@CONFERENCE{MTMT:34030843,
	title = {METABOLIKUS POLIHISZTOR VAGY EGYSZERŰ GLUTAMINGYÁR? – CITRÁTKÖR AZ ASZTROCITÁKBAN},
	url = {https://m2.mtmt.hu/api/publication/34030843},
	author = {Kokas, Márton and Kirchlechner-Farkas, Judit Mária and Gáspár, Dániel and Komlódi, Tímea and Ozohanics, Olivér and Környei, Zsuzsanna and Sváb, Gergely and Tretter, László},
	booktitle = {Membrán-Transzport konferencia : programfüzet},
	unique-id = {34030843},
	year = {2023},
	orcid-numbers = {Kokas, Márton/0000-0002-3982-4782; Komlódi, Tímea/0000-0001-9876-1411; Ozohanics, Olivér/0000-0002-2705-9921; Sváb, Gergely/0000-0002-7669-8252; Tretter, László/0000-0001-5638-2886}
}

@{MTMT:34722580,
	title = {Aminosav-, fehérje-anyagcsere},
	url = {https://m2.mtmt.hu/api/publication/34722580},
	author = {Tretter, László},
	booktitle = {Orvosi patobiokémia},
	unique-id = {34722580},
	year = {2023},
	pages = {121-142},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886}
}

@article{MTMT:33718236,
	title = {Oxoglutarate dehydrogenase complex controls glutamate-mediated neuronal death},
	url = {https://m2.mtmt.hu/api/publication/33718236},
	author = {Weidinger, A. and Milivojev, N. and Hosmann, A. and Duvigneau, J.C. and Szabo, C. and Törö, G. and Rauter, L. and Vaglio-Garro, A. and Mkrtchyan, G.V. and Trofimova, L. and Sharipov, R.R. and Surin, A.M. and Krasilnikova, I.A. and Pinelis, V.G. and Tretter, László and Moldzio, R. and Bayır, H. and Kagan, V.E. and Bunik, V.I. and Kozlov, A.V.},
	doi = {10.1016/j.redox.2023.102669},
	journal-iso = {REDOX BIOL},
	journal = {REDOX BIOLOGY},
	volume = {62},
	unique-id = {33718236},
	issn = {2213-2317},
	year = {2023},
	eissn = {2213-2317},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886}
}

@article{MTMT:32989211,
	title = {The effect of Cyclophilin D depletion on liver regeneration following associating liver partition and portal vein ligation for staged hepatectomy},
	url = {https://m2.mtmt.hu/api/publication/32989211},
	author = {Daradics, Noémi and Horváth, Gergő and Tretter, László and Paál, Ágnes and Fülöp, András and Budai, András and Szijártó, Attila},
	doi = {10.1371/journal.pone.0271606},
	journal-iso = {PLOS ONE},
	journal = {PLOS ONE},
	volume = {17},
	unique-id = {32989211},
	issn = {1932-6203},
	abstract = {Associating Liver Partition and Portal vein ligation for Staged hepatectomy (ALPPS) is a modification of two-stage hepatectomy profitable for patients with inoperable hepatic tumors by standard techniques. Unfortunately, initially poor postoperative outcome was associated with ALPPS, in which mitochondrial dysfunction played an essential role. Inhibition of cyclophilins has been already proposed to be efficient as a mitochondrial therapy in liver diseases. To investigate the effect of Cyclophilin D (CypD) depletion on mitochondrial function, biogenesis and liver regeneration following ALPPS a CypD knockout (KO) mice model was created.Male wild type (WT) (n = 30) and CypD KO (n = 30) mice underwent ALPPS procedure. Animals were terminated pre-operatively and 24, 48, 72 or 168 h after the operation. Mitochondrial functional studies and proteomic analysis were performed. Regeneration rate and mitotic activity were assessed.The CypD KO group displayed improved mitochondrial function, as both ATP production (P < 0.001) and oxygen consumption (P < 0.05) were increased compared to the WT group. The level of mitochondrial biogenesis coordinator peroxisome proliferator-activated receptor γ co-activator 1-α (PGC1-α) was also elevated in the CypD KO group (P < 0.001), which resulted in the induction of the mitochondrial oxidative phosphorylation system. Liver growth increased in the CypD KO group compared to the WT group (P < 0.001).Our study demonstrates the beneficial effect of CypD depletion on the mitochondrial vulnerability following ALPPS. Based on our results we propose that CypD inhibition should be further investigated as a possible mitochondrial therapy following ALPPS.},
	year = {2022},
	eissn = {1932-6203},
	orcid-numbers = {Daradics, Noémi/0000-0001-6918-7406; Horváth, Gergő/0000-0001-5386-9509; Tretter, László/0000-0001-5638-2886; Paál, Ágnes/0000-0003-2292-3714; Budai, András/0000-0002-4634-2140}
}

@article{MTMT:33070137,
	title = {Reverse and Forward Electron Flow-Induced H2O2 Formation Is Decreased in α-Ketoglutarate Dehydrogenase (α-KGDH) Subunit (E2 or E3) Heterozygote Knock Out Animals},
	url = {https://m2.mtmt.hu/api/publication/33070137},
	author = {Horváth, Gergő and Sváb, Gergely and Komlódi, Tímea and Ravasz, Dóra and Kacsó, Gergely and Dóczi, Judit and Chinopoulos, Christos and Ambrus, Attila and Tretter, László},
	doi = {10.3390/antiox11081487},
	journal-iso = {ANTIOXIDANTS-BASEL},
	journal = {ANTIOXIDANTS},
	volume = {11},
	unique-id = {33070137},
	abstract = {α-ketoglutarate dehydrogenase complex (KGDHc), or 2-oxoglutarate dehydrogenase complex (OGDHc) is a rate-limiting enzyme in the tricarboxylic acid cycle, that has been identified in neurodegenerative diseases such as in Alzheimer’s disease. The aim of the present study was to establish the role of the KGDHc and its subunits in the bioenergetics and reactive oxygen species (ROS) homeostasis of brain mitochondria. To study the bioenergetic profile of KGDHc, genetically modified mouse strains were used having a heterozygous knock out (KO) either in the dihydrolipoyl succinyltransferase (DLST+/−) or in the dihydrolipoyl dehydrogenase (DLD+/−) subunit. Mitochondrial oxygen consumption, hydrogen peroxide (H2O2) production, and expression of antioxidant enzymes were measured in isolated mouse brain mitochondria. Here, we demonstrate that the ADP-stimulated respiration of mitochondria was partially arrested in the transgenic animals when utilizing α-ketoglutarate (α-KG or 2-OG) as a fuel substrate. Succinate and α-glycerophosphate (α-GP), however, did not show this effect. The H2O2 production in mitochondria energized with α-KG was decreased after inhibiting the adenine nucleotide translocase and Complex I (CI) in the transgenic strains compared to the controls. Similarly, the reverse electron transfer (RET)-evoked H2O2 formation supported by succinate or α-GP were inhibited in mitochondria isolated from the transgenic animals. The decrease of RET-evoked ROS production by DLST+/− or DLD+/− KO-s puts the emphasis of the KGDHc in the pathomechanism of ischemia-reperfusion evoked oxidative stress. Supporting this notion, expression of the antioxidant enzyme glutathione peroxidase was also decreased in the KGDHc transgenic animals suggesting the attenuation of ROS-producing characteristics of KGDHc. These findings confirm the contribution of the KGDHc to the mitochondrial ROS production and in the pathomechanism of ischemia-reperfusion injury.},
	year = {2022},
	eissn = {2076-3921},
	orcid-numbers = {Horváth, Gergő/0000-0001-5386-9509; Sváb, Gergely/0000-0002-7669-8252; Komlódi, Tímea/0000-0001-9876-1411; Ravasz, Dóra/0000-0002-0510-3282; Kacsó, Gergely/0000-0003-0428-3645; Dóczi, Judit/0000-0002-5797-5074; Chinopoulos, Christos/0000-0003-0183-4149; Ambrus, Attila/0000-0001-6014-3175; Tretter, László/0000-0001-5638-2886}
}

@CONFERENCE{MTMT:34030854,
	title = {AZ α-KETOGLUTARÁT-DEHIDROGENÁZ KOMPLEX DLST+/- ÉS DLD+/- ALEGYSÉGEK KIÜTÉSÉNEK HATÁSA AZ OXIGÉNFOGYASZTÁSRA ÉS REAKTÍV OXIGÉNGYÖKKÉPZŐDÉSRE EGÉR AGYI MITOKONDRIUMOKON},
	url = {https://m2.mtmt.hu/api/publication/34030854},
	author = {Kokas, Márton and Horváth, Gergő and Tretter, László},
	booktitle = {51. Membrán-Transzport Konferencia},
	unique-id = {34030854},
	year = {2022},
	orcid-numbers = {Kokas, Márton/0000-0002-3982-4782; Horváth, Gergő/0000-0001-5386-9509; Tretter, László/0000-0001-5638-2886}
}

@misc{MTMT:34036737,
	title = {A metilénkék hatása a citokróm-c redox állapotára in vivo és in vitro körülmények között},
	url = {https://m2.mtmt.hu/api/publication/34036737},
	author = {Kokas, Márton and Sváb, Gergely and Tretter, László},
	unique-id = {34036737},
	year = {2021},
	orcid-numbers = {Kokas, Márton/0000-0002-3982-4782; Sváb, Gergely/0000-0002-7669-8252; Tretter, László/0000-0001-5638-2886}
}

@article{MTMT:31887594,
	title = {Methylene Blue Bridges the Inhibition and Produces Unusual Respiratory Changes in Complex III-Inhibited Mitochondria. Studies on Rats, Mice and Guinea Pigs},
	url = {https://m2.mtmt.hu/api/publication/31887594},
	author = {Sváb, Gergely and Kokas, Márton and Sipos, Ildikó and Ambrus, Attila and Tretter, László},
	doi = {10.3390/antiox10020305},
	journal-iso = {ANTIOXIDANTS-BASEL},
	journal = {ANTIOXIDANTS},
	volume = {10},
	unique-id = {31887594},
	year = {2021},
	eissn = {2076-3921},
	orcid-numbers = {Sváb, Gergely/0000-0002-7669-8252; Kokas, Márton/0000-0002-3982-4782; Sipos, Ildikó/0000-0003-2861-1439; Ambrus, Attila/0000-0001-6014-3175; Tretter, László/0000-0001-5638-2886}
}

@article{MTMT:31822211,
	title = {Cyclophilin D-dependent mitochondrial permeability transition amplifies inflammatory reprogramming in endotoxemia},
	url = {https://m2.mtmt.hu/api/publication/31822211},
	author = {Veres, Balázs and Erős, Krisztián and Antus, Csenge Petra and Kálmán, Nikoletta and Fónai, Fruzsina and Jakus, Péter and Boros, Éva and Hegedűs, Zoltán and Nagy, István and Tretter, László and Gallyas, Ferenc and Sümegi, Balázs},
	doi = {10.1002/2211-5463.13091},
	journal-iso = {FEBS OPEN BIO},
	journal = {FEBS OPEN BIO},
	volume = {11},
	unique-id = {31822211},
	issn = {2211-5463},
	abstract = {Microorganisms or LPS (lipopolysaccharide), an outer membrane component of Gram-negative bacteria, can induce a systemic inflammatory response that leads to sepsis, multiple organ dysfunction, and mortality. Here, we investigated the role of cyclophilin D (CypD)-dependent mitochondrial permeability transition (mPT) in the immunosuppressive phase of LPS-induced endotoxic shock. The liver plays an important role in immunity and organ dysfunction; therefore, we used liver RNA sequencing (RNAseq) data, Ingenuity® Pathway Analysis (IPA ® ) to investigate the complex role of mPT formation in inflammatory reprogramming and disease progression. LPS induced significant changes in the expression of 2844 genes, affecting 179 pathways related to mitochondrial dysfunction, defective oxidative phosphorylation, nitric oxide (NO) and reactive oxygen species (ROS) accumulation, nuclear factor, erythroid 2 like 2 (Nrf2), Toll-like receptors (TLRs), and tumor necrosis factor α receptor (TNFR)-mediated processes in wild-type mice. The disruption of CypD reduced LPS-induced alterations in gene expression and pathways involving TNFRs and TLRs, in addition to improving survival and attenuating oxidative liver damage and the related NO- and ROS-producing pathways. CypD deficiency diminished the suppressive effect of LPS on mitochondrial function, nuclear- and mitochondrial-encoded genes, and mitochondrial DNA (mtDNA) quantity, which could be critical in improving survival. Our data propose that CypD-dependent mPT is an amplifier in inflammatory reprogramming and promotes disease progression. The mortality in human sepsis and shock is associated with mitochondrial dysfunction. Prevention of mPT by CypD disruption reduces inflammatory reprogramming, mitochondrial dysfunction, and lethality; therefore, CypD can be a novel drug target in endotoxic shock and related inflammatory diseases.},
	keywords = {Inflammation; LIVER; ENDOTOXIN; ANTIOXIDANT; Mitochondria; Gene Expression; Toll-like receptor; Reprogramming; cyclophilin D; Oxidative stress},
	year = {2021},
	eissn = {2211-5463},
	pages = {684-704},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886; Gallyas, Ferenc/0000-0002-1906-4333}
}

@article{MTMT:31595275,
	title = {Bioenergetic impairment of triethylene glycol dimethacrylate- (TEGDMA-) treated dental pulp stem cells (DPSCs) and isolated brain mitochondria are amended by redox compound methylene blue},
	url = {https://m2.mtmt.hu/api/publication/31595275},
	author = {Mikulás, Krisztina Ágnes and Komlódi, Tímea and Földes, Anna and Sváb, Gergely and Horváth, Gergő and Nagy, Ádám Miklós and Ambrus, Attila and Gyulai-Gaál, Szabolcs and Gera, István and Hermann, Péter and Varga, Gábor and Tretter, László},
	doi = {10.3390/ma13163472},
	journal-iso = {MATERIALS},
	journal = {MATERIALS},
	volume = {13},
	unique-id = {31595275},
	abstract = {Background: Triethylene glycol dimethacrylate (TEGDMA) monomers released from resin matrix are toxic to dental pulp cells, induce apoptosis, oxidative stress and decrease viability. Recently, mitochondrial complex I (CI) was identified as a potential target of TEGDMA. In isolated mitochondria supported by CI, substrates oxidation and ATP synthesis were inhibited, reactive oxygen species production was stimulated. Contrary to that, respiratory Complex II was not impaired by TEGDMA. The beneficial effects of electron carrier compound methylene blue (MB) are proven in many disease models where mitochondrial involvement has been detected. In the present study, the bioenergetic effects of MB on TEGDMA-treated isolated mitochondria and on human dental pulp stem cells (DPSC) were analyzed. Methods: Isolated mitochondria and DPSC were acutely exposed to low millimolar concentrations of TEGDMA and 2 μM concentration of MB. Mitochondrial and cellular respiration and glycolytic flux were measured by high resolution respirometry and by Seahorse XF extracellular analyzer. Mitochondrial membrane potential was measured fluorimetrically. Results: MB partially restored the mitochondrial oxidation, rescued membrane potential in isolated mitochondria and significantly increased the impaired cellular O2 consumption in the presence of TEGDMA. Conclusion: MB is able to protect against TEGDMA-induced CI damage, and might provide protective effects in resin monomer exposed cells. © 2020 by the authors.},
	keywords = {Oxygen Consumption; Stem Cells; Mitochondria; Mitochondria; Substrates; Cell Death; Aromatic compounds; methylene blue; Resins; Acrylic monomers; Glycols; Triethylene glycol dimethacrylate; mitochondrial membrane potential; Mitochondrial complex; Millimolar concentrations; Dental pulp stem cells; TEGDMA; DPSC; Cellular respiration; Dental pulp stem cell (DPSC); Substrates oxidation},
	year = {2020},
	eissn = {1996-1944},
	orcid-numbers = {Mikulás, Krisztina Ágnes/0000-0002-0259-9761; Komlódi, Tímea/0000-0001-9876-1411; Földes, Anna/0000-0002-4182-7886; Sváb, Gergely/0000-0002-7669-8252; Horváth, Gergő/0000-0001-5386-9509; Nagy, Ádám Miklós/0000-0002-9568-2555; Ambrus, Attila/0000-0001-6014-3175; Gyulai-Gaál, Szabolcs/0000-0003-2419-4236; Gera, István/0000-0002-4355-7613; Hermann, Péter/0000-0002-9148-0139; Varga, Gábor/0000-0002-5506-8198; Tretter, László/0000-0001-5638-2886}
}

@article{MTMT:31523868,
	title = {The SDHB Arg230His mutation causing familial paraganglioma alters glycolysis in a new Caenorhabditis elegans model},
	url = {https://m2.mtmt.hu/api/publication/31523868},
	author = {Saskői, Éva and Hujber, Zoltán and Nyírő, Gábor and Likó, István and Mátyási, Barbara and Petővári, Gábor and Mészáros, Katalin and Kovács, Attila Lajos and Patthy, László and Supekar, Shreyas and Fan, Hao and Sváb, Gergely and Tretter, László and Sarkar, Arunabh and Nazir, Aamir and Sebestyén, Anna and Patócs, Attila Balázs and Mehta, Anil and Vellainé Takács, Krisztina},
	doi = {10.1242/dmm.044925},
	journal-iso = {DIS MODEL MECH},
	journal = {DISEASE MODELS & MECHANISMS},
	volume = {13},
	unique-id = {31523868},
	issn = {1754-8403},
	year = {2020},
	eissn = {1754-8411},
	orcid-numbers = {Saskői, Éva/0000-0001-6691-8576; Nyírő, Gábor/0000-0002-0248-0007; Likó, István/0000-0001-7668-4726; Petővári, Gábor/0000-0002-1957-2864; Sváb, Gergely/0000-0002-7669-8252; Tretter, László/0000-0001-5638-2886; Sebestyén, Anna/0000-0001-8814-4794; Patócs, Attila Balázs/0000-0001-7506-674X; Vellainé Takács, Krisztina/0000-0002-4472-0363}
}

@article{MTMT:3426954,
	title = {Mitochondrial function after associating liver partition and portal vein ligation for staged hepatectomy in an experimental model},
	url = {https://m2.mtmt.hu/api/publication/3426954},
	author = {Budai, András and Horváth, Gergő and Tretter, László and Radák, Zsolt and Koltai, Erika and Bori, Zoltán and Torma, Ferenc Gergely and Lukáts, Ákos and Röhlich, Pál and Szijártó, Attila and Fülöp, András},
	doi = {10.1002/bjs.10978},
	journal-iso = {BRIT J SURG},
	journal = {BRITISH JOURNAL OF SURGERY},
	volume = {106},
	unique-id = {3426954},
	issn = {0007-1323},
	year = {2019},
	eissn = {1365-2168},
	pages = {120-131},
	orcid-numbers = {Budai, András/0000-0002-4634-2140; Horváth, Gergő/0000-0001-5386-9509; Tretter, László/0000-0001-5638-2886; Radák, Zsolt/0000-0003-1297-6804; Koltai, Erika/0000-0002-1370-2955; Bori, Zoltán/0000-0003-1253-060X}
}

@article{MTMT:30810275,
	title = {The Mitochondrial Targets of Neuroprotective Drug Vinpocetine on Primary Neuron Cultures, Brain Capillary Endothelial Cells, Synaptosomes, and Brain Mitochondria},
	url = {https://m2.mtmt.hu/api/publication/30810275},
	author = {Sváb, Gergely and Dóczi, Judit and Gerencsér, Ákos and Ambrus, Attila and Gallyas, Ferenc and Sümegi, Balázs and Tretter, László},
	doi = {10.1007/s11064-019-02871-9},
	journal-iso = {NEUROCHEM RES},
	journal = {NEUROCHEMICAL RESEARCH},
	volume = {44},
	unique-id = {30810275},
	issn = {0364-3190},
	abstract = {Vinpocetine is considered as neuroprotectant drug and used for treatment of brain ischemia and cognitive deficiencies for decades. A number of enzymes, channels and receptors can bind vinpocetine, however the mechanisms of many effects' are still not clear. The present study investigated the effects of vinpocetine from the mitochondrial bioenergetic aspects. In primary brain capillary endothelial cells the purinergic receptor-stimulated mitochondrial Ca2+ uptake and efflux were studied. Vinpocetine exerted a partial inhibition on the mitochondrial calcium efflux. In rodent brain synaptosomes vinpocetine (30 μM) inhibited respiration in uncoupler stimulated synaptosomes and decreased H2O2 release from the nerve terminals in resting and in complex I inhibited conditions, respectively. In isolated rat brain mitochondria using either complex I or complex II substrates leak respiration was stimulated, but ADP-induced respiration was inhibited by vinpocetine. The stimulation of oxidation was associated with a small extent of membrane depolarization. Mitochondrial H2O2 production was inhibited by vinpocetine under all conditions investigated. The most pronounced effects were detected with the complex II substrate succinate. Vinpocetine also mitigated both Ca2+-induced mitochondrial Ca2+-release and Ca2+-induced mitochondrial swelling. It lowered the rate of mitochondrial ATP synthesis, while increasing ATPase activity. These results indicate more than a single mitochondrial target of this vinca alkaloid. The relevance of the affected mitochondrial mechanisms in the anti ischemic effect of vinpocetine is discussed.},
	keywords = {Oxygen Consumption; Mitochondria; Reactive oxygen species; neuroprotection; vinpocetine; Atp synthesis; UNCOUPLING; Calcium induced calcium release},
	year = {2019},
	eissn = {1573-6903},
	pages = {2435-2447},
	orcid-numbers = {Sváb, Gergely/0000-0002-7669-8252; Dóczi, Judit/0000-0002-5797-5074; Ambrus, Attila/0000-0001-6014-3175; Gallyas, Ferenc/0000-0002-1906-4333; Tretter, László/0000-0001-5638-2886}
}

@inproceedings{MTMT:30878884,
	title = {Modeling of phenylalanine metabolism and its medical relevance},
	url = {https://m2.mtmt.hu/api/publication/30878884},
	author = {Sváb, Gergely and Tretter, László and Szederkényi, Gábor},
	booktitle = {Proceedings of the Pannonian Conference on Advances in Information Technology (PCIT'2019)},
	unique-id = {30878884},
	year = {2019},
	pages = {49-58},
	orcid-numbers = {Sváb, Gergely/0000-0002-7669-8252; Tretter, László/0000-0001-5638-2886; Szederkényi, Gábor/0000-0003-4199-6089}
}

@article{MTMT:30857506,
	title = {Novel mitochondrial transition pore inhibitor N-methyl-4-isoleucine cyclosporin is a new therapeutic option in acute pancreatitis},
	url = {https://m2.mtmt.hu/api/publication/30857506},
	author = {Tóth, Emese and Maléth, József and Závogyán, Noémi and Fanczal, Júlia and Grassalkovich, Anna and Erdős, Réka and Pallagi, Petra and Horváth, Gergő and Tretter, László and Bálint, Emese Réka and Rakonczay, Zoltán and Venglovecz, Viktória and Hegyi, Péter},
	doi = {10.1113/JP278517},
	journal-iso = {J PHYSIOL-LONDON},
	journal = {JOURNAL OF PHYSIOLOGY-LONDON},
	volume = {597},
	unique-id = {30857506},
	issn = {0022-3751},
	abstract = {•Bile acids, ethanol and fatty acids deteriorate pancreatic ductal fluid and bicarbonate secretion via mitochondrial damage, ATP depletion and calcium overload. •It is known that pancreatitis inducing factors open the membrane transition pore (mPTP) channel via cyclophilin D activation in acinar cells causing calcium overload and cell death and genetic or pharmacological inhibition of mPTP improves the outcome of acute pancreatitis in animal models. •In our study we show that genetic and pharmacological inhibition of mPTP protects mitochondrial homeostasis and cell function evoked by pancreatitis-inducing factors in pancreatic ductal cells. •Our results also reveal that the novel Cyclosporin A derivative NIM811 protects mitochondrial function in acinar and ductal cells, moreover it preserves bicarbonate transport mechanisms in pancreatic ductal cells. •We found that NIM811 is highly effective in different experimental pancreatitis models and that NIM811 has no side-effects. NIM811 is a highly suitable compound to be tested in clinical trials .Background and aims Mitochondrial dysfunction plays a crucial role in the development of acute pancreatitis (AP); however, no compound is currently available with clinically acceptable effectiveness and safety. In this study, we investigated the effects of a novel mitochondrial transition pore inhibitor, N-methyl-4-isoleucine cyclosporin (NIM811), in AP. Methods Pancreatic ductal and acinar cells were isolated by enzymatic digestion from Bl/6 mice. In vitro measurements were performed by confocal microscopy and microfluorometry. Preventive effects of pharmacological (cylosporin A (2 µM), NIM811 (2 µM)) or genetic (Ppif-/- /Cyp D KO) inhibition of the mitochondrial transition pore (mPTP) during the administration of either bile acids (BA) or ethanol + fatty acids (EtOH+FA) were examined. Toxicity of mPTP inhibition was investigated by detecting apoptosis and necrosis. In vivo effects of the most promising compound, NIM811 (5 or 10 mg/kg per os), were checked in three different AP models induced by either caerulein (10 × 50 µg/kg), ethanol+ fatty acid (1.75 g/kg ethanol and 750 mg/kg palmitic acid) or 4% taurocholic acid (2 ml/kg). Results Both genetic and pharmacological inhibition of Cyp D significantly prevented the toxic effects of BA and EtOH+FA by restoring mitochondrial membrane potential (Δψ) and preventing the loss of mitochondrial mass. In vivo experiments revealed that per os administration of NIM811 has a protective effect in AP by reducing oedema, necrosis, leukocyte infiltration and serum amylase level in AP models. Administration of NIM811 had no toxic effects. Conclusion The novel mitochondrial transition pore inhibitor NIM811 seems to be an exceptionally good candidate compound for clinical trials in AP. This article is protected by copyright. All rights reserved.},
	keywords = {Acute pancreatitis; cyclophilin D; NIM811; mitochondrial transition pore},
	year = {2019},
	eissn = {1469-7793},
	pages = {5879-5898},
	orcid-numbers = {Maléth, József/0000-0001-5768-3090; Fanczal, Júlia/0000-0001-7356-3857; Pallagi, Petra/0000-0001-8906-0840; Horváth, Gergő/0000-0001-5386-9509; Tretter, László/0000-0001-5638-2886; Rakonczay, Zoltán/0000-0002-1499-3416; Venglovecz, Viktória/0000-0002-2316-7247; Hegyi, Péter/0000-0003-0399-7259}
}

@article{MTMT:30413397,
	title = {Genetic inhibition of cyclophilin d protects against bile acid or ethanol and fatty acid induced pancreatic ductal epithelial cell damage in mice},
	url = {https://m2.mtmt.hu/api/publication/30413397},
	author = {Tóth, Emese and Maléth, József and R., Erdos and N., Závogyán and Tretter, László and G., Horvath and Z.J., Rakonczay and Hegyi, Péter},
	journal-iso = {UEG JOURNAL},
	journal = {UNITED EUROPEAN GASTROENTEROLOGY JOURNAL},
	volume = {6},
	unique-id = {30413397},
	issn = {2050-6406},
	year = {2018},
	eissn = {2050-6414},
	pages = {A102},
	orcid-numbers = {Maléth, József/0000-0001-5768-3090; Tretter, László/0000-0001-5638-2886; Hegyi, Péter/0000-0003-0399-7259}
}

@article{MTMT:30318236,
	title = {GABA, glutamine, glutamate oxidation and succinic semialdehyde dehydrogenase expression in human gliomas},
	url = {https://m2.mtmt.hu/api/publication/30318236},
	author = {Hujber, Zoltán and Horváth, Gergő and Petővári, Gábor and Krencz, Ildikó and Dankó, Titanilla and Mészáros, Katalin and Rajnai, Hajnalka and Szoboszlai, Norbert and Leenders, William P J and Jeney, András and Tretter, László and Sebestyén, Anna},
	doi = {10.1186/s13046-018-0946-5},
	journal-iso = {J EXP CLIN CANC RES},
	journal = {JOURNAL OF EXPERIMENTAL AND CLINICAL CANCER RESEARCH},
	volume = {37},
	unique-id = {30318236},
	issn = {0392-9078},
	abstract = {Bioenergetic characterisation of malignant tissues revealed that different tumour cells can catabolise multiple substrates as salvage pathways, in response to metabolic stress. Altered metabolism in gliomas has received a lot of attention, especially in relation to IDH mutations, and the associated oncometabolite D-2-hydroxyglutarate (2-HG) that impact on metabolism, epigenetics and redox status. Astrocytomas and oligodendrogliomas, collectively called diffuse gliomas, are derived from astrocytes and oligodendrocytes that are in metabolic symbiosis with neurons; astrocytes can catabolise neuron-derived glutamate and gamma-aminobutyric acid (GABA) for supporting and regulating neuronal functions.Metabolic characteristics of human glioma cell models - including mitochondrial function, glycolytic pathway and energy substrate oxidation - in relation to IDH mutation status and after 2-HG incubation were studied to understand the Janus-faced role of IDH1 mutations in the progression of gliomas/astrocytomas. The metabolic and bioenergetic features were identified in glioma cells using wild-type and genetically engineered IDH1-mutant glioblastoma cell lines by metabolic analyses with Seahorse, protein expression studies and liquid chromatography-mass spectrometry.U251 glioma cells were characterised by high levels of glutamine, glutamate and GABA oxidation. Succinic semialdehyde dehydrogenase (SSADH) expression was correlated to GABA oxidation. GABA addition to glioma cells increased proliferation rates. Expression of mutated IDH1 and treatment with 2-HG reduced glutamine and GABA oxidation, diminished the pro-proliferative effect of GABA in SSADH expressing cells. SSADH protein overexpression was found in almost all studied human cases with no significant association between SSADH expression and clinicopathological parameters (e.g. IDH mutation).Our findings demonstrate that SSADH expression may participate in the oxidation and/or consumption of GABA in gliomas, furthermore, GABA oxidation capacity may contribute to proliferation and worse prognosis of gliomas. Moreover, IDH mutation and 2-HG production inhibit GABA oxidation in glioma cells. Based on these data, GABA oxidation and SSADH activity could be additional therapeutic targets in gliomas/glioblastomas.},
	keywords = {GLIOMA; glutamine; GABA; Bioenergetics; 2-hydroxyglutarate; IDH1 mutation; Succinic semialdehyde dehydrogenase},
	year = {2018},
	eissn = {1756-9966},
	orcid-numbers = {Horváth, Gergő/0000-0001-5386-9509; Petővári, Gábor/0000-0002-1957-2864; Krencz, Ildikó/0000-0003-3601-8723; Dankó, Titanilla/0000-0002-7419-4560; Rajnai, Hajnalka/0000-0003-0934-5366; Szoboszlai, Norbert/0000-0002-3991-3996; Tretter, László/0000-0001-5638-2886; Sebestyén, Anna/0000-0001-8814-4794}
}

@article{MTMT:3405043,
	title = {Membrane potential and delta pH dependency of reverse electron transport-associated hydrogen peroxide production in brain and heart mitochondria},
	url = {https://m2.mtmt.hu/api/publication/3405043},
	author = {Komlódi, Tímea and Geibl, FF and Sassani, M and Ambrus, Attila and Tretter, László},
	doi = {10.1007/s10863-018-9766-8},
	journal-iso = {J BIOENERG BIOMEMBR},
	journal = {JOURNAL OF BIOENERGETICS AND BIOMEMBRANES},
	volume = {50},
	unique-id = {3405043},
	issn = {0145-479X},
	abstract = {Succinate-driven reverse electron transport (RET) is one of the main sources of mitochondrial reactive oxygen species (mtROS) in ischemia-reperfusion injury. RET is dependent on mitochondrial membrane potential (Deltapsim) and transmembrane pH difference (DeltapH), components of the proton motive force (pmf); a decrease in Deltapsim and/or DeltapH inhibits RET. In this study we aimed to determine which component of the pmf displays the more dominant effect on RET-provoked ROS generation in isolated guinea pig brain and heart mitochondria respiring on succinate or alpha-glycerophosphate (alpha-GP). Deltapsim was detected via safranin fluorescence and a TPP(+) electrode, the rate of H2O2 formation was measured by Amplex UltraRed, the intramitochondrial pH (pHin) was assessed via BCECF fluorescence. Ionophores were used to dissect the effects of the two components of pmf. The K(+)/H(+) exchanger, nigericin lowered pHin and DeltapH, followed by a compensatory increase in Deltapsim that led to an augmented H2O2 production. Valinomycin, a K(+) ionophore, at low [K(+)] increased DeltapH and pHin, decreased Deltapsim, which resulted in a decline in H2O2 formation. It was concluded that Deltapsim is dominant over pH in modulating the succinate- and alpha-GP-evoked RET. The elevation of extramitochondrial pH was accompanied by an enhanced H2O2 release and a decreased pH. This phenomenon reveals that from the pH component not pH, but rather absolute value of pH has higher impact on the rate of mtROS formation. Minor decrease of Deltapsim might be applied as a therapeutic strategy to attenuate RET-driven ROS generation in ischemia-reperfusion injury.},
	year = {2018},
	eissn = {1573-6881},
	pages = {355-365},
	orcid-numbers = {Komlódi, Tímea/0000-0001-9876-1411; Ambrus, Attila/0000-0001-6014-3175; Tretter, László/0000-0001-5638-2886}
}

@article{MTMT:3362693,
	title = {Triethylene glycol dimethacrylate impairs bioenergetic functions and induces oxidative stress in mitochondria via inhibiting respiratory Complex I},
	url = {https://m2.mtmt.hu/api/publication/3362693},
	author = {Mikulás, Krisztina Ágnes and Hermann, Péter and Gera, István and Komlódi, Tímea and Horváth, Gergő and Ambrus, Attila and Tretter, László},
	doi = {10.1016/j.dental.2018.03.012},
	journal-iso = {DENT MATER},
	journal = {DENTAL MATERIALS},
	volume = {34},
	unique-id = {3362693},
	issn = {0109-5641},
	abstract = {OBJECTIVES: Earlier studies demonstrated that dental resin monomers lower cellular viability and provoke oxidative stress. Reactive oxygen species (ROS) formation has a key role in triethylene glycol dimethacrylate (TEGDMA) induced adverse reactions. In the present study the effects of TEGDMA on mitochondrial functions were investigated to identify a direct molecular target for cytotoxicity. METHODS: Mitochondria were isolated from guinea pig brain. The most important bioenergetic parameters, oxygen consumption, membrane potential (DeltaPsim), and ATP production were assessed. Mitochondrial H2O2 production and elimination and the NAD(P)H level reported on redox balance. RESULTS: Mitochondria were supported with respiratory substrates to be oxidized by either Complex I (CI) or Complex II (CII). DeltaPsim was depolarized, respiration and ATP production was greatly diminished when applying CI substrates in the presence of TEGDMA. The same parameters remained essentially unaffected when CII substrate plus TEGDMA were applied. H2O2 production by mitochondria was significantly stimulated by TEGDMA in the presence of CI substrates. In the presence of TEGDMA mitochondrial elimination of exogenous H2O2 was impaired. When CII substrate supported the mitochondria in the absence of ADP the H2O2 generation was decreased. NADH autofluorescence results also demonstrated the inhibitory effect of TEGDMA on CI activity. SIGNIFICANCE: TEGDMA inhibits CI in the respiratory chain, which explains effects induced by TEGDMA on redox homeostasis, apoptotic and necrotic cell deaths described in previous studies. Identification of the molecular target of TEGDMA may influence the development of relevant biomaterials and may induce new therapeutic strategies to control the adverse effects of resin monomers.},
	year = {2018},
	eissn = {1879-0097},
	pages = {e166-e181},
	orcid-numbers = {Mikulás, Krisztina Ágnes/0000-0002-0259-9761; Hermann, Péter/0000-0002-9148-0139; Gera, István/0000-0002-4355-7613; Komlódi, Tímea/0000-0001-9876-1411; Horváth, Gergő/0000-0001-5386-9509; Ambrus, Attila/0000-0001-6014-3175; Tretter, László/0000-0001-5638-2886}
}

@article{MTMT:3308092,
	title = {Versatility of microglial bioenergetic machinery under starving conditions},
	url = {https://m2.mtmt.hu/api/publication/3308092},
	author = {Nagy, Ádám Miklós and Fekete, Rebeka and Horváth, Gergő and Koncsos, Gábor and Kriston, Csilla and Sebestyén, Anna and Giricz, Zoltán and Környei, Zsuzsanna and Madarász, Emilia and Tretter, László},
	doi = {10.1016/j.bbabio.2017.12.002},
	journal-iso = {BBA-BIOENERGETICS},
	journal = {BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS},
	volume = {1859},
	unique-id = {3308092},
	issn = {0005-2728},
	abstract = {Microglia are highly dynamic cells in the brain. Their functional diversity and phenotypic versatility brought microglial energy metabolism into the focus of research. Although it is known that microenvironmental cues shape microglial phenotype, their bioenergetic response to local nutrient availability remains unclear. In the present study effects of energy substrates on the oxidative and glycolytic metabolism of primary - and BV-2 microglial cells were investigated. Cellular oxygen consumption, glycolytic activity, the levels of intracellular ATP/ADP, autophagy, mTOR phosphorylation, apoptosis and cell viability were measured in the absence of nutrients or in the presence of physiological energy substrates: glutamine, glucose, lactate, pyruvate or ketone bodies. All of the oxidative energy metabolites increased the rate of basal and maximal respiration. However, the addition of glucose decreased microglial oxidative metabolism and glycolytic activity was enhanced. Increased ATP/ADP ratio and cell viability, activation of the mTOR and reduction of autophagic activity were observed in glutamine-supplemented media. Moreover, moderate and transient oxidation of ketone bodies was highly enhanced by glutamine, suggesting that anaplerosis of the TCA-cycle could stimulate ketone body oxidation. It is concluded that microglia show high metabolic plasticity and utilize a wide range of substrates. Among them glutamine is the most efficient metabolite. To our knowledge these data provide the first account of microglial direct metabolic response to nutrients under short-term starvation and demonstrate that microglia exhibit versatile metabolic machinery. Our finding that microglia have a distinct bioenergetic profile provides a critical foundation for specifying microglial contributions to brain energy metabolism.},
	keywords = {Autophagy},
	year = {2018},
	eissn = {1879-2650},
	pages = {201-214},
	orcid-numbers = {Nagy, Ádám Miklós/0000-0002-9568-2555; Horváth, Gergő/0000-0001-5386-9509; Koncsos, Gábor/0000-0001-5451-8719; Sebestyén, Anna/0000-0001-8814-4794; Giricz, Zoltán/0000-0003-2036-8665; Tretter, László/0000-0001-5638-2886}
}

@{MTMT:3412404,
	title = {A Simple Dynamic Model for Mitochondrial Metabolism},
	url = {https://m2.mtmt.hu/api/publication/3412404},
	author = {Sváb, Gergely and Szederkényi, Gábor and Horváth, G and Tretter, László},
	booktitle = {MATHMOD 2018 Extended Abstract Volume},
	unique-id = {3412404},
	year = {2018},
	pages = {11-12},
	orcid-numbers = {Sváb, Gergely/0000-0002-7669-8252; Szederkényi, Gábor/0000-0003-4199-6089; Tretter, László/0000-0001-5638-2886}
}

@article{MTMT:3414412,
	title = {Bioenergetics: From atomic resolution structures to cancer metabolism},
	url = {https://m2.mtmt.hu/api/publication/3414412},
	author = {Tretter, László and Zimányi, László},
	doi = {10.1016/j.bbabio.2018.07.006},
	journal-iso = {BBA-BIOENERGETICS},
	journal = {BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS},
	volume = {1859},
	unique-id = {3414412},
	issn = {0005-2728},
	year = {2018},
	eissn = {1879-2650},
	pages = {631-632},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886; Zimányi, László/0000-0002-5101-2023}
}

@article{MTMT:3211755,
	title = {The Putative Drp1 Inhibitor mdivi-1 Is a Reversible Mitochondrial Complex I Inhibitor that Modulates Reactive Oxygen Species},
	url = {https://m2.mtmt.hu/api/publication/3211755},
	author = {Bordt, EA and Clerc, P and Roelofs, BA and Saladino, AJ and Tretter, László and Ádám, Veronika and Cherok, E and Khalil, A and Yadava, N and Ge, SX and Francis, TC and Kennedy, NW and Picton, LK and Kumar, T and Uppuluri, S and Miller, AM and Itoh, K and Karbowski, M and Sesaki, H and Hill, RB and Polster, BM},
	doi = {10.1016/j.devcel.2017.02.020},
	journal-iso = {DEV CELL},
	journal = {DEVELOPMENTAL CELL},
	volume = {40},
	unique-id = {3211755},
	issn = {1534-5807},
	abstract = {Mitochondrial fission mediated by the GTPase dynamin-related protein 1 (Drp1) is an attractive drug target in numerous maladies that range from heart disease to neurodegenerative disorders. The compound mdivi-1 is widely reported to inhibit Drp1-dependent fission, elongate mitochondria, and mitigate brain injury. Here, we show that mdivi-1 reversibly inhibits mitochondrial complex I-dependent O2 consumption and reverse electron transfer-mediated reactive oxygen species (ROS) production at concentrations (e.g., 50 μM) used to target mitochondrial fission. Respiratory inhibition is rescued by bypassing complex I using yeast NADH dehydrogenase Ndi1. Unexpectedly, respiratory impairment by mdivi-1 occurs without mitochondrial elongation, is not mimicked by Drp1 deletion, and is observed in Drp1-deficient fibroblasts. In addition, mdivi-1 poorly inhibits recombinant Drp1 GTPase activity (Ki > 1.2 mM). Overall, these results suggest that mdivi-1 is not a specific Drp1 inhibitor. The ability of mdivi-1 to reversibly inhibit complex I and modify mitochondrial ROS production may contribute to effects observed in disease models. © 2017 Elsevier Inc.},
	keywords = {Brain; Mitochondria; NEURON; FRAGMENTATION; FISSION; Respiration; SUPEROXIDE; Bioenergetics; SUCCINATE; reverse electron transfer},
	year = {2017},
	eissn = {1878-1551},
	pages = {583-594.e6},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886; Ádám, Veronika/0000-0002-8350-8701}
}

@article{MTMT:3228818,
	title = {Methylene blue stimulates substrate-level phosphorylation catalysed by succinyl-CoA ligase in the citric acid cycle},
	url = {https://m2.mtmt.hu/api/publication/3228818},
	author = {Komlódi, Tímea and Tretter, László},
	doi = {10.1016/j.neuropharm.2017.05.009},
	journal-iso = {NEUROPHARMACOLOGY},
	journal = {NEUROPHARMACOLOGY},
	volume = {123},
	unique-id = {3228818},
	issn = {0028-3908},
	abstract = {Methylene blue (MB), a potential neuroprotective agent, is efficient in various neurodegenerative disease models. Beneficial effects of MB have been attributed to improvements in mitochondrial functions. Substrate-level phosphorylation (SLP) results in the production of ATP independent from the ATP synthase (ATP-ase). In energetically compromised mitochondria, ATP produced by SLP can prevent the reversal of the adenine nucleotide translocase and thus the hydrolysis of glycolytic ATP. The aim of the present study was to investigate the effect of MB on mitochondrial SLP catalysed by succinyl-CoA ligase. Measurements were carried out on isolated guinea pig cortical mitochondria respiring on α-ketoglutarate, glutamate, malate or succinate. The mitochondrial functions and parameters like ATP synthesis, oxygen consumption, membrane potential, and NAD(P)H level were followed online, in parallel with the redox state of MB. SLP-mediated ATP synthesis was measured in the presence of inhibitors for ATP-ase and adenylate kinase. In the presence of the ATP-ase inhibitor oligomycin MB stimulated respiration with all of the respiratory substrates. However, the rate of ATP synthesis increased only with substrates α-ketoglutarate and glutamate (forming succinyl-CoA). MB efficiently stimulated SLP and restored the membrane potential in mitochondria also with the combined inhibition of Complex I and ATP synthase. ATP formed by SLP alleviated the energetic insufficiency generated by the lack of oxidative phosphorylation. Thus, the MB-mediated stimulation of SLP might be important in maintaining the energetic competence of mitochondria and in preventing the mitochondrial hydrolysis of glycolytic ATP. The mitochondrial effects of MB are explained by the ability to accept electrons from reducing equivalents and transfer them to cytochrome c bypassing the respiratory Complexes I and III. © 2017 Elsevier Ltd.},
	keywords = {Mitochondria; neurodegeneration; neuroprotection; methylene blue; Citric Acid Cycle; Substrate-level phosphorylation},
	year = {2017},
	eissn = {1873-7064},
	pages = {287-298},
	orcid-numbers = {Komlódi, Tímea/0000-0001-9876-1411; Tretter, László/0000-0001-5638-2886}
}

@article{MTMT:2940351,
	title = {Abolition of mitochondrial substrate-level phosphorylation by itaconic acid produced by LPS-induced Irg1 expression in cells of murine macrophage lineage},
	url = {https://m2.mtmt.hu/api/publication/2940351},
	author = {Németh, Beáta and Dóczi, Judit and Csete, Dániel and Kacsó, Gergely and Ravasz, Dóra and Daniel, Adams and Kiss, Gergely and Nagy, Ádám Miklós and Horváth, Gergő and Tretter, László and Mócsai, Attila and Csépányi-Kömi, Roland and Iordanov, Iordan and Ádám, Veronika and Chinopoulos, Christos},
	doi = {10.1096/fj.15-279398},
	journal-iso = {FASEB J},
	journal = {FASEB JOURNAL},
	volume = {30},
	unique-id = {2940351},
	issn = {0892-6638},
	year = {2016},
	eissn = {1530-6860},
	pages = {286-300},
	orcid-numbers = {Németh, Beáta/0000-0002-2334-9796; Dóczi, Judit/0000-0002-5797-5074; Csete, Dániel/0000-0001-8057-225X; Kacsó, Gergely/0000-0003-0428-3645; Ravasz, Dóra/0000-0002-0510-3282; Nagy, Ádám Miklós/0000-0002-9568-2555; Horváth, Gergő/0000-0001-5386-9509; Tretter, László/0000-0001-5638-2886; Mócsai, Attila/0000-0002-0512-1157; Csépányi-Kömi, Roland/0000-0001-6825-7142; Iordanov, Iordan/0000-0001-8251-5857; Ádám, Veronika/0000-0002-8350-8701; Chinopoulos, Christos/0000-0003-0183-4149}
}

@article{MTMT:3111904,
	title = {TP53 mutation hits energy metabolism and increases glycolysis in breast cancer},
	url = {https://m2.mtmt.hu/api/publication/3111904},
	author = {Papp, Hajnalka and Pongor, Lőrinc and Munkácsy, Gyöngyi and Horváth, Gergő and Nagy, Ádám Miklós and Ambrus, Attila and Hauser, Péter and Szabó, András and Tretter, László and Győrffy, Balázs},
	doi = {10.18632/oncotarget.11594},
	journal-iso = {ONCOTARGET},
	journal = {ONCOTARGET},
	volume = {7},
	unique-id = {3111904},
	abstract = {Promising new hallmarks of cancer is alteration of energy metabolism that involves molecular mechanisms shifting cancer cells to aerobe glycolysis. Our goal was to evaluate the correlation between mutation in the commonly mutated tumor suppressor gene TP53 and metabolism. We established a database comprising mutation and RNA-seq expression data of the TCGA repository and performed receiver operating characteristics (ROC) analysis to compare expression of each gene between TP53 mutated and wild type samples. All together 762 breast cancer samples were evaluated of which 215 had TP53 mutation. Top up-regulated metabolic genes include glycolytic enzymes (e.g. HK3, GPI, GAPDH, PGK1, ENO1), glycolysis regulator (PDK1) and pentose phosphate pathway enzymes (PGD, TKT, RPIA). Gluconeogenesis enzymes (G6PC3, FBP1) were down-regulated. Oxygen consumption and extracellular acidification rates were measured in TP53 wild type and mutant breast cell lines with a microfluorimetric analyzer. Applying metabolic inhibitors in the presence and absence of D-glucose and L-glutamine in cell culture experiments resulted in higher glycolytic and mitochondrial activity in TP53 mutant breast cancer cell lines. In summary, TP53 mutation influences energy metabolism at multiple levels. Our results provide evidence for the synergistic activation of multiple hallmarks linking to these the mutation status of a key driver gene.},
	year = {2016},
	eissn = {1949-2553},
	pages = {67183-67195},
	orcid-numbers = {Pongor, Lőrinc/0000-0001-5917-4628; Munkácsy, Gyöngyi/0000-0001-9124-4788; Horváth, Gergő/0000-0001-5386-9509; Nagy, Ádám Miklós/0000-0002-9568-2555; Ambrus, Attila/0000-0001-6014-3175; Hauser, Péter/0000-0002-8307-8975; Szabó, András/0000-0001-8320-4946; Tretter, László/0000-0001-5638-2886; Győrffy, Balázs/0000-0002-5772-3766}
}

@article{MTMT:3108583,
	title = {Differentiation-Dependent Energy Production and Metabolite Utilization: A Comparative Study on Neural Stem Cells, Neurons, and Astrocytes.},
	url = {https://m2.mtmt.hu/api/publication/3108583},
	author = {Jády, Attila and Nagy, Ádám Miklós and Kőhidi, Tímea and Ferenczi, Szilamér and Tretter, László and Madarász, Emilia},
	doi = {10.1089/scd.2015.0388},
	journal-iso = {STEM CELLS DEV},
	journal = {STEM CELLS AND DEVELOPMENT},
	volume = {25},
	unique-id = {3108583},
	issn = {1547-3287},
	abstract = {While it is evident that the metabolic machinery of stem cells should be fairly different from that of differentiated neurons, the basic energy production pathways in neural stem cells (NSCs) or in neurons are far from clear. Using the model of in vitro neuron production by NE-4C NSCs, this study focused on the metabolic changes taking place during the in vitro neuronal differentiation. O2 consumption, H(+) production, and metabolic responses to single metabolites were measured in cultures of NSCs and in their neuronal derivatives, as well as in primary neuronal and astroglial cultures. In metabolite-free solutions, NSCs consumed little O2 and displayed a higher level of mitochondrial proton leak than neurons. In stem cells, glycolysis was the main source of energy for the survival of a 2.5-h period of metabolite deprivation. In contrast, stem cell-derived or primary neurons sustained a high-level oxidative phosphorylation during metabolite deprivation, indicating the consumption of own cellular material for energy production. The stem cells increased O2 consumption and mitochondrial ATP production in response to single metabolites (with the exception of glucose), showing rapid adaptation of the metabolic machinery to the available resources. In contrast, single metabolites did not increase the O2 consumption of neurons or astrocytes. In "starving" neurons, neither lactate nor pyruvate was utilized for mitochondrial ATP production. Gene expression studies also suggested that aerobic glycolysis and rapid metabolic adaptation characterize the NE-4C NSCs, while autophagy and alternative glucose utilization play important roles in the metabolism of stem cell-derived neurons.},
	year = {2016},
	eissn = {1557-8534},
	pages = {995-1005},
	orcid-numbers = {Nagy, Ádám Miklós/0000-0002-9568-2555; Tretter, László/0000-0001-5638-2886}
}

@article{MTMT:3101389,
	title = {Diastolic dysfunction in prediabetic male rats: role of mitochondrial oxidative stress},
	url = {https://m2.mtmt.hu/api/publication/3101389},
	author = {Koncsos, Gábor and Varga, Zoltán and Baranyai, Tamás and Boengler, K and Rohrbach, S and Li, L and Schluter, KD and Schreckenberg, R and Radovits, Tamás and Oláh, Attila and Mátyás, Csaba and Lux, Árpád and Al-Khrasani, Mahmoud and Komlódi, Tímea and Bukosza, Éva Nóra and Máthé, Domokos and Deres, László and Bartekova, M and Rajtik, T and Adameova, A and Szigeti, Krisztián and Hamar, Péter and Helyes, Zsuzsanna and Tretter, László and Pacher, Pál and Merkely, Béla Péter and Giricz, Zoltán and Schulz, R and Ferdinandy, Péter},
	doi = {10.1152/ajpheart.00049.2016},
	journal-iso = {AM J PHYSIOL HEART C},
	journal = {AMERICAN JOURNAL OF PHYSIOLOGY: HEART AND CIRCULATORY PHYSIOLOGY},
	volume = {311},
	unique-id = {3101389},
	issn = {0363-6135},
	abstract = {Although incidence and prevalence of prediabetes are increasing, little is known on its cardiac effects. Therefore, our aim was to investigate the effect of prediabetes on cardiac function and to characterize parameters and pathways associated with deteriorated cardiac performance. Long-Evans rats were fed with either control or high-fat chow for 21 weeks and treated with a single low dose (20 mg/kg) streptozotocin at week 4. High-fat and streptozotocin treatment induced prediabetes as characterized by slightly elevated fasting blood glucose, impaired glucose- and insulin tolerance, increased visceral adipose tissue and plasma leptin levels, as well as sensory neuropathy. In prediabetic animals a mild diastolic dysfunction was observed, the number of myocardial lipid droplets increased, and left ventricular mass and wall thickness were elevated, however, no molecular sign of fibrosis or cardiac hypertrophy was evidenced. In prediabetes, production of reactive oxygen species was elevated in subsarcolemmal mitochondria. Expression of mitofusin-2 was increased while the phosphorylation of phospholamban and expression of Bcl-2/adenovirus E1B 19 kDa protein-interacting protein 3 (BNIP3, a marker of mitophagy) decreased. However, expression of other markers of cardiac auto- and mitophagy, mitochondrial dynamics, inflammation, heat shock proteins, Ca2+/calmodulin-dependent protein kinase II, mTOR or apoptotic pathways were unchanged in prediabetes. This is the first comprehensive analysis of cardiac effects of prediabetes indicating that mild diastolic dysfunction and cardiac hypertrophy are multifactorial phenomena which is associated with early changes in mitophagy, cardiac lipid accumulation and elevated oxidative stress, and that prediabetes-induced oxidative stress originates from the subsarcolemmal mitochondria.},
	year = {2016},
	eissn = {1522-1539},
	pages = {H927-H943},
	orcid-numbers = {Koncsos, Gábor/0000-0001-5451-8719; Varga, Zoltán/0000-0002-2758-0784; Baranyai, Tamás/0000-0002-9378-8938; Mátyás, Csaba/0000-0001-6095-7611; Lux, Árpád/0000-0002-7048-5619; Al-Khrasani, Mahmoud/0000-0001-8488-3266; Komlódi, Tímea/0000-0001-9876-1411; Hamar, Péter/0000-0002-1095-3564; Tretter, László/0000-0001-5638-2886; Pacher, Pál/0000-0001-7036-8108; Merkely, Béla Péter/0000-0001-6514-0723; Giricz, Zoltán/0000-0003-2036-8665; Ferdinandy, Péter/0000-0002-6424-6806}
}

@article{MTMT:3037326,
	title = {Succinate, an intermediate in metabolism, signal transduction, ROS, hypoxia, and tumorigenesis.},
	url = {https://m2.mtmt.hu/api/publication/3037326},
	author = {Tretter, László and Patócs, Attila Balázs and Chinopoulos, Christos},
	doi = {10.1016/j.bbabio.2016.03.012},
	journal-iso = {BBA-BIOENERGETICS},
	journal = {BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS},
	volume = {1857},
	unique-id = {3037326},
	issn = {0005-2728},
	abstract = {Succinate is an important metabolite at the cross-road of several metabolic pathways, also involved in the formation and elimination of reactive oxygen species. However, it is becoming increasingly apparent that its realm extends to epigenetics, tumorigenesis, signal transduction, endo- and paracrine modulation and inflammation. Here we review the pathways encompassing succinate as a metabolite or a signal and how these may interact in normal and pathological conditions.1.},
	year = {2016},
	eissn = {1879-2650},
	pages = {1086-1101},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886; Patócs, Attila Balázs/0000-0001-7506-674X; Chinopoulos, Christos/0000-0003-0183-4149}
}

@article{MTMT:3082316,
	title = {Chronic Activation of gamma2 AMPK Induces Obesity and Reduces beta Cell Function},
	url = {https://m2.mtmt.hu/api/publication/3082316},
	author = {Yavari, A and Stocker, CJ and Ghaffari, S and Wargent, ET and Steeples, V and Czibik, G and Pinter, K and Bellahcene, M and Woods, A and Martinez, de Morentin PB and Cansell, C and Lam, BY and Chuster, A and Petkevicius, K and Nguyen-Tu, MS and Martinez-Sanchez, A and Pullen, TJ and Oliver, PL and Stockenhuber, A and Nguyen, C and Lazdam, M and O'Dowd, JF and Harikumar, P and Tóth, Mónika and Beall, C and Kyriakou, T and Parnis, J and Sarma, D and Katritsis, G and Wortmann, DD and Harper, AR and Brown, LA and Willows, R and Gandra, S and Poncio, V and de Oliveira, Figueiredo MJ and Qi, NR and Peirson, SN and McCrimmon, RJ and Gereben, Balázs and Tretter, László and Fekete, Csaba and Redwood, C and Yeo, GS and Heisler, LK and Rutter, GA and Smith, MA and Withers, DJ and Carling, D and Sternick, EB and Arch, JR and Cawthorne, MA and Watkins, H and Ashrafian, H},
	doi = {10.1016/j.cmet.2016.04.003},
	journal-iso = {CELL METAB},
	journal = {CELL METABOLISM},
	volume = {23},
	unique-id = {3082316},
	issn = {1550-4131},
	abstract = {Despite significant advances in our understanding of the biology determining systemic energy homeostasis, the treatment of obesity remains a medical challenge. Activation of AMP-activated protein kinase (AMPK) has been proposed as an attractive strategy for the treatment of obesity and its complications. AMPK is a conserved, ubiquitously expressed, heterotrimeric serine/threonine kinase whose short-term activation has multiple beneficial metabolic effects. Whether these translate into long-term benefits for obesity and its complications is unknown. Here, we observe that mice with chronic AMPK activation, resulting from mutation of the AMPK gamma2 subunit, exhibit ghrelin signaling-dependent hyperphagia, obesity, and impaired pancreatic islet insulin secretion. Humans bearing the homologous mutation manifest a congruent phenotype. Our studies highlight that long-term AMPK activation throughout all tissues can have adverse metabolic consequences, with implications for pharmacological strategies seeking to chronically activate AMPK systemically to treat metabolic disease.},
	year = {2016},
	eissn = {1932-7420},
	pages = {821-836},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886}
}

@article{MTMT:2953634,
	title = {Formation of reactive oxygen species by human and bacterial pyruvate and 2- oxoglutarate dehydrogenase multienzyme complexes reconstituted from recombinant components},
	url = {https://m2.mtmt.hu/api/publication/2953634},
	author = {Ambrus, Attila and Nemeria, NS and Törőcsik, Beáta and Tretter, László and Nilsson, M and Jordan, F and Ádám, Veronika},
	doi = {10.1016/j.freeradbiomed.2015.10.001},
	journal-iso = {FREE RADICAL BIO MED},
	journal = {FREE RADICAL BIOLOGY AND MEDICINE},
	volume = {89},
	unique-id = {2953634},
	issn = {0891-5849},
	year = {2015},
	eissn = {1873-4596},
	pages = {642-650},
	orcid-numbers = {Ambrus, Attila/0000-0001-6014-3175; Törőcsik, Beáta/0000-0002-9838-3710; Tretter, László/0000-0001-5638-2886; Ádám, Veronika/0000-0002-8350-8701}
}

@article{MTMT:2943971,
	title = {Lack of cyclophilin D protects against the development of acute lung injury in endotoxemia.},
	url = {https://m2.mtmt.hu/api/publication/2943971},
	author = {Fónai, Fruzsina and Pribér, János Krisztián and Jakus, Péter and Kálmán, Nikoletta and Antus, Csenge Petra and Pollák, Edit and Karsai, G and Tretter, László and Sümegi, Balázs and Veres, Balázs},
	doi = {10.1016/j.bbadis.2015.09.004},
	journal-iso = {BBA-MOL BASIS DIS},
	journal = {BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE},
	volume = {1852},
	unique-id = {2943971},
	issn = {0925-4439},
	abstract = {Sepsis caused by LPS is characterized by an intense systemic inflammatory response affecting the lungs, causing acute lung injury (ALI). Dysfunction of mitochondria and the role of reactive oxygen (ROS) and nitrogen species produced by mitochondria have already been proposed in the pathogenesis of sepsis; however, the exact molecular mechanism is poorly understood. Oxidative stress induces cyclophilin D (CypD)-dependent mitochondrial permeability transition (mPT), leading to organ failure in sepsis. In previous studies mPT was inhibited by cyclosporine A which, beside CypD, inhibits cyclophilin A, B, C and calcineurin, regulating cell death and inflammatory pathways. The immunomodulatory side effects of cyclosporine A make it unfavorable in inflammatory model systems. To avoid these uncertainties in the molecular mechanism, we studied endotoxemia-induced ALI in CypD-/- mice providing unambiguous data for the pathological role of CypD-dependent mPT in ALI. Our key finding is that the loss of this essential protein improves survival rate and it can intensely ameliorate endotoxin-induced lung injury through attenuated proinflammatory cytokine release, down-regulation of redox sensitive cellular pathways such as MAPKs, Akt, and NF-kappaB and reducing the production of ROS. Functional inhibition of NF-kappaB was confirmed by decreased expression of NF-kappaB-mediated proinflammatory genes. We demonstrated that impaired mPT due to the lack of CypD reduces the severity of endotoxemia-induced lung injury suggesting that CypD specific inhibitors might have a great therapeutic potential in sepsis-induced organ failure. Our data highlight a previously unknown regulatory function of mitochondria during inflammatory response.},
	year = {2015},
	eissn = {1879-260X},
	pages = {2563-2573},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886}
}

@article{MTMT:2853101,
	title = {Cyclophilin D disruption attenuates lipopolysaccharide-induced inflammatory response in primary mouse macrophages.},
	url = {https://m2.mtmt.hu/api/publication/2853101},
	author = {Pribér, János Krisztián and Fónai, Fruzsina and Jakus, Péter and Rácz, Boglárka and Chinopoulos, Christos and Tretter, László and Gallyas, Ferenc and Sümegi, Balázs and Veres, Balázs},
	doi = {10.1139/bcb-2014-0120},
	journal-iso = {BIOCHEM CELL BIOL},
	journal = {BIOCHEMISTRY AND CELL BIOLOGY-BIOCHIMIE ET BIOLOGIE CELLULAIRE},
	volume = {93},
	unique-id = {2853101},
	issn = {0829-8211},
	abstract = {According to recent results, various mitochondrial processes can actively regulate the immune response. In the present report, we studied whether mitochondrial permeability transition (mPT) has such a role. To this end, we compared bacterial lipopolysaccharide (LPS)-induced inflammatory response in cyclophilin D (CypD) knock-out and wild-type mouse resident peritoneal macrophages. CypD is a regulator of mPT; therefore, mPT is damaged in CypD-/- cells. We chose this genetic modification-based model because the mPT inhibitor cyclosporine A regulates inflammatory processes by several pathways unrelated to the mitochondria. The LPS increased mitochondrial depolarisation, cellular and mitochondrial reactive oxygen species production, nuclear factor-kappaB activation, and nitrite- and tumour necrosis factor alpha accumulation in wild-type cells, but these changes were diminished or absent in the CypD-deficient macrophages. Additionally, LPS enhanced Akt phosphorylation/activation as well as FOXO1 and FOXO3a phosphorylation/inactivation both in wild-type and CypD-/- cells. However, Akt and FOXO phosphorylation was significantly more pronounced in CypD-deficient compared to wild-type macrophages. These results provide the first pieces of experimental evidence for the functional regulatory role of mPT in the LPS-induced early inflammatory response of macrophages.},
	year = {2015},
	eissn = {1208-6002},
	pages = {241-250},
	orcid-numbers = {Chinopoulos, Christos/0000-0003-0183-4149; Tretter, László/0000-0001-5638-2886; Gallyas, Ferenc/0000-0002-1906-4333}
}

@article{MTMT:2713247,
	title = {Comparison of proton channel, phagocyte oxidase, and respiratory burst levels between human eosinophil and neutrophil granulocytes.},
	url = {https://m2.mtmt.hu/api/publication/2713247},
	author = {Kovács, István and Horvath, M and Kovács, Tünde and Somogyi, K and Tretter, László and Geiszt, Miklós and Petheő, Gábor L.},
	doi = {10.3109/10715762.2014.938234},
	journal-iso = {FREE RADIC RES},
	journal = {FREE RADICAL RESEARCH},
	volume = {48},
	unique-id = {2713247},
	issn = {1071-5762},
	abstract = {Robust production of reactive oxygen species (ROS) by phagocyte NADPH oxidase (phox) during the respiratory burst (RB) is a characteristic feature of eosinophil and neutrophil granulocytes. In these cells the voltage-gated proton channel (Hv1) is now considered as an ancillary subunit of the phox needed for intense ROS production. Multiple sources reported that the expression of phox subunits and RB is more intensive in eosinophils than in neutrophils. In most of these studies the eosinophils were not isolated from healthy individuals, and a comparative analysis of Hv1 expression had never been carried out. We performed a systematic comparison of the levels of essential phox subunits, Hv1 expression and ROS producing capacity between eosinophils and neutrophils of healthy individuals. The expression of phox components was similar, whereas the amount of Hv1 was approximately 10-fold greater in eosinophils. Furthermore, Hv1 expression correlated with Nox2 expression only in eosinophils. Additionally, in confocal microscopy experiments co-accumulation of Hv1 and Nox2 at the cell periphery was observed in resting eosinophils but not in neutrophils. While phorbol-12-myristate-13-acetate-induced peak extracellular ROS release was approximately 1.7-fold greater in eosinophils, oxygen consumption studies indicated that the maximal intensity of the RB is only approximately 1.4-fold greater in eosinophils. Our data reinforce that eosinophils, unlike neutrophils, generate ROS predominantly extracellularly. In contrast to previous works we have found that the two granulocyte types display very similar phox subunit expression and RB capacity. The large difference in Hv1 expression suggests that its support to intense ROS production is more important at the cell surface.},
	year = {2014},
	eissn = {1029-2470},
	pages = {1190-1199},
	orcid-numbers = {Kovács, Tünde/0000-0003-1064-2616; Tretter, László/0000-0001-5638-2886; Petheő, Gábor L./0000-0002-1773-4129}
}

@article{MTMT:2769374,
	title = {Human 2-Oxoglutarate Dehydrogenase Complex E1 Component Forms a Thiamin-derived Radical by Aerobic Oxidation of the Enamine Intermediate.},
	url = {https://m2.mtmt.hu/api/publication/2769374},
	author = {Nemeria, NS and Ambrus, Attila and Patel, H and Gerfen, G and Ádám, Veronika and Tretter, László and Zhou, J and Wang, J and Jordan, F},
	doi = {10.1074/jbc.M114.591073},
	journal-iso = {J BIOL CHEM},
	journal = {JOURNAL OF BIOLOGICAL CHEMISTRY},
	volume = {289},
	unique-id = {2769374},
	issn = {0021-9258},
	abstract = {Herein are reported unique properties of the human 2-oxoglutarate dehydrogenase multienzyme complex (OGDHc), a rate-limiting enzyme in the Krebs (citric acid) cycle. (a) Functionally competent 2-oxoglutarate dehydrogenase (E1o-h) and dihydrolipoyl succinyltransferase components have been expressed according to kinetic and spectroscopic evidence. (b) A stable free radical, consistent with the C2-(C2alpha-hydroxy)-gamma-carboxypropylidene thiamin diphosphate (ThDP) cation radical was detected by electron spin resonance upon reaction of the E1o-h with 2-oxoglutarate (OG) by itself or when assembled from individual components into OGDHc. (c) An unusual stability of the E1o-h-bound C2-(2alpha-hydroxy)-gamma-carboxypropylidene thiamin diphosphate (the "ThDP-enamine"/C2alpha-carbanion, the first postdecarboxylation intermediate) was observed, probably stabilized by the 5-carboxyl group of OG, not reported before. (d) The reaction of OG with the E1o-h gave rise to superoxide anion and hydrogen peroxide (reactive oxygen species (ROS)). (e) The relatively stable enzyme-bound enamine is the likely substrate for oxidation by O2, leading to the superoxide anion radical (in d) and the radical (in b). (f) The specific activity assessed for ROS formation compared with the NADH (overall complex) activity, as well as the fraction of radical intermediate occupying active centers of E1o-h are consistent with each other and indicate that radical/ROS formation is an "off-pathway" side reaction comprising less than 1% of the "on-pathway" reactivity. However, the nearly ubiquitous presence of OGDHc in human tissues, including the brain, makes these findings of considerable importance in human metabolism and perhaps disease.},
	year = {2014},
	eissn = {1083-351X},
	pages = {29859-29873},
	orcid-numbers = {Ambrus, Attila/0000-0001-6014-3175; Ádám, Veronika/0000-0002-8350-8701; Tretter, László/0000-0001-5638-2886}
}

@article{MTMT:2770712,
	title = {Measurement of ROS homeostasis in isolated mitochondria},
	url = {https://m2.mtmt.hu/api/publication/2770712},
	author = {Tretter, László and Ambrus, Attila},
	doi = {10.1016/B978-0-12-801415-8.00012-6},
	journal-iso = {METHOD ENZYMOL},
	journal = {METHODS IN ENZYMOLOGY},
	volume = {547},
	unique-id = {2770712},
	issn = {0076-6879},
	abstract = {In this chapter, we describe the currently most advanced methods applied for the quantitative assessment of ROS homeostasis inside the mitochondrion. These techniques are of particular interest in the field of oxidative stress. After discussing the importance of quantifying mitochondrial ROS homeostasis, three major aspects of this phenomenon and the pertinent methodologies for detection are delineated in detail. First the most important methods, based on fluorimetric or spectrophotometric approaches, for the detection of mitochondrial ROS are described. Elimination of ROS generated inside the mitochondrion is another crucial mechanism that also needs to be quantified accurately to estimate the antioxidant capacity of mitochondria under specific conditions. Since ROS generation and elimination manifest in concert, there needs to exist independent methods for the estimation of the net effect. Such a sensitive biochemical marker in the mitochondrion is aconitase, a citric acid cycle enzyme which is greatly sensitive to ROS. We describe two procedures for the precise determination of aconitase activity. A few auxiliary techniques and good practices having relevance in the successful accomplishment of the more delicate approaches are also mentioned. All other relevant technical considerations including advantages/disadvantages of the various methods and the most common artifacts are also discussed. © 2014 Elsevier Inc.},
	keywords = {Animals; Humans; PH; metabolism; ARTICLE; DEPOLARIZATION; FLUORESCENCE; human; animal; priority journal; Mitochondria; nonhuman; quantitative analysis; enzyme activity; glutamic acid; Spectrophotometry; Electron Transport; Homeostasis; Spectrometry, Fluorescence; Fluorometry; hydrogen peroxide; mitochondrial membrane; spectrofluorometry; Cytochrome c; Reactive oxygen species; reactive oxygen metabolite; SUPEROXIDE; mitochondrion; BIOCHEMISTRY; RED; liver mitochondrion; brain mitochondrion; reduced nicotinamide adenine dinucleotide; Mitochondrial Proteins; horseradish peroxidase; nicotinamide adenine dinucleotide; Pyruvic Acid; rotenone; bovine serum albumin; mitochondrial protein; homovanillic acid; malic acid; Isocitrate dehydrogenase; respiratory chain; mitochondrial membrane potential; succinate dehydrogenase; Spin Trapping; hyperpolarization; succinic acid; Membrane Potential, Mitochondrial; Cytochromes c; carbonyl cyanide 4 (trifluoromethoxy)phenylhydrazone; heart mitochondrion; muscle mitochondrion; scopoletin; aconitate hydratase; procedures; reverse electron transfer; oxaloacetic acid; Reactive oxygen species homeostasis; ROS elimination; Oxidative stress; Aconitase; Amplex},
	year = {2014},
	eissn = {1557-7988},
	pages = {199-223},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886; Ambrus, Attila/0000-0001-6014-3175}
}

@article{MTMT:2749008,
	title = {Enhanced hydrogen peroxide generation accompanies the beneficial bioenergetic effects of methylene blue in isolated brain mitochondria},
	url = {https://m2.mtmt.hu/api/publication/2749008},
	author = {Tretter, László and Horváth, Gergő and Hölgyesi, Áron and Essek, F and Ádám, Veronika},
	doi = {10.1016/j.freeradbiomed.2014.09.024},
	journal-iso = {FREE RADICAL BIO MED},
	journal = {FREE RADICAL BIOLOGY AND MEDICINE},
	volume = {77},
	unique-id = {2749008},
	issn = {0891-5849},
	year = {2014},
	eissn = {1873-4596},
	pages = {317-330},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886; Horváth, Gergő/0000-0001-5386-9509; Hölgyesi, Áron/0000-0001-8131-2839; Ádám, Veronika/0000-0002-8350-8701}
}

@article{MTMT:2227476,
	title = {The role of mitochondrial dehydrogenases in the generation of oxidative stress},
	url = {https://m2.mtmt.hu/api/publication/2227476},
	author = {Ádám, Veronika and Tretter, László},
	doi = {10.1016/j.neuint.2013.01.012},
	journal-iso = {NEUROCHEM INT},
	journal = {NEUROCHEMISTRY INTERNATIONAL},
	volume = {62},
	unique-id = {2227476},
	issn = {0197-0186},
	abstract = {In addition to complexes in the respiratory chain, few dehydrogenases playing key roles in the physiological metabolism in neurons, are able to generate reactive oxygen species (ROS) in mitochondria. One of them is the Krebs cycle enzyme, α-ketoglutarate dehydrogenase (α-KGDH), which is capable of producing superoxide and hydrogen peroxide by the E3 subunit of the enzyme regulated by changes in the NADH/NAD+ ratio. Mutations in the E3 subunit known to be related to diseases in humans were shown to have increased ROS-forming ability. α-Glycerophosphate dehydrogenase (α-GPDH) located on the outer surface of the inner membrane can also generate ROS, which is stimulated by Ca2+. ROS production by α-GPDH is unique as it does not require Ca2+ uptake and it is observed in respiring as well as damaged, bioenergetically incompetent mitochondria. The possible role of ROS generation by these dehydrogenases in brain pathology is discussed in this review. © 2013 Elsevier Ltd. All rights reserved.},
	keywords = {Mitochondria; Reactive oxygen species; ALPHA-KETOGLUTARATE DEHYDROGENASE; Dehydrogenases; Alpha-glycerophosphate dehydrogenase; Oxidative stress},
	year = {2013},
	eissn = {1872-9754},
	pages = {757-763},
	orcid-numbers = {Ádám, Veronika/0000-0002-8350-8701; Tretter, László/0000-0001-5638-2886}
}

@article{MTMT:2505661,
	title = {Transglutaminase 2 Contributes to Apoptosis Induction in Jurkat T Cells by Modulating Ca(2+) Homeostasis via Cross-Linking RAP1GDS1},
	url = {https://m2.mtmt.hu/api/publication/2505661},
	author = {Yu-Fan, Hsieh and Guang-Yaw, Liu and Yi-Ju, Lee and Jiann-Jou, Yang and Dánielné Sándor, Katalin and Sarang, Zsolt and Angela, Bononi and Paolo, Pinton and Tretter, László and Szondy, Zsuzsanna and Gregory, J Tsay},
	doi = {10.1371/journal.pone.0081516},
	journal-iso = {PLOS ONE},
	journal = {PLOS ONE},
	volume = {8},
	unique-id = {2505661},
	issn = {1932-6203},
	abstract = {BACKGROUND:
		
		Transglutaminase 2 (TG2) is a protein cross-linking enzyme known to be associated with the in vivo apoptosis program of T cells. However, its role in the T cell apoptosis program was not investigated yet.
		RESULTS:
		
		Here we report that timed overexpression of both the wild type (wt) and the cross-linking mutant of TG2 induced apoptosis in Jurkat T cells, the wt being more effective. Part of TG2 colocalised with mitochondria. WtTG2-induced apoptosis was characterized by enhanced mitochondrial Ca(2+) uptake. Ca(2+)-activated wtTG2 cross-linked RAP1, GTP-GDP dissociation stimulator 1, an unusual guanine exchange factor acting on various small GTPases, to induce a yet uncharacterized signaling pathway that was able to promote the Ca(2+) release from the endoplasmic reticulum via both Ins3P and ryanodine sensitive receptors leading to a consequently enhanced mitochondrial Ca(2+)uptake.
		CONCLUSIONS:
		
		Our data indicate that TG2 might act as a Ca(2+) sensor to amplify endoplasmic reticulum-derived Ca(2+) signals to enhance mitochondria Ca(2+) uptake. Since enhanced mitochondrial Ca(2+) levels were previously shown to sensitize mitochondria for various apoptotic signals, our data demonstrate a novel mechanism through which TG2 can contribute to the induction of apoptosis in certain cell types. Since, as compared to knock out cells, physiological levels of TG2 affected Ca(2+) signals in mouse embryonic fibroblasts similar to Jurkat cells, our data might indicate a more general role of TG2 in the regulation of mitochondrial Ca(2+) homeostasis.},
	year = {2013},
	eissn = {1932-6203},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886}
}

@article{MTMT:2529233,
	title = {Mitochondrial effects of a possible neuroprotectant, methylene blue. Studies on isolated brain mitochondria and on BV-2 microglial cell line},
	url = {https://m2.mtmt.hu/api/publication/2529233},
	author = {Tretter, László and Horváth, Gergő and Ádám, Veronika},
	journal-iso = {BBA-BIOENERGETICS},
	journal = {BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS},
	volume = {1817},
	unique-id = {2529233},
	issn = {0005-2728},
	year = {2012},
	eissn = {1879-2650},
	pages = {S152-S152},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886; Horváth, Gergő/0000-0001-5386-9509; Ádám, Veronika/0000-0002-8350-8701}
}

@article{MTMT:2124569,
	title = {High Ca 2+ load promotes Hydrogen peroxide generation via activation of α-glycerophosphate dehydrogenase in brain mitochondria},
	url = {https://m2.mtmt.hu/api/publication/2124569},
	author = {Tretter, László and Ádám, Veronika},
	doi = {10.1016/j.freeradbiomed.2012.09.029},
	journal-iso = {FREE RADICAL BIO MED},
	journal = {FREE RADICAL BIOLOGY AND MEDICINE},
	volume = {53},
	unique-id = {2124569},
	issn = {0891-5849},
	abstract = {H 2O 2 generation associated with α-glycerophosphate (α-GP) oxidation was addressed in guinea pig brain mitochondria challenged with high Ca 2+ load (10μM). Exposure to 10μM Ca 2+ induced an abrupt 2.5-fold increase in H 2O 2 release compared to that measured in the presence of a physiological cytosolic Ca 2+ concentration (100nM) from mitochondria respiring on 5mM α-GP in the presence of ADP (2mM). The Ca 2+-induced stimulation of H 2O 2 generation was reversible and unaltered by the uniporter blocker Ru 360, indicating that it did not require Ca 2+ uptake into mitochondria. Enhanced H 2O 2 generation by Ca 2+ was also observed in the absence of ADP when mitochondria exhibited permeability transition pore opening with a decrease in the NAD(P)H level, dissipation of membrane potential, and mitochondrial swelling. Furthermore, mitochondria treated with the pore-forming peptide alamethicin also responded with an elevated H 2O 2 generation to a challenge with 10μM Ca 2+. Ca 2+-induced promotion of H 2O 2 formation was further enhanced by the complex III inhibitor myxothiazol. With 20mM α-GP concentration, stimulation of H 2O 2 formation by Ca 2+ was detected only in the presence, not in the absence, of ADP. It is concluded that α-glycerophosphate dehydrogenase, which is accessible to and could be activated by a rise in the level of cytosolic Ca 2+, makes a major contribution to Ca 2+-stimulated H 2O 2 generation. This work highlights a unique high-Ca 2+-stimulated reactive oxygen species-forming mechanism in association with oxidation of α-GP, which is largely independent of the bioenergetic state and can proceed even in damaged, functionally incompetent mitochondria. © 2012 Elsevier Inc.},
	keywords = {calcium; Mitochondria; Free Radicals; hydrogen peroxide; Reactive oxygen species; PERMEABILITY TRANSITION PORE; myxothiazol; Reverse electron transport; α-Glycerophosphate shuttle; α-Glycerophosphate dehydrogenase},
	year = {2012},
	eissn = {1873-4596},
	pages = {2119-2130},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886; Ádám, Veronika/0000-0002-8350-8701}
}

@article{MTMT:1666747,
	title = {Stimulation of reactive oxygen species generation by disease-causing mutations of lipoamide dehydrogenase},
	url = {https://m2.mtmt.hu/api/publication/1666747},
	author = {Ambrus, Attila and Törőcsik, Beáta and Tretter, László and Ozohanics, Olivér and Ádám, Veronika},
	doi = {10.1093/hmg/ddr202},
	journal-iso = {HUM MOL GENET},
	journal = {HUMAN MOLECULAR GENETICS},
	volume = {20},
	unique-id = {1666747},
	issn = {0964-6906},
	keywords = {Humans; Escherichia coli; Mass spectrometry; Chromatography, Gel; hydrogen peroxide; Reactive oxygen species; Circular Dichroism; Dihydrolipoamide dehydrogenase},
	year = {2011},
	eissn = {1460-2083},
	pages = {2984-2995},
	orcid-numbers = {Ambrus, Attila/0000-0001-6014-3175; Törőcsik, Beáta/0000-0002-9838-3710; Tretter, László/0000-0001-5638-2886; Ozohanics, Olivér/0000-0002-2705-9921; Ádám, Veronika/0000-0002-8350-8701}
}

@article{MTMT:1616633,
	title = {Reversible inhibition of hydrogen peroxide elimination by calcium in brain mitochondria.},
	url = {https://m2.mtmt.hu/api/publication/1616633},
	author = {Tretter, László and Angeli, BE and Ardestani, MR and Goracci, G and Ádám, Veronika},
	doi = {10.1002/jnr.22658},
	journal-iso = {J NEUROSCI RES},
	journal = {JOURNAL OF NEUROSCIENCE RESEARCH},
	volume = {89},
	unique-id = {1616633},
	issn = {0360-4012},
	year = {2011},
	eissn = {1097-4547},
	pages = {1965-1972},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886; Ádám, Veronika/0000-0002-8350-8701}
}

@article{MTMT:1430452,
	title = {Substrate-dependence of mitochondrial reactive oxygen species generation},
	url = {https://m2.mtmt.hu/api/publication/1430452},
	author = {Ádám, Veronika and Komáry, Zsófia and Tretter, László},
	doi = {10.1016/j.bbabio.2010.04.179},
	journal-iso = {BBA-BIOENERGETICS},
	journal = {BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS},
	volume = {1797},
	unique-id = {1430452},
	issn = {0005-2728},
	year = {2010},
	eissn = {1879-2650},
	pages = {55-55},
	orcid-numbers = {Ádám, Veronika/0000-0002-8350-8701; Tretter, László/0000-0001-5638-2886}
}

@article{MTMT:1430453,
	title = {Inhibition of the alpha-ketoglutarate dehydrogenase-mediated reactive oxygen species generation by lipoic acid},
	url = {https://m2.mtmt.hu/api/publication/1430453},
	author = {Ambrus, Attila and Tretter, László and Ádám, Veronika},
	doi = {10.1016/j.bbabio.2010.04.187},
	journal-iso = {BBA-BIOENERGETICS},
	journal = {BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS},
	volume = {1797},
	unique-id = {1430453},
	issn = {0005-2728},
	year = {2010},
	eissn = {1879-2650},
	pages = {57-57},
	orcid-numbers = {Ambrus, Attila/0000-0001-6014-3175; Tretter, László/0000-0001-5638-2886; Ádám, Veronika/0000-0002-8350-8701}
}

@article{MTMT:1327784,
	title = {Membrane potential-related effect of calcium on reactive oxygen species generation in isolated brain mitochondria.},
	url = {https://m2.mtmt.hu/api/publication/1327784},
	author = {Komáry, Zsófia and Tretter, László and Ádám, Veronika},
	doi = {10.1016/j.bbabio.2010.03.010},
	journal-iso = {BBA-BIOENERGETICS},
	journal = {BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS},
	volume = {1797},
	unique-id = {1327784},
	issn = {0005-2728},
	year = {2010},
	eissn = {1879-2650},
	pages = {922-928},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886; Ádám, Veronika/0000-0002-8350-8701}
}

@CONFERENCE{MTMT:3037386,
	title = {Inhibition of the alpha-ketoglutarate dehydrogenase-mediated reactive oxygen species generation by lipoic acid},
	url = {https://m2.mtmt.hu/api/publication/3037386},
	author = {Ádám, Veronika and Ambrus, Attila and Tretter, László},
	booktitle = {Frontiers in Systems Neuroscience},
	doi = {10.3389/conf.neuro.01.2009.04.136},
	unique-id = {3037386},
	year = {2009},
	pages = {online},
	orcid-numbers = {Ádám, Veronika/0000-0002-8350-8701; Ambrus, Attila/0000-0001-6014-3175; Tretter, László/0000-0001-5638-2886}
}

@article{MTMT:1234615,
	title = {Inhibition of the alpha-ketoglutarate dehydrogenase-mediated reactive oxygen species generation by lipoic acid},
	url = {https://m2.mtmt.hu/api/publication/1234615},
	author = {Ambrus, Attila and Tretter, László and Ádám, Veronika},
	doi = {10.1111/j.1471-4159.2009.05942.x},
	journal-iso = {J NEUROCHEM},
	journal = {JOURNAL OF NEUROCHEMISTRY},
	volume = {109},
	unique-id = {1234615},
	issn = {0022-3042},
	abstract = {Dihydrolipoamide dehydrogenase (LADH) is a flavo-enzyme that serves as a subunit 
		of alpha-ketoglutarate dehydrogenase complex (alpha-KGDHC). Reactive oxygen
		species (ROS) generation by alpha-KGDHC has been assigned to LADH (E3 subunit)
		and explained by the diaphorase activity of E3. Dysfunctions of alpha-KGDHC and
		concurrent ROS production have been implicated in neurodegeneration,
		ischemia-reperfusion, and other pathological conditions. In this work we
		investigated the in-depth details of ROS generation by isolated LADH and
		alpha-KGDHC. We found a parallel generation of superoxide and hydrogen peroxide
		by the E3 subunit of alpha-KGDHC which could be blocked by lipoic acid (LA)
		acting on a site upstream of the E3 subunit. The pathologically relevant ROS
		generation (at high NADH/NAD+ ratio and low pH) in the reverse mode of
		alpha-KGDHC could also be inhibited by LA. Our results contradict the previously 
		proposed mechanism for pH-dependent ROS generation by LADH, showing no
		disassembling of the E3 functional homodimer at acidic pH using a physiologically
		relevant method for the examination. It is also suggested that LA could be
		beneficial in reducing the cell damage related to excessive ROS generation under 
		pathological conditions.},
	year = {2009},
	eissn = {1471-4159},
	pages = {222-229},
	orcid-numbers = {Ambrus, Attila/0000-0001-6014-3175; Tretter, László/0000-0001-5638-2886; Ádám, Veronika/0000-0002-8350-8701}
}

@article{MTMT:1127363,
	title = {H(2)O(2) generation is decreased by calcium in isolated brain mitochondria.},
	url = {https://m2.mtmt.hu/api/publication/1127363},
	author = {Komáry, Zsófia and Tretter, László and Ádám, Veronika},
	doi = {10.1016/j.bbabio.2008.05.004},
	journal-iso = {BBA-BIOENERGETICS},
	journal = {BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS},
	volume = {1777},
	unique-id = {1127363},
	issn = {0005-2728},
	year = {2008},
	eissn = {1879-2650},
	pages = {800-807},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886; Ádám, Veronika/0000-0002-8350-8701}
}

@article{MTMT:1127361,
	title = {Uncoupling is without an effect on the production of reactive oxygen species by in situ synaptic mitochondria},
	url = {https://m2.mtmt.hu/api/publication/1127361},
	author = {Tretter, László and Ádám, Veronika},
	doi = {10.1111/j.1471-4159.2007.04891.x},
	journal-iso = {J NEUROCHEM},
	journal = {JOURNAL OF NEUROCHEMISTRY},
	volume = {103},
	unique-id = {1127361},
	issn = {0022-3042},
	year = {2007},
	eissn = {1471-4159},
	pages = {1864-1871},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886; Ádám, Veronika/0000-0002-8350-8701}
}

@article{MTMT:1127360,
	title = {Stimulation of H(2)O(2) generation by calcium in brain mitochondria respiring on alpha-glycerophosphate.},
	url = {https://m2.mtmt.hu/api/publication/1127360},
	author = {Tretter, László and Takacs, K and Kover, K and Ádám, Veronika},
	doi = {10.1002/jnr.21405},
	journal-iso = {J NEUROSCI RES},
	journal = {JOURNAL OF NEUROSCIENCE RESEARCH},
	volume = {85},
	unique-id = {1127360},
	issn = {0360-4012},
	year = {2007},
	eissn = {1097-4547},
	pages = {3471-3479},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886; Ádám, Veronika/0000-0002-8350-8701}
}

@article{MTMT:1127359,
	title = {Moderate dependence of ROS formation on ΔΨm in isolated brain mitochondria supported by NADH-linked substrates},
	url = {https://m2.mtmt.hu/api/publication/1127359},
	author = {Tretter, László and Ádám, Veronika},
	doi = {10.1007/s11064-006-9130-y},
	journal-iso = {NEUROCHEM RES},
	journal = {NEUROCHEMICAL RESEARCH},
	volume = {32},
	unique-id = {1127359},
	issn = {0364-3190},
	year = {2007},
	eissn = {1573-6903},
	pages = {569-575},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886; Ádám, Veronika/0000-0002-8350-8701}
}

@article{MTMT:1127358,
	title = {Characteristics of alpha-glycerophosphate evoked H2 O2 generation in brain mitochondria.},
	url = {https://m2.mtmt.hu/api/publication/1127358},
	author = {Tretter, László and Takacs, K and Hegedűs, V and Ádám, Veronika},
	doi = {10.1111/j.1471-4159.2006.04223.x},
	journal-iso = {J NEUROCHEM},
	journal = {JOURNAL OF NEUROCHEMISTRY},
	volume = {100},
	unique-id = {1127358},
	issn = {0022-3042},
	year = {2007},
	eissn = {1471-4159},
	pages = {650-663},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886; Ádám, Veronika/0000-0002-8350-8701}
}

@article{MTMT:1067039,
	title = {The effect of bovine serum albumin on the membrane potential and reactive oxygen species generation in succinate-supported isolated brain mitochondria},
	url = {https://m2.mtmt.hu/api/publication/1067039},
	author = {Tretter, László and Mayer-Takacs, D and Ádám, Veronika},
	doi = {10.1016/j.neuint.2006.07.010},
	journal-iso = {NEUROCHEM INT},
	journal = {NEUROCHEMISTRY INTERNATIONAL},
	volume = {50},
	unique-id = {1067039},
	issn = {0197-0186},
	year = {2007},
	eissn = {1872-9754},
	pages = {139-147},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886; Ádám, Veronika/0000-0002-8350-8701}
}

@{MTMT:2463303,
	title = {Mitochondrial production of reactive oxygen species},
	url = {https://m2.mtmt.hu/api/publication/2463303},
	author = {Tretter, László},
	booktitle = {Reactive Oxygen Species and Diseases},
	unique-id = {2463303},
	year = {2007},
	pages = {1-31},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886}
}

@article{MTMT:1030894,
	title = {Impaired regulation of pH homeostasis by oxidative stress in rat brain capillary endothelial cells},
	url = {https://m2.mtmt.hu/api/publication/1030894},
	author = {Sipos, Ildikó and Törőcsik, Beáta and Tretter, László and Ádám, Veronika},
	doi = {10.1007/s10571-004-1379-6},
	journal-iso = {CELL MOL NEUROBIOL},
	journal = {CELLULAR AND MOLECULAR NEUROBIOLOGY},
	volume = {25},
	unique-id = {1030894},
	issn = {0272-4340},
	year = {2005},
	eissn = {1573-6830},
	pages = {141-151},
	orcid-numbers = {Sipos, Ildikó/0000-0003-2861-1439; Törőcsik, Beáta/0000-0002-9838-3710; Tretter, László/0000-0001-5638-2886; Ádám, Veronika/0000-0002-8350-8701}
}

@article{MTMT:1030892,
	title = {Reactive oxygen species production by complex I in brain mitochondria. The role of reverse electron transport},
	url = {https://m2.mtmt.hu/api/publication/1030892},
	author = {Tretter, László and Ádám, Veronika},
	journal-iso = {J NEUROCHEM},
	journal = {JOURNAL OF NEUROCHEMISTRY},
	volume = {94},
	unique-id = {1030892},
	issn = {0022-3042},
	year = {2005},
	eissn = {1471-4159},
	pages = {247-247},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886; Ádám, Veronika/0000-0002-8350-8701}
}

@article{MTMT:1030889,
	title = {Dual effect of pyruvate in isolated nerve terminals: Generation of reactive oxygen species and protection of aconitase},
	url = {https://m2.mtmt.hu/api/publication/1030889},
	author = {Tretter, László and Liktor, Bálint (ifj.) and Ádám, Veronika},
	doi = {10.1007/s11064-005-8805-0},
	journal-iso = {NEUROCHEM RES},
	journal = {NEUROCHEMICAL RESEARCH},
	volume = {30},
	unique-id = {1030889},
	issn = {0364-3190},
	year = {2005},
	eissn = {1573-6903},
	pages = {1331-1338},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886; Ádám, Veronika/0000-0002-8350-8701}
}

@article{MTMT:1030888,
	title = {Alpha-ketoglutarate dehydrogenase: a target and generator of oxidative stress},
	url = {https://m2.mtmt.hu/api/publication/1030888},
	author = {Tretter, László and Ádám, Veronika},
	doi = {10.1098/rstb.2005.1764},
	journal-iso = {PHILOS T ROY SOC B},
	journal = {PHILOSOPHICAL TRANSACTIONS OF THE ROYAL SOCIETY B - BIOLOGICAL SCIENCES},
	volume = {360},
	unique-id = {1030888},
	issn = {0962-8436},
	year = {2005},
	eissn = {1471-2970},
	pages = {2335-2345},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886; Ádám, Veronika/0000-0002-8350-8701}
}

@article{MTMT:1030899,
	title = {Initiation of neuronal damage by complex I deficiency and oxidative stress in Parkinson's disease},
	url = {https://m2.mtmt.hu/api/publication/1030899},
	author = {Tretter, László and Sipos, Ildikó and Ádám, Veronika},
	doi = {10.1023/B:NERE.0000014827.94562.4b},
	journal-iso = {NEUROCHEM RES},
	journal = {NEUROCHEMICAL RESEARCH},
	volume = {29},
	unique-id = {1030899},
	issn = {0364-3190},
	year = {2004},
	eissn = {1573-6903},
	pages = {569-577},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886; Sipos, Ildikó/0000-0003-2861-1439; Ádám, Veronika/0000-0002-8350-8701}
}

@article{MTMT:1030897,
	title = {Generation of reactive oxygen species in the reaction catalyzed by alpha-ketoglutarate dehydrogenase},
	url = {https://m2.mtmt.hu/api/publication/1030897},
	author = {Tretter, László and Ádám, Veronika},
	doi = {10.1523/JNEUROSCI.1842-04.2004},
	journal-iso = {J NEUROSCI},
	journal = {JOURNAL OF NEUROSCIENCE},
	volume = {24},
	unique-id = {1030897},
	issn = {0270-6474},
	year = {2004},
	eissn = {1529-2401},
	pages = {7771-7778},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886; Ádám, Veronika/0000-0002-8350-8701}
}

@article{MTMT:109265,
	title = {Non-synaptic release of H³noradrenaline in response to oxidative stress combined with mitochondrial dysfunction in rat hippocampal slices},
	url = {https://m2.mtmt.hu/api/publication/109265},
	author = {Milusheva, Elisaveta and Sperlágh, Beáta and Shikova, L and Baranyi, Mária and Tretter, László and Ádám, Veronika and Vizi, E. Szilveszter},
	doi = {10.1016/S0306-4522(03)00340-3},
	journal-iso = {NEUROSCIENCE},
	journal = {NEUROSCIENCE},
	volume = {120},
	unique-id = {109265},
	issn = {0306-4522},
	year = {2003},
	eissn = {1873-7544},
	pages = {771-781},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886; Ádám, Veronika/0000-0002-8350-8701; Vizi, E. Szilveszter/0000-0002-9557-4597}
}

@article{MTMT:1030907,
	title = {Quantitative relationship between inhibition of respiratory complexes and formation of reactive oxygen species in isolated nerve terminals},
	url = {https://m2.mtmt.hu/api/publication/1030907},
	author = {Sipos, Ildikó and Tretter, László and Ádám, Veronika},
	doi = {10.1046/j.1471-4159.2003.01513.x},
	journal-iso = {J NEUROCHEM},
	journal = {JOURNAL OF NEUROCHEMISTRY},
	volume = {84},
	unique-id = {1030907},
	issn = {0022-3042},
	year = {2003},
	eissn = {1471-4159},
	pages = {112-118},
	orcid-numbers = {Sipos, Ildikó/0000-0003-2861-1439; Tretter, László/0000-0001-5638-2886; Ádám, Veronika/0000-0002-8350-8701}
}

@article{MTMT:1030903,
	title = {Reactive oxygen species production in synaptosomes is independent of Delta Psi(m)},
	url = {https://m2.mtmt.hu/api/publication/1030903},
	author = {Sipos, Ildikó and Tretter, László and Ádám, Veronika},
	doi = {10.1046/j.1471-4159.85.s2.19_2.x},
	journal-iso = {J NEUROCHEM},
	journal = {JOURNAL OF NEUROCHEMISTRY},
	volume = {85},
	unique-id = {1030903},
	issn = {0022-3042},
	year = {2003},
	eissn = {1471-4159},
	pages = {28-28},
	orcid-numbers = {Sipos, Ildikó/0000-0003-2861-1439; Tretter, László/0000-0001-5638-2886; Ádám, Veronika/0000-0002-8350-8701}
}

@article{MTMT:1030901,
	title = {The production of reactive oxygen species in intact isolated nerve terminals is independent of the mitochondrial membrane potential},
	url = {https://m2.mtmt.hu/api/publication/1030901},
	author = {Sipos, Ildikó and Tretter, László and Ádám, Veronika},
	doi = {10.1023/A:1025634728227},
	journal-iso = {NEUROCHEM RES},
	journal = {NEUROCHEMICAL RESEARCH},
	volume = {28},
	unique-id = {1030901},
	issn = {0364-3190},
	year = {2003},
	eissn = {1573-6903},
	pages = {1575-1581},
	orcid-numbers = {Sipos, Ildikó/0000-0003-2861-1439; Tretter, László/0000-0001-5638-2886; Ádám, Veronika/0000-0002-8350-8701}
}

@article{MTMT:1030906,
	title = {Endogenous glutamate contributes to the maintenance of glutathione level under oxidative stress in isolated nerve terminals},
	url = {https://m2.mtmt.hu/api/publication/1030906},
	author = {Tretter, László and Repassy, R and Ádám, Veronika},
	doi = {10.1016/S0197-0186(02)00140-7},
	journal-iso = {NEUROCHEM INT},
	journal = {NEUROCHEMISTRY INTERNATIONAL},
	volume = {42},
	unique-id = {1030906},
	issn = {0197-0186},
	year = {2003},
	eissn = {1872-9754},
	pages = {393-400},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886; Ádám, Veronika/0000-0002-8350-8701}
}

@article{MTMT:1030908,
	title = {Glutamate release by an Na+ load and oxidative stress in nerve terminals: relevance to ischemia/reperfusion},
	url = {https://m2.mtmt.hu/api/publication/1030908},
	author = {Tretter, László and Ádám, Veronika},
	doi = {10.1046/j.1471-4159.2002.01191.x},
	journal-iso = {J NEUROCHEM},
	journal = {JOURNAL OF NEUROCHEMISTRY},
	volume = {83},
	unique-id = {1030908},
	issn = {0022-3042},
	year = {2002},
	eissn = {1471-4159},
	pages = {855-862},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886; Ádám, Veronika/0000-0002-8350-8701}
}

@article{MTMT:244300,
	title = {Analysis of high intracellular [Na⁺]-induced release of ³noradrenaline in rat hippocampal slices},
	url = {https://m2.mtmt.hu/api/publication/244300},
	author = {Gerevich, Zoltán and Tretter, László and Ádám, Veronika and Baranyi, Mária and Kiss, János and Zelles, Tibor and Vizi, E. Szilveszter},
	doi = {10.1016/S0306-4522(01)00102-6},
	journal-iso = {NEUROSCIENCE},
	journal = {NEUROSCIENCE},
	volume = {104},
	unique-id = {244300},
	issn = {0306-4522},
	abstract = {Our aim was to investigate the mechanisms involved in the high intracellular sodium-induced transmitter release in the CNS through the characterisation of the veratridine-evoked (40 μM) noradrenaline release from rat hippocampal slices. The response to veratridine was completely inhibited by tetrodotoxin (1 μM), indicating that the effect is due to the activation of sodium channels. Omission of Ca2+ from the superfusion fluid inhibited the veratridine-evoked release by 72%, showing that the majority of release results from external Ca2+-dependent exocytosis. The residual Ca2+-independent release was not blocked by the intracellular Ca2+ chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N,N-tetraacetic acid acetoxymethyl ester (100 μM) suggesting that intracellular Ca2+ stores are not involved in this component of veratridine effect. The noradrenaline uptake blockers, desipramine (10 μM) and nisoxetine (10 μM), inhibited the external Ca2+-independent release by 50 and 46%, respectively, indicating that the release partly originates from the reversal of transporters (carrier-mediated release). In contrast to uptake blockers, lowering the temperature, another possibility to inhibit transporter function, completely inhibited the effect of veratridine in the absence of Ca2+. Further experiments revealed that low temperature (20 and 12°C) reduces the veratridine-induced increase of intracellular sodium concentration ([Na+]i) in rat cortical synaptosomes (68 and 78% inhibition, respectively). The clinical relevance of our data is that during ischemia a massive release of transmitters occurs mainly due to the elevation of [Na+]i, which contributes to the development of ischemic brain injury. Our results show that low temperature may be a better therapeutic approach to the treatment of ischemia because it has a dual action on this process. Firstly, it inhibits the function of uptake transporters and hence reduces the carrier-mediated outflow of transmitters. Secondly, it inhibits the sodium influx and therefore prevents the unwanted elevation of [Na+]i. Our data also suggest that veratridine stimulation can be a suitable model for ischemic conditions. © 2001 IBRO.},
	year = {2001},
	eissn = {1873-7544},
	pages = {761-768},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886; Ádám, Veronika/0000-0002-8350-8701; Zelles, Tibor/0000-0002-0357-0469; Vizi, E. Szilveszter/0000-0002-9557-4597}
}

@article{MTMT:244296,
	title = {The effects of oxidative stress on calcium and pH homeostasis in rat brain capillary endothelial cells},
	url = {https://m2.mtmt.hu/api/publication/244296},
	author = {Sipos, Ildikó and Tretter, László and Ádám, Veronika},
	journal-iso = {J NEUROCHEM},
	journal = {JOURNAL OF NEUROCHEMISTRY},
	volume = {77},
	unique-id = {244296},
	issn = {0022-3042},
	year = {2001},
	eissn = {1471-4159},
	pages = {38-39},
	orcid-numbers = {Sipos, Ildikó/0000-0003-2861-1439; Tretter, László/0000-0001-5638-2886; Ádám, Veronika/0000-0002-8350-8701}
}

@article{MTMT:1030912,
	title = {Oxidative stress and sodium load influence glutamate homeostasis and glutamate release in isolated nerve terminals},
	url = {https://m2.mtmt.hu/api/publication/1030912},
	author = {Tretter, László and Rozsa, A and Ádám, Veronika},
	journal-iso = {J NEUROCHEM},
	journal = {JOURNAL OF NEUROCHEMISTRY},
	volume = {78},
	unique-id = {1030912},
	issn = {0022-3042},
	year = {2001},
	eissn = {1471-4159},
	pages = {72-72},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886; Ádám, Veronika/0000-0002-8350-8701}
}

@article{MTMT:244283,
	title = {The role of endogenous glutamate in the maintenance of glutathione-dependent antioxidant capacity of isolated nerve terminals.},
	url = {https://m2.mtmt.hu/api/publication/244283},
	author = {Tretter, László and Repassy, R and Ádám, Veronika},
	journal-iso = {J NEUROCHEM},
	journal = {JOURNAL OF NEUROCHEMISTRY},
	volume = {77},
	unique-id = {244283},
	issn = {0022-3042},
	year = {2001},
	eissn = {1471-4159},
	pages = {32-32},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886; Ádám, Veronika/0000-0002-8350-8701}
}

@article{MTMT:1030923,
	title = {Exacerbated responses to oxidative stress by an Na+ load in isolated nerve terminals: the role of ATP depletion and rise of [Ca2+](i)},
	url = {https://m2.mtmt.hu/api/publication/1030923},
	author = {Chinopoulos, Christos and Tretter, László and Rózsa, Adrienn and Ádám, Veronika},
	journal-iso = {J NEUROSCI},
	journal = {JOURNAL OF NEUROSCIENCE},
	volume = {20},
	unique-id = {1030923},
	issn = {0270-6474},
	year = {2000},
	eissn = {1529-2401},
	pages = {2094-2103},
	orcid-numbers = {Chinopoulos, Christos/0000-0003-0183-4149; Tretter, László/0000-0001-5638-2886; Ádám, Veronika/0000-0002-8350-8701}
}

@article{MTMT:1030922,
	title = {Reversible depolarization of in situ mitochondria by oxidative stress parallels a decrease in NAD(P)H level in nerve terminals},
	url = {https://m2.mtmt.hu/api/publication/1030922},
	author = {Chinopoulos, Christos and Tretter, László and Ádám, Veronika},
	doi = {10.1016/S0197-0186(99)00161-8},
	journal-iso = {NEUROCHEM INT},
	journal = {NEUROCHEMISTRY INTERNATIONAL},
	volume = {36},
	unique-id = {1030922},
	issn = {0197-0186},
	year = {2000},
	eissn = {1872-9754},
	pages = {483-488},
	orcid-numbers = {Chinopoulos, Christos/0000-0003-0183-4149; Tretter, László/0000-0001-5638-2886; Ádám, Veronika/0000-0002-8350-8701}
}

@article{MTMT:1507629,
	title = {Dinoflagellates from marine algal blooms produce neurotoxic compounds: effects on free calcium levels in neuronal cells and synaptosomes},
	url = {https://m2.mtmt.hu/api/publication/1507629},
	author = {Perovic, S and Tretter, László and Brummer, F and Wetzler, C Brenner J and Donner, G and Schroder, HC and Muller, WE},
	doi = {10.1016/S1382-6689(99)00035-6},
	journal-iso = {ENVIRON TOXICOL PHAR},
	journal = {ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY},
	volume = {8},
	unique-id = {1507629},
	issn = {1382-6689},
	year = {2000},
	eissn = {1872-7077},
	pages = {83-94},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886}
}

@article{MTMT:1030917,
	title = {Inhibition of Krebs cycle enzymes by hydrogen peroxide: A key role of alpha-ketoglutarate dehydrogenase in limiting NADH production under oxidative stress},
	url = {https://m2.mtmt.hu/api/publication/1030917},
	author = {Tretter, László and Ádám, Veronika},
	journal-iso = {J NEUROSCI},
	journal = {JOURNAL OF NEUROSCIENCE},
	volume = {20},
	unique-id = {1030917},
	issn = {0270-6474},
	year = {2000},
	eissn = {1529-2401},
	pages = {8972-8979},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886; Ádám, Veronika/0000-0002-8350-8701}
}

@article{MTMT:1030931,
	title = {Depolarization of in situ mitochondria due to hydrogen peroxide-induced oxidative stress in nerve terminals: Inhibition of alpha-ketoglutarate dehydrogenase},
	url = {https://m2.mtmt.hu/api/publication/1030931},
	author = {Chinopoulos, Christos and Tretter, László and Ádám, Veronika},
	doi = {10.1046/j.1471-4159.1999.0730220.x},
	journal-iso = {J NEUROCHEM},
	journal = {JOURNAL OF NEUROCHEMISTRY},
	volume = {73},
	unique-id = {1030931},
	issn = {0022-3042},
	year = {1999},
	eissn = {1471-4159},
	pages = {220-228},
	orcid-numbers = {Chinopoulos, Christos/0000-0003-0183-4149; Tretter, László/0000-0001-5638-2886; Ádám, Veronika/0000-0002-8350-8701}
}

@article{MTMT:1507670,
	title = {Changes of ICE protease activities caused by toxic supernatants of dinoflagellates (Prorocentrum species) from marine algal blooms},
	url = {https://m2.mtmt.hu/api/publication/1507670},
	author = {Perovic, S and Wetzler, C and Brummer, F and Elbrachter, M and Tretter, László and Wichels, A and Muller, WEG and Schröder, HC},
	journal-iso = {EUR J PROTISTOL},
	journal = {EUROPEAN JOURNAL OF PROTISTOLOGY},
	volume = {35},
	unique-id = {1507670},
	issn = {0932-4739},
	year = {1999},
	eissn = {1618-0429},
	pages = {267-274},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886}
}

@article{MTMT:1059589,
	title = {Inhibition of alpha-ketoglutarate dehydrogenase due to H2O2-induced oxidative stress in nerve terminals. Oxidative/Energy Metabolism in Neurodegenerative Disorders},
	url = {https://m2.mtmt.hu/api/publication/1059589},
	author = {Tretter, László and Ádám, Veronika},
	doi = {10.1111/j.1749-6632.1999.tb07867.x},
	journal-iso = {ANN NY ACAD SCI},
	journal = {ANNALS OF THE NEW YORK ACADEMY OF SCIENCES},
	volume = {893},
	unique-id = {1059589},
	issn = {0077-8923},
	year = {1999},
	eissn = {1749-6632},
	pages = {412-416},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886; Ádám, Veronika/0000-0002-8350-8701}
}

@article{MTMT:1030929,
	title = {Oxidative stress-induced changes in the redox state and citric acid cycle function in isolated nerve endings},
	url = {https://m2.mtmt.hu/api/publication/1030929},
	author = {Tretter, László and Rózsa, Adrienn and Chinopoulos, Christos and Ádám, Veronika},
	journal-iso = {J NEUROCHEM},
	journal = {JOURNAL OF NEUROCHEMISTRY},
	volume = {73},
	unique-id = {1030929},
	issn = {0022-3042},
	year = {1999},
	eissn = {1471-4159},
	pages = {S200-S200},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886; Chinopoulos, Christos/0000-0003-0183-4149; Ádám, Veronika/0000-0002-8350-8701}
}

@article{MTMT:1030933,
	title = {Mitochondrial membrane potential in isolated nerve terminals under peroxidative stress.},
	url = {https://m2.mtmt.hu/api/publication/1030933},
	author = {Chinopoulos, Christos and Tretter, László and Ádám, Veronika},
	journal-iso = {J NEUROCHEM},
	journal = {JOURNAL OF NEUROCHEMISTRY},
	volume = {71},
	unique-id = {1030933},
	issn = {0022-3042},
	year = {1998},
	eissn = {1471-4159},
	pages = {S16-S16},
	orcid-numbers = {Chinopoulos, Christos/0000-0003-0183-4149; Tretter, László/0000-0001-5638-2886; Ádám, Veronika/0000-0002-8350-8701}
}

@article{MTMT:108534,
	title = {Effects of retinoic acid on rat forebrain cells derived from embryonic and perinatal rats},
	url = {https://m2.mtmt.hu/api/publication/108534},
	author = {Környei, Zsuzsanna and Tóth, B and Tretter, László and Madarász, Emilia},
	doi = {10.1016/S0197-0186(98)00063-1},
	journal-iso = {NEUROCHEM INT},
	journal = {NEUROCHEMISTRY INTERNATIONAL},
	volume = {33},
	unique-id = {108534},
	issn = {0197-0186},
	year = {1998},
	eissn = {1872-9754},
	pages = {541-549},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886}
}

@article{MTMT:1030935,
	title = {Plasma membrane depolarization and disturbed Na+ homeostasis induced by the protonophore carbonyl cyanide-p-trifluoromethoxyphenyl-hydrazon in isolated nerve terminals},
	url = {https://m2.mtmt.hu/api/publication/1030935},
	author = {Tretter, László and Chinopoulos, Christos and Ádám, Veronika},
	doi = {10.1124/mol.53.4.734},
	journal-iso = {MOL PHARMACOL},
	journal = {MOLECULAR PHARMACOLOGY},
	volume = {53},
	unique-id = {1030935},
	issn = {0026-895X},
	year = {1998},
	eissn = {1521-0111},
	pages = {734-741},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886; Chinopoulos, Christos/0000-0003-0183-4149; Ádám, Veronika/0000-0002-8350-8701}
}

@article{MTMT:1030934,
	title = {The neuroprotective drug vinpocetine prevents veratridine-induced [Na+](i) and [Ca2(+)](i) rise in synaptosomes},
	url = {https://m2.mtmt.hu/api/publication/1030934},
	author = {Tretter, László and Ádám, Veronika},
	doi = {10.1097/00001756-199806010-00034},
	journal-iso = {NEUROREPORT},
	journal = {NEUROREPORT},
	volume = {9},
	unique-id = {1030934},
	issn = {0959-4965},
	year = {1998},
	eissn = {1473-558X},
	pages = {1849-1853},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886; Ádám, Veronika/0000-0002-8350-8701}
}

@article{MTMT:1030859,
	title = {Enhanced stimulation-evoked Ca2+-signal and impaired ATP production by hydrogen peroxide in synaptosomes. Comparison with the effect of protonophores},
	url = {https://m2.mtmt.hu/api/publication/1030859},
	author = {Ádám, Veronika and Tretter, László and Chinopoulos, Christos},
	journal-iso = {J NEUROCHEM},
	journal = {JOURNAL OF NEUROCHEMISTRY},
	volume = {69},
	unique-id = {1030859},
	issn = {0022-3042},
	year = {1997},
	eissn = {1471-4159},
	pages = {S214-S214},
	orcid-numbers = {Ádám, Veronika/0000-0002-8350-8701; Tretter, László/0000-0001-5638-2886; Chinopoulos, Christos/0000-0003-0183-4149}
}

@article{MTMT:1030858,
	title = {Enhanced depolarization-evoked calcium signal and reduced [ATP]/[ADP] ratio are unrelated events induced by oxidative stress in synaptosomes},
	url = {https://m2.mtmt.hu/api/publication/1030858},
	author = {Tretter, László and Chinopoulos, Christos and Ádám, Veronika},
	doi = {10.1046/j.1471-4159.1997.69062529.x},
	journal-iso = {J NEUROCHEM},
	journal = {JOURNAL OF NEUROCHEMISTRY},
	volume = {69},
	unique-id = {1030858},
	issn = {0022-3042},
	year = {1997},
	eissn = {1471-4159},
	pages = {2529-2537},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886; Chinopoulos, Christos/0000-0003-0183-4149; Ádám, Veronika/0000-0002-8350-8701}
}

@article{MTMT:1030860,
	title = {Early events in isolated nerve terminals due to free radicals},
	url = {https://m2.mtmt.hu/api/publication/1030860},
	author = {Ádám, Veronika and Tretter, László},
	journal-iso = {J NEUROCHEM},
	journal = {JOURNAL OF NEUROCHEMISTRY},
	volume = {66},
	unique-id = {1030860},
	issn = {0022-3042},
	year = {1996},
	eissn = {1471-4159},
	pages = {S31-S31},
	orcid-numbers = {Ádám, Veronika/0000-0002-8350-8701; Tretter, László/0000-0001-5638-2886}
}

@article{MTMT:1030862,
	title = {Early events in free radical-mediated damage of isolated nerve terminals: Effects of peroxides on membrane potential and intracellular Na+ and Ca+ concentrations},
	url = {https://m2.mtmt.hu/api/publication/1030862},
	author = {Tretter, László and Ádám, Veronika},
	doi = {10.1046/j.1471-4159.1996.66052057.x},
	journal-iso = {J NEUROCHEM},
	journal = {JOURNAL OF NEUROCHEMISTRY},
	volume = {66},
	unique-id = {1030862},
	issn = {0022-3042},
	year = {1996},
	eissn = {1471-4159},
	pages = {2057-2066},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886; Ádám, Veronika/0000-0002-8350-8701}
}

@article{MTMT:1030861,
	title = {Free radicals enhance Ca2+-signal and inhibit glutamate release in response to K+-depolarization in synaptosomes},
	url = {https://m2.mtmt.hu/api/publication/1030861},
	author = {Tretter, László and Ádám, Veronika},
	journal-iso = {J NEUROCHEM},
	journal = {JOURNAL OF NEUROCHEMISTRY},
	volume = {66},
	unique-id = {1030861},
	issn = {0022-3042},
	year = {1996},
	eissn = {1471-4159},
	pages = {S59-S59},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886; Ádám, Veronika/0000-0002-8350-8701}
}

@article{MTMT:1030864,
	title = {RELATION OF [CA2+](I) TO DOPAMINE RELEASE IN STRIATAL SYNAPTOSOMES - ROLE OF CA2+ CHANNELS},
	url = {https://m2.mtmt.hu/api/publication/1030864},
	author = {Carvalho, C M and Ferreira, I L and Duarte, C B and Malva, J O and Tretter, László and Ádám, Veronika and Carvalho, A P},
	doi = {10.1016/0006-8993(94)01252-D},
	journal-iso = {BRAIN RES},
	journal = {BRAIN RESEARCH},
	volume = {669},
	unique-id = {1030864},
	issn = {0006-8993},
	year = {1995},
	eissn = {1872-6240},
	pages = {234-244},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886; Ádám, Veronika/0000-0002-8350-8701}
}

@article{MTMT:1030866,
	title = {THE EFFECT OF FREE-RADICALS ON SYNAPTOSOMAL IONIC HOMEOSTASIS},
	url = {https://m2.mtmt.hu/api/publication/1030866},
	author = {Tretter, László and Bors, P and Ádám, Veronika},
	journal-iso = {J NEUROCHEM},
	journal = {JOURNAL OF NEUROCHEMISTRY},
	volume = {63},
	unique-id = {1030866},
	issn = {0022-3042},
	year = {1994},
	eissn = {1471-4159},
	pages = {S92-S92},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886; Ádám, Veronika/0000-0002-8350-8701}
}

@article{MTMT:1030871,
	title = {LACK OF INVOLVEMENT OF [CA2+]I IN THE EXTERNAL CA2+-INDEPENDENT RELEASE OF ACETYLCHOLINE EVOKED BY VERATRIDINE, OUABAIN AND ALPHA-LATROTOXIN - POSSIBLE ROLE OF [NA+]I},
	url = {https://m2.mtmt.hu/api/publication/1030871},
	author = {Ádám, Veronika and Deri, Z and Bors, P and Tretter, László},
	doi = {10.1016/0928-4257(93)90023-M},
	journal-iso = {J PHYSIOL (PARIS 1992-)},
	journal = {JOURNAL OF PHYSIOLOGY (PARIS 1992-)},
	volume = {87},
	unique-id = {1030871},
	issn = {0928-4257},
	year = {1993},
	eissn = {1769-7115},
	pages = {43-50},
	orcid-numbers = {Ádám, Veronika/0000-0002-8350-8701; Tretter, László/0000-0001-5638-2886}
}

@article{MTMT:1030868,
	title = {RELATIONSHIP BETWEEN SYNAPTOSOMAL ION DISTRIBUTION AND NEUROTRANSMITTER RELEASE - EFFECT OF HYDROPEROXIDES},
	url = {https://m2.mtmt.hu/api/publication/1030868},
	author = {Bors, P and Tretter, László and Ádám, Veronika},
	journal-iso = {J NEUROCHEM},
	journal = {JOURNAL OF NEUROCHEMISTRY},
	volume = {61},
	unique-id = {1030868},
	issn = {0022-3042},
	year = {1993},
	eissn = {1471-4159},
	pages = {S144-S144},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886; Ádám, Veronika/0000-0002-8350-8701}
}

@article{MTMT:1507442,
	title = {SEVERE DEPLETION OF CELLULAR THIOLS AND GLUTATHIONE-RELATED ENZYMES OF A CARMUSTINE-RESISTANT L1210 STRAIN ASSOCIATES WITH COLLATERAL SENSITIVITY TO CYCLOPHOSPHAMIDE},
	url = {https://m2.mtmt.hu/api/publication/1507442},
	author = {INSTITORIS, E and Tretter, László and GAAL, D},
	doi = {10.1007/BF00686029},
	journal-iso = {CANCER CHEMOTH PHARM},
	journal = {CANCER CHEMOTHERAPY AND PHARMACOLOGY},
	volume = {33},
	unique-id = {1507442},
	issn = {0344-5704},
	year = {1993},
	eissn = {1432-0843},
	pages = {85-88},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886}
}

@article{MTMT:1030870,
	title = {EFFECT OF HYDROPEROXIDES ON THE INTRACELLULAR [CA2+] AND MEMBRANE-POTENTIAL OF SYNAPTOSOMES},
	url = {https://m2.mtmt.hu/api/publication/1030870},
	author = {Tretter, László and Bors, P and Ádám, Veronika},
	journal-iso = {J NEUROCHEM},
	journal = {JOURNAL OF NEUROCHEMISTRY},
	volume = {61},
	unique-id = {1030870},
	issn = {0022-3042},
	year = {1993},
	eissn = {1471-4159},
	pages = {S156-S156},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886; Ádám, Veronika/0000-0002-8350-8701}
}

@inproceedings{MTMT:1059125,
	title = {Effects of free radical-generating agents on snaptosomal functions},
	url = {https://m2.mtmt.hu/api/publication/1059125},
	author = {Tretter, László and Bors, P and Berencsi, Andrea and Ádám, Veronika},
	booktitle = {Oxygen free radicals and scavengers in the natural sciences},
	unique-id = {1059125},
	year = {1993},
	pages = {115-118},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886; Ádám, Veronika/0000-0002-8350-8701}
}

@article{MTMT:1506658,
	title = {THE EFFECT OF THE RADIOPROTECTOR WR-2721 AND WR-1065 ON MITOCHONDRIAL LIPID-PEROXIDATION},
	url = {https://m2.mtmt.hu/api/publication/1506658},
	author = {Tretter, László and RONAI, E and Szabados, György and HERMANN, R and ANDO, A and HORVATH, I},
	doi = {10.1080/09553009014552611},
	journal-iso = {INT J RADIAT BIOL},
	journal = {INTERNATIONAL JOURNAL OF RADIATION BIOLOGY},
	volume = {57},
	unique-id = {1506658},
	issn = {0955-3002},
	year = {1990},
	eissn = {1362-3095},
	pages = {467-478},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886}
}

@article{MTMT:1506659,
	title = {LIPID-PEROXIDATION IN LIVER AND EHRLICH ASCITES CELL MITOCHONDRIA},
	url = {https://m2.mtmt.hu/api/publication/1506659},
	author = {Szabados, György and Tretter, László and HORVATH, I},
	doi = {10.3109/10715768909087938},
	journal-iso = {FREE RADIC RES COMM},
	journal = {FREE RADICAL RESEARCH COMMUNICATIONS},
	volume = {7},
	unique-id = {1506659},
	issn = {8755-0199},
	year = {1989},
	pages = {161-170},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886}
}

@article{MTMT:1506660,
	title = {LIPID-PEROXIDATION IN EHRLICH ASCITES CELL MITOCHONDRIA IS NOT DETERMINED BY THE POLY-UNSATURATED FATTY-ACID CONTENT OF THE MEMBRANE},
	url = {https://m2.mtmt.hu/api/publication/1506660},
	author = {Tretter, László and NGUYEN, TH and Szabados, György and HORVATH, I},
	doi = {10.1016/0006-291X(89)92143-8},
	journal-iso = {BIOCHEM BIOPH RES CO},
	journal = {BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS},
	volume = {163},
	unique-id = {1506660},
	issn = {0006-291X},
	year = {1989},
	eissn = {1090-2104},
	pages = {356-362},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886}
}

@article{MTMT:1506661,
	title = {THE INHIBITORY EFFECT OF SUCCINATE ON RADIATION-ENHANCED MITOCHONDRIAL LIPID-PEROXIDATION},
	url = {https://m2.mtmt.hu/api/publication/1506661},
	author = {RONAI, E and Tretter, László and Szabados, György and HORVATH, I},
	doi = {10.1080/09553008414552141},
	journal-iso = {INT J RADIAT BIOL},
	journal = {INTERNATIONAL JOURNAL OF RADIATION BIOLOGY},
	volume = {51},
	unique-id = {1506661},
	issn = {0955-3002},
	year = {1987},
	eissn = {1362-3095},
	pages = {611-617},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886}
}

@article{MTMT:1506662,
	title = {EFFECT OF SUCCINATE ON MITOCHONDRIAL LIPID-PEROXIDATION .1. COMPARATIVE-STUDIES ON FERROUS ION AND ADP.FE/NADPH-INDUCED PEROXIDATION},
	url = {https://m2.mtmt.hu/api/publication/1506662},
	author = {Szabados, György and ANDO, A and Tretter, László and HORVATH, I},
	journal-iso = {J BIOENERG BIOMEMBR},
	journal = {JOURNAL OF BIOENERGETICS AND BIOMEMBRANES},
	volume = {19},
	unique-id = {1506662},
	issn = {0145-479X},
	year = {1987},
	eissn = {1573-6881},
	pages = {21-30},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886}
}