@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}
}

@mastersthesis{MTMT:34509339,
	title = {Neuroprotektív vegyületek hatásmechanizmusának vizsgálata: a metilénkék és a vinpocetin mitokondriális célpontjai},
	url = {https://m2.mtmt.hu/api/publication/34509339},
	author = {Sváb, Gergely},
	doi = {10.14753/SE.2023.2792},
	unique-id = {34509339},
	year = {2023},
	orcid-numbers = {Sváb, Gergely/0000-0002-7669-8252}
}

@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}
}

@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: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:30677034,
	title = {The Arg244His missense mutation in SDHB-1 leads to altered metabolism in Caenorhabditis elegans: a new disease model},
	url = {https://m2.mtmt.hu/api/publication/30677034},
	author = {Saskői, Éva and Hujber, Zoltán and Likó, István and Meszaros, Katalin and Sarkadi, Balázs and Mátyási, Barbara and Kovács, Attila Lajos and Patthy, Laszlo and Nyírő, Gábor and Sváb, Gergely and Tretter, Laszlo and Mehta, Anil and Sebestyen, Anna and Patócs, Attila Balázs and Vellainé Takács, Krisztina},
	doi = {10.1530/endoabs.63.P444},
	journal-iso = {ENDOCR ABSTR},
	journal = {ENDOCRINE ABSTRACTS},
	volume = {63},
	unique-id = {30677034},
	issn = {1470-3947},
	year = {2019},
	eissn = {1479-6848},
	orcid-numbers = {Saskői, Éva/0000-0001-6691-8576; Likó, István/0000-0001-7668-4726; Sarkadi, Balázs/0000-0002-5839-1601; Nyírő, Gábor/0000-0002-0248-0007; Sváb, Gergely/0000-0002-7669-8252; Patócs, Attila Balázs/0000-0001-7506-674X; Vellainé Takács, Krisztina/0000-0002-4472-0363}
}

@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}
}

@{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}
}

@inproceedings{MTMT:3412391,
	title = {Modeling of the Citric Acid Cycle and its Two Shuttle Systems},
	url = {https://m2.mtmt.hu/api/publication/3412391},
	author = {Sváb, Gergely and Horváth, G and Szederkényi, Gábor},
	booktitle = {MED 2018},
	doi = {10.1109/MED.2018.8442579},
	unique-id = {3412391},
	year = {2018},
	pages = {70-77},
	orcid-numbers = {Sváb, Gergely/0000-0002-7669-8252; Szederkényi, Gábor/0000-0003-4199-6089}
}

@article{MTMT:30882909,
	title = {Dynamical modeling of the most important pathways in cellular metabolism},
	url = {https://m2.mtmt.hu/api/publication/30882909},
	author = {Sváb, Gergely and Szederkényi, Gábor},
	journal-iso = {JEDLIK LABOR REP},
	journal = {JEDLIK LABORATORIES REPORTS},
	volume = {5},
	unique-id = {30882909},
	issn = {2064-3942},
	year = {2017},
	pages = {1-24},
	orcid-numbers = {Sváb, Gergely/0000-0002-7669-8252; Szederkényi, Gábor/0000-0003-4199-6089}
}