TY  - CHAP
AU  - Tretter, László
ED  - Mandl, József
ED  - Csala, Miklós
TI  - Aminosav-, fehérje-anyagcsere
T2  - Orvosi patobiokémia
PB  - Medicina Könyvkiadó Zrt.
CY  - Budapest
SN  - 9789632267821
PY  - 2023
SP  - 121
EP  - 142
PG  - 22
UR  - https://m2.mtmt.hu/api/publication/34722580
ID  - 34722580
LA  - Hungarian
DB  - MTMT
ER  - 

TY  - CONF
AU  - Kokas, Márton
AU  - Kirchlechner-Farkas, Judit Mária
AU  - Gáspár, Dániel
AU  - Komlódi, Tímea
AU  - Ozohanics, Olivér
AU  - Környei, Zsuzsanna
AU  - Sváb, Gergely
AU  - Tretter, László
TI  - METABOLIKUS POLIHISZTOR VAGY EGYSZERŰ GLUTAMINGYÁR? – CITRÁTKÖR AZ ASZTROCITÁKBAN
T2  - Membrán-Transzport konferencia : programfüzet
PB  - Pécsi Tudományegytem
C1  - Sümeg
C1  - Pécs
PY  - 2023
UR  - https://m2.mtmt.hu/api/publication/34030843
ID  - 34030843
LA  - Hungarian
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Weidinger, A.
AU  - Milivojev, N.
AU  - Hosmann, A.
AU  - Duvigneau, J.C.
AU  - Szabo, C.
AU  - Törö, G.
AU  - Rauter, L.
AU  - Vaglio-Garro, A.
AU  - Mkrtchyan, G.V.
AU  - Trofimova, L.
AU  - Sharipov, R.R.
AU  - Surin, A.M.
AU  - Krasilnikova, I.A.
AU  - Pinelis, V.G.
AU  - Tretter, László
AU  - Moldzio, R.
AU  - Bayır, H.
AU  - Kagan, V.E.
AU  - Bunik, V.I.
AU  - Kozlov, A.V.
TI  - Oxoglutarate dehydrogenase complex controls glutamate-mediated neuronal death
JF  - REDOX BIOLOGY
J2  - REDOX BIOL
VL  - 62
PY  - 2023
PG  - 15
SN  - 2213-2317
DO  - 10.1016/j.redox.2023.102669
UR  - https://m2.mtmt.hu/api/publication/33718236
ID  - 33718236
LA  - English
DB  - MTMT
ER  - 

TY  - CONF
AU  - Kokas, Márton
AU  - Horváth, Gergő
AU  - Tretter, László
TI  - AZ α-KETOGLUTARÁT-DEHIDROGENÁZ KOMPLEX DLST+/- ÉS DLD+/- ALEGYSÉGEK KIÜTÉSÉNEK HATÁSA AZ OXIGÉNFOGYASZTÁSRA ÉS REAKTÍV OXIGÉNGYÖKKÉPZŐDÉSRE EGÉR AGYI MITOKONDRIUMOKON
T2  - 51. Membrán-Transzport Konferencia
PY  - 2022
UR  - https://m2.mtmt.hu/api/publication/34030854
ID  - 34030854
LA  - Hungarian
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Horváth, Gergő
AU  - Sváb, Gergely
AU  - Komlódi, Tímea
AU  - Ravasz, Dóra
AU  - Kacsó, Gergely
AU  - Dóczi, Judit
AU  - Chinopoulos, Christos
AU  - Ambrus, Attila
AU  - Tretter, László
TI  - Reverse and Forward Electron Flow-Induced H2O2 Formation Is Decreased in α-Ketoglutarate Dehydrogenase (α-KGDH) Subunit (E2 or E3) Heterozygote Knock Out Animals
JF  - ANTIOXIDANTS
J2  - ANTIOXIDANTS-BASEL
VL  - 11
PY  - 2022
IS  - 8
PG  - 19
SN  - 2076-3921
DO  - 10.3390/antiox11081487
UR  - https://m2.mtmt.hu/api/publication/33070137
ID  - 33070137
N1  - Cited By :1            
            Export Date: 7 October 2022            
            Correspondence Address: Tretter, L.; Department of Biochemistry, Hungary; email: tretter.laszlo@med.semmelweis-univ.hu            
            Funding details: Semmelweis Egyetem, STIA-OTKA-2021, TKP2021-EGA-25            
            Funding details: Nemzeti Kutatási, Fejlesztési és Innovaciós Alap, NKFIA, EFOP-3.6.3-VEKOP-16-2017-00009            
            Funding text 1: This research was funded by the Hungarian Brain Research Program 2 (2017-1.2.1-NKP-2017-00002 to Vera Adam-Vizi, Semmelweis University), STIA-OTKA-2021 grant (from the Semmelweis University, to A.A.), TKP2021-EGA-25 grant to A.A. and C.C., Project no. TKP2021-EGA-25 has been implemented with the support provided by the Ministry of Innovation and Technology of Hungary from the National Research, Development and Innovation Fund, financed under the TKP2021-EGA funding scheme. EFOP-3.6.3-VEKOP-16-2017-00009 support to G.S.
AB  - 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.
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Daradics, Noémi
AU  - Horváth, Gergő
AU  - Tretter, László
AU  - Paál, Ágnes
AU  - Fülöp, András
AU  - Budai, András
AU  - Szijártó, Attila
TI  - The effect of Cyclophilin D depletion on liver regeneration following associating liver partition and portal vein ligation for staged hepatectomy
JF  - PLOS ONE
J2  - PLOS ONE
VL  - 17
PY  - 2022
IS  - 7
PG  - 15
SN  - 1932-6203
DO  - 10.1371/journal.pone.0271606
UR  - https://m2.mtmt.hu/api/publication/32989211
ID  - 32989211
N1  - These authors contributed equally to this work: Andras Budai, Attila Szijarto
AB  - 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.
LA  - English
DB  - MTMT
ER  - 

TY  - GEN
AU  - Kokas, Márton
AU  - Sváb, Gergely
AU  - Tretter, László
TI  - A metilénkék hatása a citokróm-c redox állapotára in vivo és in vitro körülmények között
PY  - 2021
UR  - https://m2.mtmt.hu/api/publication/34036737
ID  - 34036737
LA  - Hungarian
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Sváb, Gergely
AU  - Kokas, Márton
AU  - Sipos, Ildikó
AU  - Ambrus, Attila
AU  - Tretter, László
TI  - Methylene Blue Bridges the Inhibition and Produces Unusual Respiratory Changes in Complex III-Inhibited Mitochondria. Studies on Rats, Mice and Guinea Pigs
JF  - ANTIOXIDANTS
J2  - ANTIOXIDANTS-BASEL
VL  - 10
PY  - 2021
IS  - 2
PG  - 18
SN  - 2076-3921
DO  - 10.3390/antiox10020305
UR  - https://m2.mtmt.hu/api/publication/31887594
ID  - 31887594
N1  - Funding details: KTIA_13_NAP-A-III/6            
            Funding details: 61826 690289, 61830Z0100            
            Funding details: Hungarian Scientific Research Fund, OTKA, NK 112230            
            Funding details: Magyar Tudományos Akadémia, MTA, MTA TKI 02001            
            Funding text 1: Funding: This research was funded by grants from the Hungarian Brain Research Program (KTIA_13_NAP-A-III/6 and 2017-1.2.1-NKP-2017-00002), OTKA (NK 112230), Hungarian Academy of Sciences (MTA TKI 02001) [all to Vera Adam-Vizi], and Hungarian Higher Education Institution Excellence Program (FIKP grants 61826 690289 EATV and 61830Z0100 EATV) [to A.A.].
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Veres, Balázs
AU  - Erős, Krisztián
AU  - Antus, Csenge Petra
AU  - Kálmán, Nikoletta
AU  - Fónai, Fruzsina
AU  - Jakus, Péter
AU  - Boros, Éva
AU  - Hegedűs, Zoltán
AU  - Nagy, István
AU  - Tretter, László
AU  - Gallyas, Ferenc
AU  - Sümegi, Balázs
TI  - Cyclophilin D-dependent mitochondrial permeability transition amplifies inflammatory reprogramming in endotoxemia
JF  - FEBS OPEN BIO
J2  - FEBS OPEN BIO
VL  - 11
PY  - 2021
IS  - 3
SP  - 684
EP  - 704
PG  - 21
SN  - 2211-5463
DO  - 10.1002/2211-5463.13091
UR  - https://m2.mtmt.hu/api/publication/31822211
ID  - 31822211
AB  - 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.
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Mikulás, Krisztina Ágnes
AU  - Komlódi, Tímea
AU  - Földes, Anna
AU  - Sváb, Gergely
AU  - Horváth, Gergő
AU  - Nagy, Ádám Miklós
AU  - Ambrus, Attila
AU  - Gyulai-Gaál, Szabolcs
AU  - Gera, István
AU  - Hermann, Péter
AU  - Varga, Gábor
AU  - Tretter, László
TI  - Bioenergetic impairment of triethylene glycol dimethacrylate- (TEGDMA-) treated dental pulp stem cells (DPSCs) and isolated brain mitochondria are amended by redox compound methylene blue
JF  - MATERIALS
J2  - MATERIALS
VL  - 13
PY  - 2020
IS  - 16
PG  - 19
SN  - 1996-1944
DO  - 10.3390/ma13163472
UR  - https://m2.mtmt.hu/api/publication/31595275
ID  - 31595275
N1  - Funding Agency and Grant Number: Hungarian Brain Research Program [KTIA_13_NAP-A-III/6, 2017-1.2.1-NKP-2017-00002]; OTKAOrszagos Tudomanyos Kutatasi Alapprogramok (OTKA) [NK 112230]; Hungarian Academy of SciencesHungarian Academy of Sciences [MTA TKI 02001]; Hungarian Human Resources Development Operational Program [EFOP-3.6.2-16-2017-00006]; Competition of Faculty of Dentistry, Semmelweis University; Higher Education Institutional Excellence Programme of the Ministry for Innovation and Technology in Hungary of the Semmelweis University [FIKP 61826 690289 EATV]
            Funding text: This work was supported by grants to the Hungarian Brain Research Program (KTIA_13_NAP-A-III/6 and 2017-1.2.1-NKP-2017-00002), OTKA (NK 112230), and the Hungarian Academy of Sciences (MTA TKI 02001), all to Vera Adam-Vizi, Hungarian Human Resources Development Operational Program (EFOP-3.6.2-16-2017-00006) to Gabor Varga and Anna Foldes, Competition of Faculty of Dentistry, Semmelweis University 2016 to Krisztina Mikulas. "The research was also financed by the Higher Education Institutional Excellence Programme of the Ministry for Innovation and Technology in Hungary, within the framework of the Neurology thematic programme of the Semmelweis University to Attila Ambrus (FIKP 61826 690289 EATV).
AB  - 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.
LA  - English
DB  - MTMT
ER  -