期刊
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS
卷 474, 期 1, 页码 119-127出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.abb.2008.03.008
关键词
glutathione; dicarboxylates; transport; liver; mitochondria; hepatoma cells; oxidative stress
资金
- NIDDK NIH HHS [R01 DK040725, R01-DK40725] Funding Source: Medline
- NIEHS NIH HHS [P30 ES006639, P30-ES06639] Funding Source: Medline
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK040725] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES [P30ES006639] Funding Source: NIH RePORTER
Glutathione (GSH) is transported into renal mitochondria by the dicarboxylate (DIC: Slc25a10) and 2-oxo-glutarate carriers (OGC; Slc25a11). To determine whether these carriers function similarly in liver mitochondria, we assessed the effect of competition with specific substrates or inhibitors on GSH uptake in isolated rat liver mitochondria. GSH uptake was uniphasic, independent of ATP hydrolysis, and exhibited K-m, and V-max values of 4.08 mM and 3.06 nmol/min per mg protein, respectively. Incubation with butylmalonate and phenylsuccinate inhibited GSH uptake by 45-50%, although the individual inhibitors had no effect, suggesting in rat liver mitochondria, the DIC and OGC are only partially responsible for GSH uptake. H4IIE cells, a Fat hepatoma cell line, were stably transfected with the cDNA for the OGC, and exhibited increased uptake of GSH and 2-oxoglutarate and were protected from cytotoxicity induced by H2O2, methyl vinyl ketone, or cisplatin, demonstrating the protective function of increased mitochondrial GSH transport in the liver. (C) 2008 Elsevier Inc. All rights reserved.
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