The role of glutathione in the retention of Ca2+ by liver mitochondria.

摘要: Concentrations of rhein and nitrofurantoin in the micromolar range induce Ca2+ release development increased inner membrane permeability liver mitochondria. Both compounds inhibit mitochondrial glutathione reductase causing a depletion GSH an accumulation GSSG energized Under these conditions, also alter oxidation state pyridine nucleotides, NADH becoming oxidized while NADPH remains reduced. Using or nitrofurantoin, together with t-butyl-hydroperoxide beta-hydroxybutyrate, it is possible to selectively NAD/NADH, NADP/NADPH, GSSG/GSH ratios determine effect different states on ability produce permeable membrane. No correlation between nucleotide sensitivity was observed. Mitochondria are stable when content high, but become present converted GSSG. It proposed that ratio, by controlling reduction critical sulfhydryl groups, regulates lysophospholipid acyltransferase activity and, therefore, mitochondria remain impermeable upon activation intramitochondrial requiring phospholipase A2.