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• W1548077438 endingPage "2003" @default.
• W1548077438 startingPage "1995" @default.
• W1548077438 abstract "Cyclosporin A (CsA) is a potent inhibitor of the prooxidant-induced release of Ca2+ from isolated mitochondria. In this investigation, pretreatment of hepatocytes with CsA before exposure to the prooxidants tert-butyl hydroperoxide (tBH), cumene hydroperoxide or 3,5-dimethyl-N-acetyl-p-benzoquinone imine (3,5-Me2-NAPQI) prevented the loss of cell viability. HPLC analysis of adenine and pyridine nucleotide concentrations in hepatocytes treated with 3,5-Me2-NAPQI showed a rapid depletion of ATP prior to the loss of cell viability versus the maintenance of near control levels of ATP in hepatocytes treated with CsA before 3,5-Me2-NAPQI. In 3,5-Me2-NAPQI-exposed hepatocytes there was also a rapid loss of cellular NAD+ which could be accounted for initially by a transient increase in NADP+. Measurement of the intracellular Ca2+ pools showed an early depletion of the mitochondrial Ca2+ pool in hepatocytes exposed to 3,5-Me2-NAPQI, tBH or cumene hydroperoxide; this loss was prevented by CsA. In conclusion, these results show that CsA protected hepatocytes from prooxidant injury by preventing mitochondrial Ca2+ cycling and subsequent mitochondrial dysfunction. This suggests that in prooxidant injury, excessive Ca2+ cycling is an early and important event leading to mitochondrial damage and subsequently to cell death." @default.
• W1548077438 created "2016-06-24" @default.
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• W1548077438 date "1992-11-01" @default.
• W1548077438 modified "2023-09-30" @default.
• W1548077438 title "Cyclosporin a protects hepatocytes against prooxidant-induced cell killing" @default.
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• W1548077438 doi "https://doi.org/10.1016/0006-2952(92)90102-o" @default.
• W1548077438 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/1449518" @default.
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