Cyclosporin A protects hepatocytes subjected to high Ca2+ and oxidative stress

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Abstract
Hepatocytes incubated with 0.8 mM t -butylhydroperoxide are protected by cyclosporin A when the medium Ca 2+ concentration is 10 mM, but not when it is 2.5 mM. The highest Ca 2+ level is associated with an inhibition of t -butylhydroperoxide-dependent malondialdehyde accumulation and with mitochondrial Ca 2+ loading within the cells. These findings are new evidence that t -butylhydroperoxide can kill cells by peroxidation-dependent and -independent mechanisms, and suggest that the mitochondrial permeability transition and the resultant de-energization are components of the peroxidation-independent mechanism. Cyclosporin A may have considerable utility for the protection of cells subjected to oxidative stress.