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Cyclosporin A protects hepatocytes subjected to high Ca 2+ and oxidative stress
Author(s) -
Brockemeier Kimberly M.,
Carpenter-Deyo Laurie,
Reed Donald J.,
Pfeiffer Douglas R.
Publication year - 1992
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(92)80616-o
Subject(s) - oxidative stress , oxidative phosphorylation , chemistry , microbiology and biotechnology , biophysics , biochemistry , biology
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.