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- W2066380764 abstract "Hypoxia/reperfusion injury is a major clinical problem. One of its hallmarks is an increased cytosolic Ca 2+ content and an increased generation of reactive oxygen species in the cytosol and in mitochondria. In the present study of an in vitro model of hypoxia/reperfusion injury, mitochondria are exposed to Ca 2+ in combination with extra‐ and intramitochondrially acting prooxidants. In this model mitochondria are damaged in a Ca 2+ ‐dependent manner. The extent and the site(s) of damage depend on both the kind of respiratory substrate and prooxidant used. The major damage occurs specifically at site I of the respiratory chain, and is due to hydrolysis of oxidized pyridine nucleotides and Ca 2+ release followed by Ca 2+ re‐uptake (Ca 2+ ‘cycling’). Cyclosporine A completely protects against this damage. The protection is due to inhibition of pyridine nucleotide hydrolysis, an obligatory step in the sequence of events that links prooxidants to Ca 2+ release from intact mitochondria." @default.
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- W2066380764 title "Cyclosporine A protects mitochondria in an in vitro model of hypoxia/reperfusion injury" @default.
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- W2066380764 doi "https://doi.org/10.1016/0014-5793(93)80682-k" @default.
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