Mitochondrial dysfunction during anoxia and acute cell injury.
Mitochondrial function is closely linked to the maintenance of mitochondrial integrity. During short-term anoxia, ion-transport systems in the inner membrane are inhibited to protect against loss of the promotive force and associated osmotic imbalance that can cause irreversible loss of mitochondrial integrity and function. In two models of chemically induced mitochondrial failure, a prostaglandin B1 derivative, di-calciphor, protected against mitochondrial failure and prevented cell death. Characteristics were similar to those observed in mitochondria during short-term anoxia. Thus, the results indicate that di-calciphor may represent a new type of mitochondrial protectant that inhibits ion transport and thus slows the loss of osmotic stability and delays mitochondrial dysfunction under traumatic and toxicologic conditions.
Jones
D P
DP
Department of Biochemistry, Emory University, Atlanta, GA 30322, USA.
D000818:Animals; D016923:Cell Death / Q000187:drug effects; D015687:Cell Hypoxia; D002470:Cell Survival / Q000187:drug effects; D002477:Cells / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D008099:Liver / Q000166:cytology* / Q000187:drug effects; D008930:Mitochondria, Liver / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D011190:Potassium Cyanide / Q000494:pharmacology; D011456:Prostaglandins B / Q000494:pharmacology; D051381:Rats
D011456:Prostaglandins B; C076722:di-Calciphor; D011190:Potassium Cyanide