Calcium requirement for anoxic liver cell injury.
There is disagreement as to whether Ca2+ entrance into the cell constitutes a final common pathway in cell death by a variety of injurious conditions. Pre-necrotic lesions and leakage of lactate dehydrogenase were induced both in isolated perfused rat livers and in freshly isolated hepatocytes by short exposure to anoxic conditions. Removal of Ca2+ from the media markedly reduced cell damage induced by anoxia in the perfused liver preparation but not in freshly isolated hepatocytes. Data obtained support the hypothesis that Ca2+ ions play a role in the process of cell death in intact preparations and possibly in vivo, and suggest that mechanism of cell necrosis may be different in the perfused liver than in freshly isolated suspended hepatocytes.
D000818:Animals; D002118:Calcium / Q000502:physiology*; D002470:Cell Survival / Q000187:drug effects; D000860:Hypoxia / Q000201:enzymology / Q000473:pathology; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008099:Liver / Q000098:blood supply; D008107:Liver Diseases / Q000201:enzymology / Q000473:pathology*; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains
D007770:L-Lactate Dehydrogenase; D002118:Calcium