Hypoxia-reoxygenation injury and the generation of reactive oxygen in isolated hepatocytes.
Reoxygenation following hypoxia enhanced loss of viability of isolated hepatocytes compared to cells maintained under hypoxic conditions. Cell damage due to reoxygenation was not dependent on the conversion of xanthine dehydrogenase to xanthine oxidase which occurred at a time when almost all the hepatocytes had lost their viability. The effect of reoxygenation was critically linked to the duration of the hypoxic period. During the hypoxic period degradation of endogenous glycogen may have provided sufficient substrate for glycolysis to contribute to maintenance of cell integrity by preservation of adenine nucleotides.
de Groot
H
H
Institut für Physiologische Chemie I, Universität Düsseldorf, FRG.
Anundi
I
I
Littauer
A
A
D000332:Aerobiosis; D000693:Anaerobiosis; D000818:Animals; D002470:Cell Survival; D002478:Cells, Cultured; D000860:Hypoxia / Q000473:pathology; D008099:Liver / Q000166:cytology / Q000201:enzymology / Q000473:pathology*; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D014969:Xanthine Oxidase / Q000378:metabolism
D014969:Xanthine Oxidase