Suppression of mitochondrial respiratory function after short-term anoxia.
Exposure of rat hepatocytes to 30 min anoxia resulted in a substantial decrease in O2 consumption on reoxygenation. Measurement of the sequestered Ca2+ pool of mitochondria by selective release with the protonophore, carbonylcyanide-p-trifluoromethoxyphenylhydrazone (FCCP), and quantitation with the metallochromic indicator, arsenazo III, showed that anoxia caused a marked decrease in mitochondrial Ca2+. This loss could, in part, be due to decreased electrophoretic uptake resulting from a 20% decrease in the magnitude of the mitochondrial transmembranal potential. The decrease was associated with a decrease in ATP synthase activity as expected from the Ca2+ dependence of endogenous inhibitor binding to the ATP synthase. These results show that short-term anoxia suppresses mitochondrial function in hepatocytes and suggest that mitochondrial Ca2+ content may be important in this regulation. Regulation of the ATP synthase and other ion transport systems may provide a means to preserve ion distribution and protonmotive force and thereby prolong the period during which cells can tolerate anoxia.
D000818:Animals; D002118:Calcium / Q000502:physiology*; D004579:Electron Transport; D004721:Endoplasmic Reticulum / Q000502:physiology; D000860:Hypoxia / Q000503:physiopathology*; D007425:Intracellular Membranes / Q000502:physiology; D008297:Male; D008564:Membrane Potentials; D008930:Mitochondria, Liver / Q000502:physiology*; D010085:Oxidative Phosphorylation; D010101:Oxygen Consumption; D006180:Proton-Translocating ATPases / Q000378:metabolism; D051381:Rats; D013997:Time Factors
D006180:Proton-Translocating ATPases; D002118:Calcium