Suppression of mitochondrial respiratory function after short-term anoxia.

Abstract

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.

• Authors: T Y Aw, B S Andersson, D P Jones
• Journal: The American journal of physiology (Am J Physiol) Vol. 252 Issue 4 Pt 1 Pg. C362-8 (Apr 1987) ISSN: 0002-9513 [Print] United States
• PMID: 2882683 (Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)

Chemical References

• Proton-Translocating ATPases
• Calcium

Topics

• Animals
• Calcium (physiology)
• Electron Transport
• Endoplasmic Reticulum (physiology)
• Hypoxia (physiopathology)
• Intracellular Membranes (physiology)
• Male
• Membrane Potentials
• Mitochondria, Liver (physiology)
• Oxidative Phosphorylation
• Oxygen Consumption
• Proton-Translocating ATPases (metabolism)
• Rats
• Time Factors