SUPPRESSION OF MITOCHONDRIAL RESPIRATORY-FUNCTION AFTER SHORT-TERM ANOXIA
SUPPRESSION OF MITOCHONDRIAL RESPIRATORY-FUNCTION AFTER SHORT-TERM ANOXIA
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DOI：
10.1152/ajpcell.1987.252.4.c362
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发表时间：
1987-04-01
影响因子：
--
通讯作者：
JONES, DP
中科院分区：
文献类型：
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作者：
AW, TY;ANDERSSON, BS;JONES, DP
暴露大鼠肝细胞缺氧30分钟导致在复氧的O2消耗量大幅下降。测量螯合的钙池的线粒体通过选择性释放的质子载体，羰基氰-对-三氟甲氧基苯腙（FCCP），和定量的金属显色指示剂，偶氮胂III，表明缺氧引起线粒体Ca 2+显着下降。这种损失可能，在某种程度上，是由于减少电泳吸收导致的线粒体跨膜电位的幅度下降20%。这种减少与ATP合酶活性的降低有关，正如从内源性抑制剂与ATP合酶结合的Ca 2+依赖性所预期的那样。这些结果表明，短期缺氧抑制肝细胞线粒体功能，并建议线粒体Ca 2+含量可能是重要的，在这种调节。ATP合成酶和其他离子转运系统的调节可以提供一种手段，以保持离子分布和质子动力，从而延长细胞可以耐受缺氧的时间。
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.