Das A M, Byrd D J, Brodehl J
Department of Pediatric Nephrology and Metabolic Disorders, Children's Hospital, Hannover Medical School, Germany.
Clin Chim Acta. 1994 Nov;231(1):61-8. doi: 10.1016/0009-8981(94)90254-2.
The F1F0-ATPase activity of mitochondrial complex V can be rapidly measured in sonicated preparations of monolayer skin fibroblast cultures from children. We show that direct regulation at the level of ATP-synthase occurs in these cell preparations. ATP-synthase capacity is decreased in response to blocking of the respiratory chain by cyanide (mimicking anoxia) or uncoupling of mitochondria. ATP-synthase capacity falls to 60% and 35% of control, respectively. Up-regulation of ATP-synthase can be demonstrated in fibroblasts exposed to 4 mmol/l calcium (127% of control). Mitochondrial recovery was unchanged under the different incubation conditions as judged by the activity of mitochondrial marker enzymes. We conclude that direct regulation at the level of ATP-synthase occurs in vivo in human fibroblasts. The naturally occurring inhibitor protein IF1 and the calcium binding inhibitor protein CaBI may be involved in this regulation of ATP-synthase.
儿童单层皮肤成纤维细胞培养物的超声处理制剂中，线粒体复合物V的F1F0 - ATP酶活性可被快速测定。我们发现，在这些细胞制剂中，ATP合酶水平存在直接调控。氰化物阻断呼吸链（模拟缺氧）或线粒体解偶联时，ATP合酶活性降低。ATP合酶活性分别降至对照的60%和35%。暴露于4 mmol/l钙的成纤维细胞中，可证明ATP合酶上调（为对照的127%）。根据线粒体标记酶的活性判断，不同孵育条件下线粒体恢复情况未变。我们得出结论，ATP合酶水平的直接调控在人成纤维细胞体内发生。天然存在的抑制蛋白IF1和钙结合抑制蛋白CaBI可能参与了ATP合酶的这种调控。
