Lemmi C A, Pelikan P C, Sikka S C, Hirschberg R, Geesaman B, Miller R L, Park K S, Liu S C, Koyle M, Rajfer J
Department of Anatomy and Cell Biology, University of California, Los Angeles 90024.
Am J Physiol. 1989 Nov;257(5 Pt 2):F837-41. doi: 10.1152/ajprenal.1989.257.5.F837.
The in vivo action of cyclosporine A (CS) on rat renal cortical mitochondria was investigated. CS (30 mg.kg-1.day-1) given orally to rats for 30 days caused an augmentation of renal mitochondrial oxidative phosphorylation. The ADP-stimulated respiratory rate was increased by 37.0% with glutamate plus malate as respiratory substrates (P less than 0.025) but not with succinate-supported respiration, indicating enhancement of mitochondrial complex I activity. This reaction may be a response to the 32.5% reduction of renal blood (P less than 0.005) in the CS-treated group, possibly serving to maximize ATP synthesis during ischemia. Ligation-induced decreases in renal blood flow also resulted in enhancement of mitochondrial complex I activity.
研究了环孢素A(CS)对大鼠肾皮质线粒体的体内作用。以30mg.kg-1.day-1的剂量给大鼠口服CS 30天,可使肾线粒体氧化磷酸化增强。以谷氨酸加苹果酸作为呼吸底物时,ADP刺激的呼吸速率增加了37.0%(P<0.025),而以琥珀酸支持呼吸时则未增加,表明线粒体复合体I活性增强。该反应可能是对CS处理组肾血流量降低32.5%(P<0.005)的一种反应,可能有助于在缺血期间使ATP合成最大化。结扎诱导的肾血流量减少也导致线粒体复合体I活性增强。