缺血性细胞损伤的发病机制研究[j]。缺血细胞损伤后肾组织立方体、肾线粒体和亚线粒体颗粒的质子梯度和呼吸作用

W.J. Mergner, L. Marzella, C. Mergner, M.W. Kahng, M.W. Smith, B.F. Trump
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引用次数: 11

摘要

研究了组织立方体、离体线粒体和亚线粒体颗粒中的电子传递随缺血时间的变化。发现在缺血2小时后,所有系统的电子传递仍保持活跃。然而,NADH刺激的呼吸在ASU(氨-葡二酸-尿素)颗粒缺血2小时后下降,随后是基质脱氢酶的呼吸,底物如谷氨酸、α-酮戊二酸和丙酮酸加苹果酸。琥珀酸盐依赖性呼吸在控制水平下保持活跃。相比之下,质子梯度显示了两个阶段的变化:阶段A的特征是梯度逐渐增加,没有万霉素,在培养基中有万霉素,梯度迅速下降。阶段B的特点是质子梯度下降,有或没有valinomycin。提示缺血1 ~ 2小时质子梯度的改变是导致细胞不可逆损伤的重要因素。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Studies on the pathogenesis of ischemic cell injury VII. Proton gradient and respiration of renal tissue cubes, renal mitochondrial and submitochondrial particles following ischemic cell injury

Electron transport in tissue cubes, isolated mitochondria and submitochondria particles were examined as a function of ischemie time. It was found that electron transport remains active in all systems beyond the 2 hour ischemie time interval. The NADH stimulated respiration, however, declined after 2 hours of ischemia in ASU (Ammonia-Sephadex-Urea) particles followed by respiration with matrix-located dehydrogenases tested by substrates such as glutamate, α-ketoglutarate and pyruvate plus malate. Succinate dependent respiration remains active at control levels. In contrast proton gradient reveals changes in two phases: Phase A is characterized by gradually increasing gradient without valinomycin and by a rapidly declining gradient with valinomycin in the medium. Phase B is characterized by a declining proton gradient with or without valinomycin. It is suggested that the alteration of the proton gradient between 1 and 2 hours ischemia is an important factor contributing to irreversible cell injury.

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