脂肪酸和 Ca2+对脑线粒体 NADH：泛醌氧化还原酶（复合体 I）的协同抑制作用。

Synergetic inhibition of the brain mitochondrial NADH:ubiquinone oxidoreductase (complex I) by fatty acids and Ca2+.

机构信息

Department of Biochemistry, Biological Faculty, Lomonosov Moscow State University, Moscow, 119992, Russia.

出版信息

Biochemistry (Mosc). 2011 Aug;76(8):968-75. doi: 10.1134/S000629791108013X.

PMID:22022971

Abstract

The NADH:ubiquinone oxidoreductase (respiratory complex I) activity of inside-out pig brain submitochondrial particles is inhibited by endogenous or externally added free fatty acids in time-dependent fashion. The rate and degree of the inhibition is dramatically increased by Ca2+. The Ca2+-promoted, fatty acid-induced inhibition is pH dependent, this being particularly evident at pH > 8.0. The inhibition is completely reversed by either EGTA or by bovine serum albumin (BSA). BSA prevents previously described (Kotlyar, A. B., Sled, V. D., and Vinogradov, A. D. (1992) Biochim. Biophys. Acta, 1098, 144-150) inhibitory effect of Ca2+ and alkaline pH on the de-active-to-active form transition of complex I. A possible mechanism of synergetic inhibition on complex I by Ca2+ and fatty acids is discussed.

摘要

线粒体内膜小泡的 NADH：泛醌氧化还原酶（呼吸复合物 I）的活性可被内源性或外加的游离脂肪酸按时间依赖性方式抑制。Ca2+ 显著增强抑制的速度和程度。Ca2+ 促进的、脂肪酸诱导的抑制依赖于 pH 值，在 pH 值 > 8.0 时尤为明显。抑制作用可被 EGTA 或牛血清白蛋白（BSA）完全逆转。BSA 可预防先前描述的（Kotlyar，A. B.，Sled，V. D.，和 Vinogradov，A. D.（1992）生物化学。生物物理。学报，1098，144-150）Ca2+ 和碱性 pH 值对复合物 I 的去活-活化形式转变的抑制作用。讨论了 Ca2+ 和脂肪酸对复合物 I 协同抑制的可能机制。