Synergetic inhibition of the brain mitochondrial NADH:ubiquinone oxidoreductase (complex I) by fatty acids and Ca2+.
Synergetic inhibition of the brain mitochondrial NADH:ubiquinone oxidoreductase (complex I) by fatty acids and Ca2+.
复制标题
脂肪酸和 Ca2 协同抑制脑线粒体 NADH：泛醌氧化还原酶（复合物 I）。
DOI：
10.1134/s000629791108013x
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发表时间：
2011
期刊：
影响因子：
--
通讯作者：
Vinogradov,AD
中科院分区：
文献类型：
--
作者：
Kalashnikov,DS;Grivennikova,VG;Vinogradov,AD
内源性或外部添加的游离脂肪酸以时间依赖性方式抑制由内而外猪脑亚线粒体颗粒的NADH：泛醌氧化还原酶（呼吸复合物I）活性。Ca ~（2+）可显著提高抑制率和抑制程度。Ca 2+促进的、脂肪酸诱导的抑制是pH依赖性的，这在pH > 8.0时特别明显。EGTA或牛血清白蛋白（BSA）可完全逆转该抑制作用。BSA阻止先前描述的（Kotlyar，A. B.，斯莱德，弗吉尼亚，和Vinogradov，A. D.（1992）Biochim. Biophys. Acta，1098，144-150）Ca 2+和碱性pH对络合物I的失活至活性形式转变的抑制作用。讨论了Ca ~（2+）和脂肪酸协同抑制复合物Ⅰ的可能机理。
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.