胍衍生物对线粒体功能的影响。II. 游离脂肪酸对胍衍生物抑制作用的逆转。
Effects of guanidine derivatives on mitochondrial function. II. Reversal of guanidine-derivative inhibiton by free fatty acids.
作者信息
Davidoff F
出版信息
J Clin Invest. 1968 Oct;47(10):2344-58. doi: 10.1172/JCI105919.
Abstract
Long chain free fatty acids interfere with the inhibitory action of phenethylbiguanide and related compounds on mitochondrial respiration in vitro. This interference depends on binding of fatty acids to mitochondria and diminishes with decreasing chain length. Reversal of guanidine-derivative inhibition by fatty acids differs from that caused by dinitrophenol in that the effect of fatty acid is achieved without alteration in coupling or respiratory control. The binding of phenethylbiguanide to mitochondria is inhibited by both fatty acid and dinitrophenol. Serum albumin potentiates the inhibitory potency of guanidine derivatives, probably by removing endogenous mitochondrial free fatty acids.
摘要
长链游离脂肪酸在体外干扰苯乙双胍及相关化合物对线粒体呼吸的抑制作用。这种干扰取决于脂肪酸与线粒体的结合，并且随着链长的缩短而减弱。脂肪酸对胍衍生物抑制作用的逆转与二硝基苯酚所引起的不同，因为脂肪酸的作用是在不改变偶联或呼吸控制的情况下实现的。脂肪酸和二硝基苯酚均可抑制苯乙双胍与线粒体的结合。血清白蛋白可能通过去除内源性线粒体游离脂肪酸来增强胍衍生物的抑制效力。
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