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棕色脂肪组织线粒体:脂肪酸和嘌呤核苷酸对32000道尔顿解偶联蛋白的调节

Brown-adipose-tissue mitochondria: the regulation of the 32000-Mr uncoupling protein by fatty acids and purine nucleotides.

作者信息

Rial E, Poustie A, Nicholls D G

出版信息

Eur J Biochem. 1983 Dec 1;137(1-2):197-203. doi: 10.1111/j.1432-1033.1983.tb07815.x.

DOI:10.1111/j.1432-1033.1983.tb07815.x
PMID:6317384
Abstract

The increased proton permeability induced by the addition of a synthetic proton translocator to non-respiring hamster brown-fat mitochondria is unaffected by purine nucleotide addition. In contrast the permeability induced by fatty acids is inhibited by nucleotide, indicating that fatty acids act at the 32000-Mr uncoupling protein. Fatty acids lower the affinity of nucleotide binding to the 32000-Mr protein, but not sufficiently to explain their uncoupling action. The sensitivity of the fatty acid modulation of permeability is dependent on chain length, extent of unsaturation and pH. There is a requirement for an unesterified carboxyl group. In respiring mitochondria fatty acids act in the presence of nucleotide by lowering the 'break-point' potential at which the conductance of the 32000-Mr protein increases. Fatty acids have no effect on the chloride uniport activity of the 32000-Mr protein, but decouple the interference between chloride and protons when the simultaneous transport of both ions is attempted.

摘要

向不进行呼吸作用的仓鼠棕色脂肪线粒体中添加合成质子转运体所诱导的质子通透性增加不受嘌呤核苷酸添加的影响。相比之下,脂肪酸所诱导的通透性受到核苷酸的抑制,这表明脂肪酸作用于分子量为32000的解偶联蛋白。脂肪酸降低了核苷酸与分子量为32000的蛋白结合的亲和力,但不足以解释它们的解偶联作用。脂肪酸对通透性调节的敏感性取决于链长、不饱和度和pH值。需要一个未酯化的羧基。在进行呼吸作用的线粒体中,脂肪酸在核苷酸存在的情况下通过降低分子量为32000的蛋白电导增加时的“断点”电位而起作用。脂肪酸对分子量为32000的蛋白的氯离子单向转运活性没有影响,但当尝试同时转运氯离子和质子时,脂肪酸可消除氯离子和质子之间的干扰。

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