Mitochondrial protonophoric activity induced by a thyromimetic fatty acid analogue

被引：12

作者：

Hermesh, O ^{[1
]}

Kalderon, B ^{[1
]}

Berman, B ^{[1
]}

Bar-Tana, J ^{[1
]}

机构：

[1] Hebrew Univ Jerusalem, Sch Med, Fac Med, Dept Human Nutr & Metab, IL-91120 Jerusalem, Israel

来源：

BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS | 2000年 / 1457卷 / 03期

关键词：

mitochondria; uncoupling; fatty acid; thyroid hormone;

D O I：

10.1016/S0005-2728(00)00097-9

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Calcium-dependent uncoupling of liver mitochondrial oxidative phosphorylation by a non-metabolizable long chain fatty acyl analogue was compared with uncoupling induced by in vivo thyroid hormone treatment. beta,beta'-Methyl-substituted hexadecane alpha,omega-dioic acid (Medica 16) is reported heir to induce a saturable 20-30% decrease in liver mitochondrial Delta Psi, Delta pH and protonmotive force which proceeds in the presence of added Ca2+ to cyclosporin A-sensitive mitochondrial permeabilization. Ca2+-dependent uncoupling by Medica 16 was accompanied by atractylate-enhanced, bongkrekic-inhibited activation of mitochondrial Ca2+ efflux, The direct mitochondrial effect exerted in vitro by Medica 16 is similar to that induced by in vivo thyroid hormone treatment, Hence, the thyromimetic protonophoric activity of Medica 16 and the uncoupling activity of TH converge onto components of the mitochondrial permeabilization transition pore, (C) 2000 Elsevier Science B.V, All rights reserved.

引用

页码：166 / 174

页数：9

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