Mutter T, Dolinsky V W, Ma B J, Taylor W A, Hatch G M
Department of Pharmacology and Therapeutics, University of Manitoba, A307 Chown Building, 753 McDermot Avenue, Winnipeg, Manitoba, Canada R3E OW3.
Biochem J. 2000 Mar 1;346 Pt 2(Pt 2):403-6.
Treatment of rats with thyroxine has been shown to elevate the biosynthesis and content of cardiolipin in the heart [Cao, Cheng, Angel and Hatch (1995) Biochim. Biophys. Acta 1256, 241-244]. Treatment with thyroxine resulted in a 1.8-fold increase (P<0.025) in [1-(14)C]linoleate and a 1.7-fold increase (P<0.025) in [1-(14)C]oleate incorporated into cardiolipin in perfused hearts, compared with controls. The mechanism for the elevation in incorporation of unsaturated fatty acids into cardiolipin was a 1. 6-fold (P<0.025) increase in mitochondrial monolysocardiolipin acyltransferase activity. The results demonstrate that the acylation of cardiac monolysocardiolipin is regulated by thyroid hormone. Thus an elevation in cardiolipin biosynthesis is accompanied by an elevation in monolysocardiolipin acyltransferase activity to maintain the appropriate molecular species composition of cardiolipin in the cardiac mitochondrial membrane. We postulate that monolysocardiolipin acyltransferase might be a rate-limiting enzyme for the molecular remodelling of cardiolipin in the heart.
已证明用甲状腺素处理大鼠可提高心脏中心磷脂的生物合成及含量[曹、程、安吉尔和哈奇（1995年）《生物化学与生物物理学报》1256卷，241 - 244页]。与对照组相比，用甲状腺素处理导致灌注心脏中掺入心磷脂的[1 - （14）C]亚油酸增加1.8倍（P<0.025），[1 - （14）C]油酸增加1.7倍（P<0.025）。不饱和脂肪酸掺入心磷脂增加的机制是线粒体单溶血心磷脂酰基转移酶活性增加1.6倍（P<0.025）。结果表明心脏单溶血心磷脂的酰化受甲状腺激素调节。因此，心磷脂生物合成的增加伴随着单溶血心磷脂酰基转移酶活性的增加，以维持心脏线粒体膜中心磷脂适当的分子种类组成。我们推测单溶血心磷脂酰基转移酶可能是心脏中心磷脂分子重塑的限速酶。
