Thyroxine regulation of monolysocardiolipin acyltransferase activity in rat heart

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-C-14]linoleate and a 1.7-fold incr ease (P < 0.025) in [1-C-14]oleate incorporated into cardiolipin in perfuse d hearts, compared with controls. The mechanism for the elevation in incorp oration of unsaturated fatty acids into cardiolipin was a 1.6-fold (P < 0.0 25) 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 biosynthe sis is accompanied by an elevation in monolysocardiolipin acyltransferase a ctivity to maintain the appropriate molecular species composition of cardio lipin in the cardiac mitochondrial membrane. We postulate that monolysocard iolipin acyltransferase might be a rate-limiting enzyme for the molecular r emodelling of cardiolipin in the heart.