Role of the Thyroid in the Synthesis of Heart, Liver and Kidney Mitochondrial Phospholipids1

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Abstract
The effect of thyroxine in vivo on the concentration and rate of incorporation of Pi32 into mitochondrial phospholipids and ATP has been investigated. The administration of thyroxine, 40 mg/kg/day for 6 days to produce hyperthyroidism, increased the incorporation of Pi32 into phosphatidyl inositol, sphingo-myelin, phosphatidyl choline, phosphatidyl serine and phosphatidyl ethanolamine of liver mitochondria and also increased the concentration of these phospholipid fractions. A similar increase was observed in phosphatidyl ethanolamine of kidney mitochondria, and phosphatidyl choline and phosphatidyl ethanolamine of heart mitochondria. The administration of propylthiouracil, 50 mg/kg/day for 11 days to produce hypothyroidism, decreased incorporation of Pi32 into all the phospholipid fractions of the liver, except phosphatidyl ethanolamine. Phosphatidyl choline and phosphatidyl ethanolamine fractions were decreased in the kidney. This dose of thyroxine stimulated the incorporation of Pi32 into liver mitochondrial ATP, and there was observed a decrease in the concentration of ATP in whole liver and in liver mitochondria. Thyroxine administration resulted in an increase in whole liver ATPase activity. There is a progressive increase of incorporation of Pi32 into ATP after continued daily injections of thyroxine.