P. Fatterpaker

Effect of thyroid deficiency on oxidative phosphorylation in rat liver, kidney, and brain mitochondria.

Abstract The effect of thyroidectomy on oxidative metabolism of rat liver, kidney, and brain mitochondria has been examined. The respiration in liver, kidney, and brain mitochondria was affected differentially after thyroidectomy, the common effect in all the tissues being the impairment in state 3 as well as state 4 rates of succinate oxidation. Thyroidectomy did not have any effect on ADP O ratios; however, compared to normal, respiratory control indexes were, in general, somewhat higher. Thyroidectomy also did not alter total ATPase activity of liver, kidney, and brain mitochondria, although the basal ATPase activity had decreased significantly under these conditions. The cytochrome content of the mitochondria also showed tissue-specific changes after thyroidectomy; however, no significant changes in the absorption characteristics of the cytochromes were seen. The succinate and glutamate dehydrogenase activities of mitochondria from liver, kidney, and brain were not affected by thyroidectomy, thereby ruling out the possibility that the decrease in substrate oxidation may be due to alterations in the primary dehydrogenase levels. It is concluded that thyroid hormone(s) may have a tissue-specific role in regulating the metabolic functions of mitochondria.

Effect of 2, 4-dinitrophenol (DNP) on oxidative phosphorylation in rat liver mitochondria.

The effects of a range of DNP concentrations on ADP/O ratio, respiratory control index (RCI), and stimulation of latent ATPase activity of mitochondria have been studied using various substrates. The first and third sites of phosphorylation were found to be more sensitive to DNP action as compared to the second site. No correlation could be seen between any of the three parameters studied. Fluoride was inhibitory to the stimulation of ATPase by DNP only in presence of high concentrations of DNP, but had no inhibitory effect at low DNP concentrations. The inhibitory effects of fluoride and substrates were not additive.

Occurrence of α-tocopherol binding protein in rat liver cell sap

An α-tocopherol binding lipoprotein, from rat liver cell sap has been isolated and purified. Its possible involvement in the intracellular transport and distribution of the vitamin is discussed.

REGULATION OF MITOCHONDRIAL MEMBRANE PROTEIN TURNOVER BY THYROID HORMONE(S)

Effects of thyroidectomy on turnover rate of proteins of rat liver mitochondria, mitochondrial membranes and microsomes were examined. Thyroidectomy resulted in a significant increase in the half-lives of whole mitochondria and inner membrane-matrix, the effect being less pronounced on the half-lives of outer mitochondrial membrane and microsomes.

Effect of protein deficiency on absorption, transport and distribution of α-tocopherol in the rat

The absorption, transport and distribution of alpha-[3H]tocopherol were greatly decreased in protein deficiency. This was reflected in the subcellular distribution of alpha-[3H]tocopherol in livers of protein-deficient rats. The ratio, bound:free for alpha-[3H]tocopherol, also decreased in both serum and liver cytosol. After protein refeeding, absorption, transport and distribution patterns of alpha-[3H]tocopherol for the protein-deficient rats were restored to patterns similar to those of control animals.

Effect of vitamin E deficiency on lipid composition of CNS-myelin in the rat

Vitamin E deficiency in the rat is accompanied by a decrease in total lipids and in cholesterol and an elevation in the lysolecithin content of CNS-myelin.

Effect of tri-iodothyronine treatment on electrophoretic mobilities of rat liver mitochondrial fractions

Abstract Heterogeneity of mitochondrial fractions, observed earlier in respect of membrane-bound enzyme profiles and protein turnover, is not reflected in their electrophoretic mobilities. Administration of tri-iodothyronine to thyroidectomised rats results in decreased electrophoretic mobilities of all the mitochondrial fractions.