Thyroid hormone administered in vivo increased carrier-mediated (atractyloside-sensitive) ADP uptake by rat liver mitochondria. 3 Days after a single large dose of triiodothyronine (20 ;g/100 g of body weight), mitochondrial uptake of ADP measured at 60 was 2.35 4 0.17 nmol/min per mg of protein, compared with an uptake of 1.81 i 0.19 nmol/min per mg of protein in mitochondria from untreated rats (P < 0.025). Cyanide (1.33 mM) had no effect on ADP uptake by mitochondria from either untreated or triiodothyronine-treated animals. Uptake of ADP by mitochondria from thyroidectomized rats treated with thyroxine for 7 days was 2.89 4 0.40 nmol/min per mg in mitochondria from thyrotoxic rats (20 ug of thyroxine per 100 g per day) and 1.98 -0.22 nmol/min per mg in mitochondria from euthyroid rats (2 ug of thyroxine per 100 g per day) (P < 0.025). Mitochondria from both untreated and thyroid hormone-treated rats displayed a highly significant linear correlation between ADP uptake and ADP-dependent (i.e., state 3 minus state 4) oxygen consumption. There was, however, no difference in respiratory control ratios between mitochondria from euthyroid and thyrotoxic animals. Administration of dinitrophenol (2 mg/100 g) also stimulated carrier-mediated ADP uptake, but respiratory control of mitochondria from dinitrophenol-treated animals was virtually abolished. Triiodothyronine in vitro, at concentrations of 100 and 0.1 nM, appeared to inhibit rather than stimulate the uptake of mitochondrial ADP. The relationship between these observations and the clinical manifestations of thyrotoxicosis is discussed from the point of view of the possible effects of increased mitochondrial ADP transport on oxidative phosphorylation and adenosyl nucleotide metabolism.It has long been known that an increase in metabolic rate follows administration of a sufficient dose of thyroid hormone. Animals treated with large doses of thyroxine manifest an increased rate of oxygen consumption, a rise in body temperature, and a loss in weight, all consequent to an increase in the rate of oxidation of substrate (1, 2). Since most substrate oxidation takes place in mitochondria, many studies on the mechanism of action of thyroid hormone have involved these organelles. These studies have shown, for example, that * To whom to address correspondence. thyroid hormone increases the rate of mitochondrial oxidation of succinate, glutamate, ,-hydroxybutyrate, and isocitrate (3); the activity of the electron transport chain is increased without an increase in the concentrations of the chain components (4); and there is an increase in the activity of membrane-bound a-glycerophosphate dehydrogenase (5).In addition, thyroid hormone affects mitochondrial swelling (6, 7) and respiratory control (8), but these effects are only observed with rather large doses of hormone.The mitochondrion is composed of an outer membrane, an inner membrane, and two spaces: the intermembrane space, which lies between the membranes, and the matrix, which is enclosed within the inner me...

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In 182 black and 155 white men aged 20 to 50 years, all presently employed and living in southern Georgia, the following parameters related to fibrinolysis and its inhibitors were determined: Plasma fibrinolytic activity, fibrinolytic activity of euglobulins, plasminogen in euglobulins, antiplasmin, alpha1 antitrypsin and alpha2 macroglobulin. The first 4 components were determined by means of a fibrin plate technique while the last 2 were assayed using immunodiffusion and electro immunodiffusion, respectively. Whites were similar to blacks with respect to age, height, weight, physical activity and serum cholesterol. Blacks, however, had lower serum triglyceride level and a greater proportion of blacks than whites were cigarette smokers. In addition, the blacks in the sample had a lower socio-economic status as determined by data on education and occupation. Resting fibrinolytic activity was detected in the plasma of 26.6% of blacks and in only 9.3% of whites, this difference being highly significant by the K-S test (P = .02). Antiplasmin levels were significantly lower in blacks than in whites (P < 0.001). While mean values of both alpha1 antitrypsin and alpha2 maeroglobulin were lower in blacks than whites, these differences were not statistically significant. There was no correlation between cigarette smoking and the fibrinolytic components studied. From regression analysis, it is apparent that differences in fibrinolysis between blacks and whites in the sample were not merely secondary to differences in triglyceride levels. Blacks, but not whites, demonstrated the decrease in fibrinolytic activity and alpha1 antitiypsin with rise in social class. The results obtained indicate that in a community where the incidence of coronary heart disease has been previously shown to be markedly higher in white than in black men. whites also exhibit a significant impairment of fibrinolysis in comparison with blacks.