Kohtaro Asayama

Oxidative muscular injury and its relevance to hyperthyroidism.

In experimental hyperthyroidism, acceleration of lipid peroxidation occurs in heart and slow-oxidative muscles, suggesting the contribution of reactive oxygen species to the muscular injury caused by thyroid hormones. This article reviews various models of oxidative muscular injury and considers the relevance of the accompanying metabolic derangements to thyrotoxic myopathy and cardiomyopathy, which are the major complications of hyperthyroidism. The muscular injury models in which reactive oxygen species are supposed to play a role are ischemia/reperfusion syndrome, exercise-induced myopathy, heart and skeletal muscle diseases related to the nutritional deficiency of selenium and vitamin E and related disorders, and genetic muscular dystrophies. These models provide evidence that mitochondrial function and the glutathione-dependent antioxidant system are important for the maintenance of the structural and functional integrity of muscular tissues. Thyroid hormones have a profound effect on mitochondrial oxidative activity, synthesis and degradation of proteins and vitamin E, the sensitivity of the tissues to catecholamine, the differentiation of muscle fibers, and the levels of antioxidant enzymes. The large volume of circumstantial evidence presented here indicates that hyperthyroid muscular tissues undergo several biochemical changes that predispose them to free radical-mediated injury.

Prenatal development of antioxidant enzymes in rat lung, kidney, and heart: Marked increase in immunoreactive superoxide dismutases, glutathione peroxidase, and catalase in the kidney

ABSTRACT: The immaturity of antioxidant capacity in the lung in preterm newborn infants is postulated to contribute to the development of hyperoxic lung injury. Antioxidant enzymes in fetal lung, comprised of copper-zinc (cytosolic) and manganese (mitochondrial) superoxide dismutases, glutathione peroxidase, and catalase, have been reported to increase during the late gestational period. To determine whether such maturation of antioxidant capacity occurs in other tissues, we have evaluated the development of these four enzymes from d 18 to 22 of gestation in rat lung, kidney, and heart. To resolve the confusion in the reported levels of lung superoxide dismutases, the two isoenymes were assayed separately by specific RIA. The growth of the kidney exceeded that of the whole body during this period, while the growth of the lung and heart did not. The concentrations of the four antioxidant enzymes in lung and kidney increased in a stepwise manner during this period, and the magnitude of the change for each enzyme was greater in the kidney than in the lung. On the other hand, the only significant change in the concentrations of heart antioxidant enzymes observed was a mild increase in the glutathione peroxidase concentration from d 20 to 22. These results suggest that the prenatal maturation of antioxidant capacity occurs earlier in the heart and later in the kidney than in the lung, and that the immaturity of antioxidant capacity could make the fetal rat kidney vulnerable to free radical-mediated injury.

Increased plasma isoprostane is associated with visceral fat, high molecular weight adiponectin, and metabolic complications in obese children

Oxidative stress is considered to be increased in obese subjects. However, the association of oxidative stress with visceral adiposity and adiponectin level is not fully understood in children. Forty-four obese Japanese children and adolescents, 28 boys and 16 girls, with median age of 9.9xa0years [5.2–13.8xa0years], and the 28 age-matched non-obese healthy controls, 15 boys and 13 girls, were enrolled in this study. The median BMI Z scores were +2.21 [1.31–4.38] for the obese subjects and −0.72 [−2.11–1.31] for the control. Plasma concentrations of 8-epi-prostaglandin

Peroxisomes of the rat cardiac and soleus muscles increase after starvation

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Antioxidant enzyme status and lipid peroxidation in various tissues of diabetic and starved rats.

(isoprostane), a marker of oxidative stress, and adiponectin fractions were assayed using ELISA. 8-epi-PGF

IMMUNOHISTOCHEMICAL LOCALIZATION OF COPPER-ZINC AND MANGANESE SUPEROXIDE DISMUTASES IN RAT TISSUES

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