Search Results
You are looking at 1 - 5 of 5 items for
- Author: T Mokuno x
- Refine by access: All content x
Search for other papers by T Mano in
Google Scholar
PubMed
Search for other papers by R Sinohara in
Google Scholar
PubMed
Search for other papers by Y Sawai in
Google Scholar
PubMed
Search for other papers by N Oda in
Google Scholar
PubMed
Search for other papers by Y Nishida in
Google Scholar
PubMed
Search for other papers by T Mokuno in
Google Scholar
PubMed
Search for other papers by M Kotake in
Google Scholar
PubMed
Search for other papers by M Hamada in
Google Scholar
PubMed
Search for other papers by R Masunaga in
Google Scholar
PubMed
Search for other papers by A Nakai in
Google Scholar
PubMed
Search for other papers by A Nagasaka in
Google Scholar
PubMed
Abstract
Active oxygen species are reported to cause organ damage. This study was therefore designed to determine the behaviour of antioxidants and free radical scavengers so as to reveal changes in animals in the hyper- and hypothyroid state.
Levels of antioxidant factors (i.e. coenzyme Q (CoQ)10, CoQ9 and vitamin E) and free radical scavengers (catalase, glutathione peroxidase (GSH-PX) and superoxide dismutase (SOD)) were measured in the heart muscles of rats rendered hyper- or hypothyroid by 4 weeks of thyroxine (T4) or methimazol treatment. Serum levels of CoQ9 and total SOD were also measured.
A significant reduction in CoQ9 levels was observed in the heart muscles of both hyper- and hypothyroid rats when compared with control hearts. There was no difference in serum CoQ9 levels in thyroid dysfunction when compared with control animals. Levels of vitamin E in the heart muscles of hyperthyroid rats were significantly increased, and there was no reduction in vitamin E levels in hypothyroid rats when compared with control hearts. GSH-PX levels in the heart muscle were reduced in hyperthyroid rats and increased in hypothyroid rats when compared with control hearts. However, there were no differences in catalase levels in heart muscle between hyper- and hypothyroid rats. The concentration of SOD in heart muscle was increased in hyperthyroid rats and was not decreased in hypothyroid rats compared with control rats, suggesting the induction of SOD by excessive production of O2 −.
These data suggest that the changes in these scavengers have some role in cardiac dysfunction in the hyper- and hypothyroid state in the rat.
Journal of Endocrinology (1995) 145, 131–136
Search for other papers by T Mano in
Google Scholar
PubMed
Search for other papers by R Sinohara in
Google Scholar
PubMed
Search for other papers by Y Sawai in
Google Scholar
PubMed
Search for other papers by N Oda in
Google Scholar
PubMed
Search for other papers by Y Nishida in
Google Scholar
PubMed
Search for other papers by T Mokuno in
Google Scholar
PubMed
Search for other papers by K Asano in
Google Scholar
PubMed
Search for other papers by Y Ito in
Google Scholar
PubMed
Search for other papers by M Kotake in
Google Scholar
PubMed
Search for other papers by M Hamada in
Google Scholar
PubMed
Search for other papers by A Nakai in
Google Scholar
PubMed
Search for other papers by A Nagasaka in
Google Scholar
PubMed
Abstract
To determine how lipid peroxides and free radical scavengers are changed in the brain of hyper- or hypothyroid rats, we examined the behavior of lipid peroxide and free radical scavengers in the cerebral cortex of aged (1·5 years old) rats that had been made hyper- or hypothyroid by the administration of thyroxine or methimazol for 4 weeks. Concentrations of catalase, Mn-superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) were increased in hyperthyroid rats compared with euthyroid rats. Concentrations of total SOD, Cu,Zn-SOD and GSH-PX were increased but that of Mn-SOD was decreased in hypothyroid animals. There were no differences among hyperthyroid, hypothyroid and euthyroid rats in the levels of coenzymes 9 or 10. The concentration of lipid peroxides, determined indirectly by the measurement of thiobarbituric acid reactants, was decreased in hyperthyroid rats but not in hypothyroid rats when compared with euthyroid animals.
These findings suggest that free radicals and lipid peroxides are scavenged to compensate for the changes induced by hyper- or hypothyroidism.
Journal of Endocrinology (1995) 147, 361–365
Search for other papers by T Mano in
Google Scholar
PubMed
Search for other papers by K Iwase in
Google Scholar
PubMed
Search for other papers by Y Sawai in
Google Scholar
PubMed
Search for other papers by N Oda in
Google Scholar
PubMed
Search for other papers by Y Nishida in
Google Scholar
PubMed
Search for other papers by T Mokuno in
Google Scholar
PubMed
Search for other papers by Y Itoh in
Google Scholar
PubMed
Search for other papers by M Kotake in
Google Scholar
PubMed
Search for other papers by R Masunaga in
Google Scholar
PubMed
Search for other papers by A Nakai in
Google Scholar
PubMed
Search for other papers by T Tujimura in
Google Scholar
PubMed
Search for other papers by A Nagasaka in
Google Scholar
PubMed
Search for other papers by H Hidaka in
Google Scholar
PubMed
Abstract
To investigate the effect of thyroid hormone on cardiac muscle dysfunction in hyper- and hypothyroid states, we evaluated cyclic 3′, 5′-nucleotide metabolism by measuring cyclic 3′, 5′-nucleotide phosphodiesterase activity and calmodulin concentrations in the cardiac muscles of hyper- and hypothyroid rats.
Cyclic AMP (cAMP) concentration was significantly high in the cardiac muscle of hyperthyroid rats and low in that from hypothyroid rats compared with control rats. Cyclic AMP and cyclic GMP phosphodiesterase activities were significantly decreased in the soluble fraction of cardiac muscle from hyperthyroid rats and markedly increased in this fraction in hypothyroid rats compared with normal animals. Calmodulin concentration was high in hyperthyroid and low in hypothyroid rats.
It was concluded from these findings that low cAMP-phosphodiesterase activity might, in part, bring about the high concentration of cAMP. Calmodulin was sigificantly high in the cardiac muscle of hyperthyroid rats and the reverse was the case in hypothyroid rats compared with normal rats. The implication is that, in hyper- and hypothyroid states, these changes may play an important role in cardiac function via their effect on cyclic nucleotide and Ca2+ metabolism.
Journal of Endocrinology (1994) 143, 515–520
Search for other papers by T Mano in
Google Scholar
PubMed
Search for other papers by K Iwase in
Google Scholar
PubMed
Search for other papers by I Yoshimochi in
Google Scholar
PubMed
Search for other papers by Y Sawai in
Google Scholar
PubMed
Search for other papers by N Oda in
Google Scholar
PubMed
Search for other papers by Y Nishida in
Google Scholar
PubMed
Search for other papers by T Mokuno in
Google Scholar
PubMed
Search for other papers by M Kotake in
Google Scholar
PubMed
Search for other papers by A Nakai in
Google Scholar
PubMed
Search for other papers by N Hayakawa in
Google Scholar
PubMed
Search for other papers by R Kato in
Google Scholar
PubMed
Search for other papers by A Nagasaka in
Google Scholar
PubMed
Search for other papers by H Hidaka in
Google Scholar
PubMed
Abstract
Hyper- and hypothyroid states occasionally induce skeletal muscle dysfunction i.e. periodic paralysis and thyroid myopathy. The etiology of these diseases remains unclear, but several findings suggest that the catecholamine-β-receptor-cAMP system or other messenger systems are disturbed in these diseases. In this context, we evaluated changes in the cyclic 3′,5′-nucleotide metabolic enzyme, cyclic 3′,5′-nucleotide phosphodiesterase (PDE) and calmodulin concentrations in skeletal muscles of hyper- and hypothyroid rats.
Activities of cyclic AMP-PDE were low in skeletal muscle both from hyper- and hypothyroid rats, and calmodulin concentration was high in hyperthyroid and low in hypothyroid rats, as compared with normal rats. DE-52 column chromatographic analysis showed that the cGMP hydrolytic activity in peak I and the cAMP hydrolytic activity in peak II were decreased in hypothyroid rats, whereas cAMP hydrolytic activity in peak III was unchanged. The cAMP hydrolytic activity in peak III was decreased in hyperthyroid rats, but the activities in peaks I and II were unchanged. These findings indicate that cAMP and calmodulin may have some role in skeletal muscle function in the hyperthyroid state, and that cAMP and calmodulin-dependent metabolism may be suppressed in the hypothyroid state.
Journal of Endocrinology (1995) 146, 287–292
Search for other papers by T Mokuno in
Google Scholar
PubMed
Search for other papers by K Uchimura in
Google Scholar
PubMed
Search for other papers by R Hayashi in
Google Scholar
PubMed
Search for other papers by N Hayakawa in
Google Scholar
PubMed
Search for other papers by M Makino in
Google Scholar
PubMed
Search for other papers by M Nagata in
Google Scholar
PubMed
Search for other papers by H Kakizawa in
Google Scholar
PubMed
Search for other papers by Y Sawai in
Google Scholar
PubMed
Search for other papers by M Kotake in
Google Scholar
PubMed
Search for other papers by N Oda in
Google Scholar
PubMed
Search for other papers by A Nakai in
Google Scholar
PubMed
Search for other papers by A Nagasaka in
Google Scholar
PubMed
Search for other papers by M Itoh in
Google Scholar
PubMed
The deterioration of glucose metabolism frequently observed in hyperthyroidism may be due in part to increased gluconeogenesis in the liver and glucose efflux through hepatocyte plasma membranes. Glucose transporter 2 (GLUT 2), a facilitative glucose transporter localized to the liver and pancreas, may play a role in this distorted glucose metabolism. We examined changes in the levels of GLUT 2 in livers from rats with l-thyroxine-induced hyperthyroidism or methimazole-induced hypothyroidism by using Western blotting to detect GLUT 2. An oral glucose tolerance test revealed an oxyhyperglycemic curve (impaired glucose tolerance) in hyperthyroid rats (n=7) and a flattened curve in hypothyroid rats (n=7). GLUT 2 levels in hepatocyte plasma membranes were significantly increased in hyperthyroid rats and were not decreased in hypothyroid rats compared with euthyroid rats. The same results were obtained with a densitometric assay. These findings suggest that changes in the liver GLUT 2 concentration may contribute to abnormal glucose metabolism in thyroid disorders.
