Search Results
You are looking at 1 - 6 of 6 items for
- Author: T Mano x
- Refine by access: All content x
Search for other papers by F. Miyauchi in
Google Scholar
PubMed
Search for other papers by H. Kato in
Google Scholar
PubMed
Search for other papers by H. Yamashita in
Google Scholar
PubMed
Search for other papers by K. Ueda in
Google Scholar
PubMed
Search for other papers by H. Tamura in
Google Scholar
PubMed
Search for other papers by T. Mano in
Google Scholar
PubMed
Search for other papers by T. Torigoe in
Google Scholar
PubMed
ABSTRACT
The effects of a conceptus-derived substance on the activity of 3β-hydroxysteroid dehydrogenase (3β-HSD) and 20α-HSD in the ovary were studied in the rat. On day 7 of pregnancy (day 1 = insemination), rats were laparotomized and the desired number of conceptuses was aspirated from the uterus; thus, rats carrying one, two, three, four, five to seven or eight to ten conceptuses were prepared. They were autopsied on day 15 and 3β-HSD and 20α-HSD activity in the corpus luteum (CL) or non-luteal ovarian tissue (NLO) was determined. Conceptus number was directly related to 3β-HSD and inversely related to 20α-HSD activity in the CL. The serum progesterone level and CL weight were also directly related to conceptus number. Neither 3β-HSD nor 20α-HSD activity in the NLO was affected by conceptus number. These results indicated that 3β-HSD and 20α-HSD in the CL are probably regulated by placental hormone secreted in proportion to the number of conceptuses; in the NLO these enzymes may be controlled by a different mechanism.
J. Endocr. (1984) 101, 285–288
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 R Shinohara in
Google Scholar
PubMed
Search for other papers by T Mano in
Google Scholar
PubMed
Search for other papers by A Nagasaka in
Google Scholar
PubMed
Search for other papers by R Hayashi in
Google Scholar
PubMed
Search for other papers by K Uchimura in
Google Scholar
PubMed
Search for other papers by I Nakano in
Google Scholar
PubMed
Search for other papers by F Watanabe in
Google Scholar
PubMed
Search for other papers by T Tsugawa in
Google Scholar
PubMed
Search for other papers by M Makino in
Google Scholar
PubMed
Search for other papers by H Kakizawa in
Google Scholar
PubMed
Search for other papers by M Nagata in
Google Scholar
PubMed
Search for other papers by K Iwase in
Google Scholar
PubMed
Search for other papers by Y Ishizuki in
Google Scholar
PubMed
Search for other papers by M Itoh in
Google Scholar
PubMed
Free radicals, hydroxyperoxides and H(2)O(2) are all known to damage cell components. This study was designed to compare the concentrations of hydroxyperoxide and free radical scavengers in the cardiac muscles of old rats in the hyper- or hypothyroid condition, to determine whether rates of peroxidation would differ with age, thyroid status, or both. Rats were rendered hyper- or hypothyroid by administration of l-thyroxine or methimazole for 4 weeks. Among the old rats, the lipid peroxide (LPO) concentrations, measured as thiobarbituric acid (TBA) reactants, were significantly greater in the hyperthyroid than in the euthyroid state and the LPO concentrations measured as TBA+Fe(3+) reactants, which may be precursors of LPO, were significantly greater in the hyperthyroid state, whereas in young rats, the LPO concentrations measured by TBA or TBA+Fe(3+) methods did not differ significantly in the hyperthyroid state. In the euthyroid state, the concentration of LPO measured as TBA+Fe(3+) reactants was significantly reduced with age. Xanthine oxidase (XOD) activity also was markedly increased with age, being more pronounced in the hyperthyroid than in the euthyroid state. The Mn and Cu/Zn superoxide dismutase activities were greater in the hyperthyroid than in the euthyroid state. Glutathione peroxidase activity decreased with age in the euthyroid and, particularly, in the hyperthyroid state. Catalase activity was not affected in the old rats. Concentrations of alpha-tocopherol in the old rats were high in the hyperthyroid state and low in the hypothyroid state, whereas the levels of beta- and gamma-tocopherols in these rats were unchanged in both conditions as compared with the euthyroid state findings. Data suggest that the site of free radical generation differs in older rats, with additional shifts in the location of intracellular lipid peroxidation being noted during hyperthyroidism. Thus, as rats age, the reduction of the free radical scavenger system and the increase in LPO and XOD activities might induce myocardial dysfunction.
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
