Search Results
You are looking at 1 - 8 of 8 items for
- Author: Y Nishida x
- Refine by access: All content x
Search for other papers by J. Kawada in
Google Scholar
PubMed
Search for other papers by Y. Shirakawa in
Google Scholar
PubMed
Search for other papers by Y. Yoshimura in
Google Scholar
PubMed
Search for other papers by M. Nishida in
Google Scholar
PubMed
The role of xanthine oxidase in thyroid function was studied in the rat in vivo by different approaches. Allopurinol, an inhibitor of xanthine oxidase, was administered by mixing it with a powdered diet (16 mg/100 g body wt per day for 10 days). This treatment significantly reduced the total uptake of iodide and inhibited the organification of iodide in the rat thyroid gland. Thyroid xanthine oxidase and dehydrogenase were almost completely inactivated by tungstate, which was given to rats (100 p.p.m./animal per day in drinking water for 10 days) maintained on a purified diet containing low levels of molybdenum. Under these conditions, no inhibitory effect was observed on synthesis of thyroid hormones. It therefore seemed reasonable to assume that the suppressive effect of allopurinol on the biosynthesis of thyroid hormones is not mediated by xanthine oxidase.
Search for other papers by M. Nukatsuka in
Google Scholar
PubMed
Search for other papers by Y. Yoshimura in
Google Scholar
PubMed
Search for other papers by M. Nishida in
Google Scholar
PubMed
Search for other papers by J. Kawada in
Google Scholar
PubMed
ABSTRACT
The effects of streptozotocin (STZ) and N-methyl-N′-nitro-N-nitrosoguanidine (MNNG) on monolayer cultures of rat pancreatic β cells were compared. The intracellular NAD concentration was markedly decreased by both 2 mmol STZ/l and 13·6 μmol MNNG/l, but insulin secretion was decreased significantly only by STZ. The intracellular ATP level decreased rapidly and in a time-dependent manner with STZ, but decreased less on treatment with MNNG: 80% decrease with STZ but only 35% decrease with MNNG in 12 h in the cells exposed to the chemicals for 1 h and then washed thoroughly. STZ decreased oxygen consumption of rat liver mitochondria in a time- and dose-dependent manner and enhanced the generation of hydroxyl radicals (DMPO-adducts). This enhancement was doubled on the addition of succinate as a substrate. Mitochondrial ATP production was also decreased significantly by STZ, but not by MNNG. Thus the marked depletion of intracellular ATP in β cells by STZ seems to be due mainly to a direct effect on mitochondrial production. From these results, we suggest that the cytotoxic effect of STZ in pancreatic β cells is due to a reduction in the intracellular level of ATP, rather than of NAD.
Journal of Endocrinology (1990) 127, 161–165
Search for other papers by M. Sofue in
Google Scholar
PubMed
Search for other papers by Y. Yoshimura in
Google Scholar
PubMed
Search for other papers by M. Nishida in
Google Scholar
PubMed
Search for other papers by J. Kawada in
Google Scholar
PubMed
ABSTRACT
Exposure of rat pancreatic β cells in monolayer culture to 2 mmol streptozotocin (STZ)/1 for 1 h followed by thorough washing inhibited their uptake of [14C]nicotinamide and [3H]2-deoxyglucose ([2H]2-DG) to about 50% and also reduced the intracellular ATP concentration to 50% of that in control cells. These changes were not due to a lethal cytotoxic effect of STZ, because cell viability, as estimated by succinic dehydrogenase activity, was 90% of that of control cells. Oligomycin and carbonylcyanide-m-chlorophenylhydrazone (CCCP), an uncoupler of oxidative phosphorylation, caused a dose-dependent decrease in intracellular ATP concentration while maintaining high cell viability. These ATP-depleted cells showed a decrease in insulin release and an inhibition of the uptake of [14C]nicotinamide and [3H]2-DG in a dose-dependent manner. Therefore oligomycin and CCCP reproduced the same effects as those found in β cells treated with STZ. These results suggest that the uptake of nicotinamide and 2-DG by β cells might be regulated by their intracellular ATP concentration. The decreased uptake of nicotinamide in ATP-depleted β cells caused by STZ might explain the lack of protective effect of nicotinamide against STZ cytotoxicity when administered after the latter. Furthermore, the radiotracer experiments demonstrated that the transport of nicotinamide by intact β cells was inhibited in a dose-dependent manner by 2-DG and vice versa, i.e. the transport of 2-DG was inhibited by nicotinamide. These findings suggest the existence of a common transport mechanism in β cells responsible for the uptake of nicotinamide and 2-DG, the transport of which is known to occur by facilitated diffusion.
Journal of Endocrinology (1991) 131, 135–138
Search for other papers by J. Kawada in
Google Scholar
PubMed
Search for other papers by M. Okita in
Google Scholar
PubMed
Search for other papers by M. Nishida in
Google Scholar
PubMed
Search for other papers by Y. Yoshimura in
Google Scholar
PubMed
Search for other papers by K. Toyooka in
Google Scholar
PubMed
Search for other papers by S. Kubota in
Google Scholar
PubMed
ABSTRACT
Ethylidene glucose (4,6-O-ethylidene glucose; EG) is known to bind the outer surface of the glucose transporter in the membranes of human erythrocytes and other mammalian cells. If a glucose transport system is present on pancreatic β cells and recognizes the glucose moiety of streptozotocin (STZ), EG should protect β cells from the cytotoxicity of STZ when it is administered with STZ. This possibility was examined in in-vivo experiments in rats. When EG and STZ were injected into rats together the animals did not become diabetic, as judged by (1) their blood glucose levels, (2) response in a glucose-tolerance test, and (3) insulin secretion in response to feeding. These results suggest that there is a glucose transporter present in β cells and also the transport of streptozotocin into β cells through this system.
J. Endocr. (1987) 112, 375–378
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 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 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
