1995 Fiscal Year Final Research Report Summary
Development of specific substances evaluated by the regulation of glucose transporter involved in aging of brain
| Project/Area Number |
05557107
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| Research Category |
Grant-in-Aid for Developmental Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Biological pharmacy
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| Research Institution | HIROSHIMA UNIVERSITY |
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Principal Investigator |
ISHIBASHI Sadahiko Hiroshima University School of Medicine, Professor, 医学部, 教授 (90012616)
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| Co-Investigator(Kenkyū-buntansha) |
KUROKAWA Tomonori Hiroshima University School of Medicine, Associate Professor, 医学部, 助教授 (00124793)
KIMURA Eiichi Hiroshima University School of Medicine, Professor, 医学部, 教授 (30034010)
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| Project Period (FY) |
1993 – 1995
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| Keywords | Senescence-accelerated mouse (SAM) / Glucose metabolism / Oxidative stress / Active oxygen / Peroxisome |
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| Research Abstract |
First, we tried to clarify the characteristic of the energy metabolism in the brain cells of SAMP8, a substrain of accelerated senescence-prone strain. We found that the rate of D-glucose oxidation at 4- to 8-weeks of age, just before the appearance of deficits in the brain, was higher than that in age-matched SAMR1 and SAMR2 and that the increase in glucose transporter protein in the cell surface membrane was involved in the increased metabolism. Both the increases were restricted at 4- to 8-weeks of age and the cerebral cortex.
Next, we examined the involvement of oxygen free radicals in relation to the above-mentioned change in the cnergy metabolism. We found the transient increase in the contents of lipid peroxides and protein carbonyl only in the cerebral cortex of SAMP8 at 4- to 8-weeks of age in comparison with SAMR1. Accordingly, the content of hydrogen peroxide was increased in the cerebral cells of SAMP8 at 4- to 8-weeks of age. In comparison of the various enzyme activities in the peroxisome in the cerebral cortex between the two strains. The decrease in the catalase activity and increase in acyl-CoA oxidase activity were observed in SAMP8.
It is quite likely that these results provide some clues towards understanding the mechanism responsible for initiating the process of senile memory impairment in the brain and contribute the development of new therapeutic substances for aging.
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