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低剂量γ射线照射对小鼠大脑抗氧化能力的提升及其对1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)诱导的脑损伤的影响。

Elevation of antioxidant potency in the brain of mice by low-dose gamma-ray irradiation and its effect on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced brain damage.

作者信息

Kojima S, Matsuki O, Nomura T, Yamaoka K, Takahashi M, Niki E

机构信息

Research Institute for Biological Sciences, Science University of Tokyo, Chiba, Japan.

出版信息

Free Radic Biol Med. 1999 Feb;26(3-4):388-95. doi: 10.1016/s0891-5849(98)00200-7.

DOI:10.1016/s0891-5849(98)00200-7
PMID:9895231
Abstract

The elevation of endogenous thiol-related antioxidants and free radical scavenging enzymes in the brain of C57BL/6 female mice after low-dose gamma-ray irradiation and its inhibitory effect on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced brain damage were investigated. The brain level of the reduced form of glutathione (GSH) increased soon after irradiation with 50 cGy of gamma-rays, reached a maximum at 3 h post-treatment, and remained elevated until 12 h. Thioredoxin (TRX) was also transiently increased after irradiation. The activities of free radical scavenging enzymes, including Cu/Zn-superoxide dismutase, catalase and glutathione peroxidase, were significantly induced after irradiation as well. Cerebral malondialdehyde was remarkably elevated by MPTP treatment, and this elevation was suppressed by pre-irradiation (50 cGy). The contents of GSH and TRX were significantly decreased by MPTP treatment in comparison with those of the control group. These reductions both seemed to be attenuated by pre-irradiation with gamma-rays. These results suggest that low-dose gamma-ray irradiation induces endogenous antioxidative potency in the brain of mice and might be effective for the prevention and/or therapy of various reactive oxygen species-related neurodegenerative disorders, such as Parkinson's disease and Alzheimer's disease.

摘要

研究了低剂量γ射线照射后C57BL/6雌性小鼠脑内内源性硫醇相关抗氧化剂和自由基清除酶的升高及其对1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)诱导的脑损伤的抑制作用。照射50 cGy的γ射线后,还原型谷胱甘肽(GSH)的脑水平很快升高,在治疗后3小时达到最大值,并一直升高到12小时。照射后硫氧还蛋白(TRX)也短暂增加。照射后,包括铜/锌超氧化物歧化酶、过氧化氢酶和谷胱甘肽过氧化物酶在内的自由基清除酶的活性也显著诱导。MPTP处理使脑丙二醛显著升高,而预照射(50 cGy)可抑制这种升高。与对照组相比,MPTP处理使GSH和TRX的含量显著降低。γ射线预照射似乎减弱了这两种降低。这些结果表明,低剂量γ射线照射可诱导小鼠脑内的内源性抗氧化能力,可能对预防和/或治疗各种与活性氧相关的神经退行性疾病,如帕金森病和阿尔茨海默病有效。

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