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

Citation
S. Kojima et al., 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, FREE RAD B, 26(3-4), 1999, pp. 388-395
Citations number
47
Categorie Soggetti
Biochemistry & Biophysics
Journal title
FREE RADICAL BIOLOGY AND MEDICINE
ISSN journal
08915849 → ACNP
Volume
26
Issue
3-4
Year of publication
1999
Pages
388 - 395
Database
ISI
SICI code
0891-5849(199902)26:3-4<388:EOAPIT>2.0.ZU;2-W
Abstract
The elevation of endogenous thiol-related antioxidants and free radical sca venging enzymes in the brain of C57BL/6 female mice after low-dose gamma-ra y irradiation and its inhibitory effect on 1-methyl-4-phenyl-1,2,3,6-tetrah ydropyridine (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 rem ained elevated until 12 h. Thioredoxin (TRX) was also transiently increased after irradiation. The activities of free radical scavenging enzymes, incl uding 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 suppresse d by pre- irradiation (50 cGy). The contents of GSH and TRX were significan tly decreased by MPTP treatment in comparison with those of the control gro up. These reductions both seemed to be attenuated by pre-irradiation with g amma-rays. These results suggest that low-dose gamma-ray irradiation induce s endogenous antioxidative potency in the brain of mice and might be effect ive for the prevention and/or therapy of various reactive oxygen species-re lated neurodegenerative disorders, such as Parkinson's disease and Alzheime r's disease. (C) 1998 Elsevier Science Inc.