Role of Oxidative Stress in Ethanol-induced Neurotoxicity in the Developing Cerebellum | ||
| Iranian Journal of Basic Medical Sciences | ||
| مقاله 10، دوره 15، شماره 4، مهر 2012، صفحه 965-974 اصل مقاله (199.05 K) | ||
| نوع مقاله: Original Article | ||
| شناسه دیجیتال (DOI): 10.22038/ijbms.2012.4894 | ||
| نویسندگان | ||
| Azam Ramezani؛ Iran Goudarzi* ؛ Taghi Lashkarboluki؛ Mohammad Taghi Ghorbanian؛ Kataneh Abrari؛ Mahmoud Elahdadi Salmani | ||
| Faculty of Biology, Damghan University, Damghan, Iran | ||
| چکیده | ||
| Objective(s) The purpose of this study was to investigate the role of oxidative stress in Purkinje cell neurotoxicity ofethanol-treated rat. Materials and Methods Male rat pups 4-day-old was used in this study. Ethanol was administered to rat pups at a dose of 6 g/kg from postnatal days (PDs) 4 to 5. Pups were killed 90 min after the second alcohol treatment on PD 5 by decapitation and the brain was immediately removed. The cerebellum was dissected for analyzing the oxidative stress parameters and histological study. The activities of several antioxidant enzymes including superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) in vermis of cerebellum were assayed. Thiobarbituric acid reactive substances (TBARS) levels were also measured as a marker of lipid peroxidation. Results Administration of ethanol significantly increased TBARS levels in the cerebellum compared to control pups (P< 0.01). The treated pups with ethanol exhibited a marked decrease in the GPx activity (P< 0.01) whereas, in spite of decrease in the activities of SOD and CAT, when compared to control, there were not significant differences. The spherical cell bodies of Purkinje cells in control rats are aligned nicely between the granular and molecular layers. In ethanol treated pups, Purkinje cells scattered within the Purkinje cell layer and shrinkage of the cell somata is seen. Conclusion The results of the present work demonstrated that ethanol exposure during the vulnerable window could increase TBARS levels (lipid peroxidation) and decrease GPx levels in pup's cerebellum. Also, the results confirmed ethanol-induced microencephaly, cerebellar Purkinje cell loss. These findings suggest that Purkinje cell loss is, in part through decrease in the activity of GPx and increase of lipid peroxidation in the rat cerebellum. | ||
| کلیدواژهها | ||
| Cerebellum؛ Ethanol؛ Oxidative stress؛ Purkinje cell؛ Rat | ||
| مراجع | ||
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