ROLE OF RADIATION AS EFFECTIVE INTERVENTION IN Aβ INDUCED OXIDATIVE STRESS IN ANIMAL MODEL OF ALZHEIMER'S DISEASE

Objective: The present study was undertaken to study the therapeutic effects of low dose fractionated cranial X-irradiation on reducing the amyloid-beta (Aβ) induced oxidative stress burden in an animal model of Alzheimer's disease (AD). Methods: S.D. female rats received an intracerebroventricular injection of Aβ peptide at stereotaxically defined points. Experimental sessions were conducted by randomly dividing animals into four groups, namely sham-operated, Aβ-injected, and Aβ injection followed by cranial X-irradiation and only cranial X-irradiated. Anesthetized animals received 5 μl synthetic Aβ peptide injection with a 10 μl Hamilton microsyringe with the needle kept in place for a period of 2min following injection. Sham-operated group received 5 μl of bidistilled water instead of Aβ peptide. Animals were treated 6 weeks post-surgery with fractionated radiation of 2Gy for 5 days. Neurobehavior studies were undertaken to confirm memory impairment along with biochemical indices involved in the antioxidant defense system. Results: Fractionated cranial X-irradiation proved effective in restoration of activity of enzymes involved in the antioxidant defense system; the lipid peroxidation and catalase levels that showed a significant increase in Aβ-treated group decreased on subsequent X-irradiation. Moreover, the decrease in the superoxide dismutase, glutathione, glutathione-S-transferase, and glutathione reductase levels witnessed an increase post-irradiation, implicating the X-irradiation to be an effective intervention to restore the redox status of the oxidatively stressed brain cells in AD condition. Conclusion: The present study evaluated the therapeutic potential of low dose fractionated cranial X- irradiation by mitigating the amyloid-induced oxidative stress suggesting a novel treatment for AD-associated pathologies

Neuroprotective effects of zinc on antioxidant defense system in lithium treated rat brain

954-958With a view to find out whether zinc affords protection against lithium toxicity the activities of antioxidant enzymes and lipid peroxidation profile were determined in the cerebrum and cerebellum of lithium treated female Sprague Dawley rats. Lipid peroxidation was significantly increased in both the cerebrum and the cerebellum of animals administered with lithium for a total duration of 4 months as compared to the normal control group. On the contrary, the activities of catalase and glutathione-s-transferase (GST) were significantly reduced after 4 months of lithium treatment. The activity of superoxide dismutase (SOD) was significantly increased in the cerebrum after 4 months lithium administration, whereas in the cerebellum the enzyme activity was unaffected. No significant change in the levels of reduced glutathione (GSH) was found in either cerebrum or cerebellum after 2 months of lithium treatment. However, 4 months lithium treatment did produce significant changes in GSH levels in the cerebrum and in the cerebellum. Zinc supplementation for 4 months in lithium-treated rats significantly increased the activities of catalase and GST in the cerebellum, showing that the treatment with zinc reversed the lithium induced depression in these enzyme activities. Though, zinc treatment tended to normalize the SOD activity in the cerebrum yet it was still significantly higher in comparison to normal levels. From the present study, it can be concluded that the antiperoxidative property of zinc is effective in reversing the oxidative stress induced by lithium toxicity in the rat brain