Volume 13, Issue 1 (Spring 2009)                   Physiol Pharmacol 2009, 13(1): 18-27 | Back to browse issues page

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Abstract:   (13933 Views)
Introduction: resent studies have been shown that normobaric hyperoxia (HO) can induce excitotoxicity and stress oxidative tolerance (ETT) in variety of organs such as brain. In this study, we examined the intermittent dose of normobaric hyperoxia (HO) on neurologic deficit, and superoxide dismutase activity in brain tissue of Huntington animal model. Method: The rats were divided to three groups. First group were exposed with HO intermittently (4h×6days HO) and second two main group acted as controls, and were exposed to 21% oxygen in the same chamber (room air, RA) discontinuously (4h×6days InRA). Immediately, HO and RA groups were subjected to Huntington animal model (20mg/kg of 3-nitropropionic acid for 6 days), Because Huntington disease is a neurodegenerative disorder. Then, ETT induced by HO were measured by neurologic deficits such as string, limb withdrawal, inclined plane, beam balance test, and assessment of superoxide dismutase activity. Result: Our findings indicated that HO is involved in the induction of ETT. Pretreatment with HO improved neurologic deficits including string, limb withdrawal, inclined plane, beam balance test significantly. Preconditioning with HO increased superoxide dismutase activity significantly. Conclusion: Although further studies are needed to clarify the mechanisms of excitotoxicity tolerance, pretreatment with HO seem to partly exert their effects via increase cell viability and superoxide dismutase activity.
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Types of Manuscript: Original Research | Subject: Nervous system (others)

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