THE EFFECT OF NORMOBARIC HYPEROXIA ON SUPEROXIDE DISMUTASE ACTIVITY AND NEUROLOGICAL DEFICITS IN AN ANIMAL MODEL OF HUNTINGTON DISEASE

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BIGDELI M.R.; RAHNAMA M.

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Journal: Physiology and Pharmacology Year:2009 | Volume:13 | Issue:1 Page(s): 18-27

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Title

THE EFFECT OF NORMOBARIC HYPEROXIA ON SUPEROXIDE DISMUTASE ACTIVITY AND NEUROLOGICAL DEFICITS IN AN ANIMAL MODEL OF HUNTINGTON DISEASE

Author(s)

BIGDELI M.R. | RAHNAMA M. | Issue Writer Certificate

Keywords

BRAIN PRECONDITIONINGQ3

NORMOBARIC HYPEROXIAQ3

HUNTINGTONQ2

EXCITOTOXICITYQ3

TOLERANCEQ3

NEUROLOGICAL DEFICITSQ3

Abstract

Introduction: recent studies have shown that NORMOBARIC HYPEROXIA (HO) can induce EXCITOTOXICITY and oxidative stress TOLERANCE (ETT) in a variety of organs such as brain. In this study, we examined the effect of intermittent doses of NORMOBARIC HYPEROXIA (HO) on the neurological deficit and superoxide dismutase activity in the brain tissue of an animal model of HUNTINGTON’s disease. Methods: Rats were divided into 3 groups. The first group was exposed to HO intermittently (4h × 6 days; HO) and the second 2 main groups acted as controls, and were exposed to 21% oxygen in the same chamber (room air, RA) or discontinuously (4h × 6 days; InRA). HO and RA groups were immediately given 20 mg/kg of 3-nitropropionic acid for 6 days, Administration of 3-nitropropionic acid generates an animal model of HUNTINGTON disease, because HUNTINGTON disease is a neurodegenerative disorder. Then, ETT induced by HO was measured by the evaluation of NEUROLOGICAL DEFICITS such as string, limb withdrawal, inclined plane, beam balance test, and assessment of superoxide dismutase activity. Results: Our findings indicated that HO is involved in the induction of ETT. Pretreatment with HO significantly improved NEUROLOGICAL DEFICITS including string, limb withdrawal, inclined plane, beam balance test. Preconditioning with HO significantly increased superoxide dismutase activity.Conclusion: Although further studies are needed to clarify the mechanisms of EXCITOTOXICITY TOLERANCE, pretreatment with HO seems to partly exert its effects through the enhancement of cell viability and superoxide dismutase activity.

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APA: Copy

BIGDELI, M.R., & RAHNAMA, M.. (2009). THE EFFECT OF NORMOBARIC HYPEROXIA ON SUPEROXIDE DISMUTASE ACTIVITY AND NEUROLOGICAL DEFICITS IN AN ANIMAL MODEL OF HUNTINGTON DISEASE. PHYSIOLOGY AND PHARMACOLOGY, 13(1), 18-27. SID. https://sid.ir/paper/75133/en

Vancouver: Copy

BIGDELI M.R., RAHNAMA M.. THE EFFECT OF NORMOBARIC HYPEROXIA ON SUPEROXIDE DISMUTASE ACTIVITY AND NEUROLOGICAL DEFICITS IN AN ANIMAL MODEL OF HUNTINGTON DISEASE. PHYSIOLOGY AND PHARMACOLOGY[Internet]. 2009;13(1):18-27. Available from: https://sid.ir/paper/75133/en

IEEE: Copy

M.R. BIGDELI, and M. RAHNAMA, “THE EFFECT OF NORMOBARIC HYPEROXIA ON SUPEROXIDE DISMUTASE ACTIVITY AND NEUROLOGICAL DEFICITS IN AN ANIMAL MODEL OF HUNTINGTON DISEASE,” PHYSIOLOGY AND PHARMACOLOGY, vol. 13, no. 1, pp. 18–27, 2009, [Online]. Available: https://sid.ir/paper/75133/en

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