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- Title
NITRIC OXIDE, LIPIDPEROXIDATION AND TOTAL ANTIOXIDANT STATUS IN DIFFERENT REGIONS OF RAT BRAIN IN KAINIC ACID MEDIATED EXCITOTOXICITY.
- Authors
Swamy, M.; Sirajudeen, K. N. S.; Govindasamy, Chandran
- Abstract
Introduction: Neuronal excitation involving the excitatory glutamate receptors is recognized as an important underlying mechanism in neurodegenerative disorders. Nitric oxide (NO) is known to be involved in the pathophysiology of many epilepsy models resulting from increased action of excitatory neurotransmitter namely glutamate. Reactive Oxygen Species (ROS)/Reactive Nitrogen Species (RNS) have been implicated in the pathogenesis of various neurological disorders including epilepsy. To understand the NO production and oxidative status in excitotoxicity, nitrate /nitrite (NOx), lipid peroxidation products as Thiobarbituricacid reactive substances (TBARS) and Total antioxidant status (TAS) were analyzed in cerebral cortex (CC), cerebellum (CB) and brain stem (BS) of rats subjected to excitotoxicity by kainic acid. Methodology: Male Sprague-Dawley rats (weighing 200-250 grams) were used as experimental animal and divided into control and test group (n=6 rats/group). Control group received normal saline and in the test group excitotoxicity was produced by subcutaneous administration of kainic acid (15mg/kg body weight, dissolved in normal saline). The animals were sacrificed after 2 hours of injection and brain regions (CC, CB and BS) were separated and homogenized. In the homogenates, the NO was estimated as Nitrate/Nitrite colorimetrically and the oxidative stress parameters TBARS and TAS were estimated by colorimetric methods. The results were analyzed by independent student t-test. Results: The concentration of NOx was significantly increased (p<0.001 in CC, CB and p<0.01 in BS) and TBARS level was also showed an increase (P<0.001 in CB, BS and p<0.01 in CC) in excitotoxicity. TAS level showed a significant decrease (p<0.001 in CC, CB and BS) in kainic acid mediated excitotoxicity. Conclusions: The results of this study clearly demonstrated the increased formation of NO and suggest the involvement of NO in the pathophysiology of excitotoxicity. The increased formation of TBARS and decreased TAS indicate the presence of oxidative stress in excitotoxicity and support the beneficial role of antioxidant therapy in excitotoxicity.
- Publication
Malaysian Journal of Medical Sciences, 2007, Vol 14, p169
- ISSN
1394-195X
- Publication type
Academic Journal