Journal
NEUROCHEMISTRY INTERNATIONAL
Volume 55, Issue 7, Pages 648-654Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuint.2009.06.008
Keywords
Oxidative stress; Japanese encephalitis; Oxidant/antioxidant imbalance; Lipid peroxidation; Glutathione
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Funding
- Indian Council of Medical Research, New Delhi [80/562/ECD-1/2007]
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The imbalance in redox equilibrium is associated with several viral diseases however its role in Japanese encephalitis (JE) has not been reported. In the present study, we report the status of oxidant/antioxidant system in different brain regions in rat model of JE. Twelve days old Wistar strain rats were inoculated intracerebrally with a dose of 3 x 10(6) pfu of JE virus (JEV). The activity of manganese superoxide dismutase (Mn-SOD), catalase (CAT), glutathione peroxidase (GPx) and the levels of reduced glutathione (GSH) and malonaldialdehyde (MDA) were estimated in corpus striatum, frontal cortex, thalamus and midbrain on 0, 10 and 20 days post-inoculation (dpi). A significant increase in MDA levels in striatum (p < 0.01), cortex (p < 0.01), thalamus (p < 0.01) and midbrain (p < 0.01) was observed in JEV infected rats on 10 and 20 dpi compared to controls. The activity of CAT, GPx and the levels of GSH were significantly decreased in all the brain regions studied on 10 and 20 dpi compared to controls. However, the activity of Mn-SOD in striatum (p < 0.01). cortex (p < 0.05), thalamus (p < 0.01) and midbrain (p < 0.01) were significantly increased on 10 and 20 dpi in JEV infected rats compared to controls. The activity of Mn-SOD and MDA levels were significantly increased whereas the activity of CAT, GPx and GSH levels were significantly decreased in all the brain regions studied as the disease progressed from 0 to 20 dpi. The maximum alteration in oxidant/antioxidant balance was observed in thalamus and midbrain. The results of the present study demonstrate that antioxidant defense mechanism is impaired after the infection of JE virus suggesting its critical role in cellular injury in brain regions. The findings could be beneficial to understand the role of oxidative stress in the pathogenesis of JE and therapeutic interventions. (C) 2009 Elsevier Ltd. All rights reserved.
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