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Oxidative stress is the primary event: Effects of ethanol consumption in brain

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Abstract

Damaging effects of reactive oxygen species on living systems are well documented. They include oxidative attack on vital cell constituents. Chronic ethanol administration is able to induce an oxidative stress in the central nervous system. In the present study, 16–18 week-old male albino rats of Wistar strain were exposed to different concentration of ethanol for 4 weeks. This exposure showed profound effect on body weight. Ascorbic acid level; and activities of alkaline phosphatase and aspartate transaminase in the brain are dependent on the concentration of ethanol exposure. Chronic ethanol ingestion elicits statistically significant increase in thiobarbituric acid reactive substances level and decrease in gluatathione level in the brain. It reduces superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase activities in a dose dependent manner. However, histological examination could not reveal any pathophysiological changes. Therefore, we conclude that biochemical alterations and oxidative stress related parameters respond early in alcoholism than the histopathological changes in brain.

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Authors and Affiliations

  1. Department of Biochemistry, Amrita Institute of Medical Sciences, Elamakkara, 682 026, Cochin

    Subir Kumar Das, Sukhes Mukherjee & D. M. Vasudevan

  2. Department of Pathology, Amrita Institute of Medical Sciences, Elamakkara, 682026, Cochin, Kerala

    Hiran K. R.

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  1. Subir Kumar Das
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  4. D. M. Vasudevan
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Correspondence to Subir Kumar Das.

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Das, S.K., Hiran, K.R., Mukherjee, S. et al. Oxidative stress is the primary event: Effects of ethanol consumption in brain. Indian J Clin Biochem 22, 99–104 (2007). https://doi.org/10.1007/BF02912890

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