A STUDY ON THE EFFECT OF ISOBARIC HYPOXIA ON ANTIOXIDANT ENZYME ACTIVITY AND LIPID PEROXIDATION IN RAT BRAIN
AbstractIn the present work, an attempt was made to study the effect of isobaric hypoxic hypoxia (10%) on rat brain. Since literatures support generation of free radicals during post ischemic/hypoxic period, here hypoxia followed by reoxygenation is dealt with as the single problem. Subsequently, as brain shows regional variations in its function and metabolic activities an attempt was made to study effect of hypoxia reoxygenation in five brain regions i.e. cerebrum, cerebellum, medulla, hippocampus and hypothalamus. The changes in the antioxidant defense enzymes such as superoxide dismutase, catalase and glutathione peroxidase activity and lipid peroxidation levels in brain associated with hypoxia-reoxygenation was analyzed in this study. Antioxidant enzyme activity and lipid peroxidation levels showed a significant (P< 0.0001) regional variation among the five brain regions chosen for the study. Interestingly, the hippocampus region of the rat brain depicted the lowest SOD and GPx activity and highest level of lipid peroxidation. Hypoxia (10%) for 3 hours brought about significant decrease (P<0.05) in the activities of superoxide dismutase, catalase and glutathione peroxidase in rat brain regions. After hypoxia, hippocampus region showed a highly significant (P<0.0001) reduction in SOD activity and GPx activity and highest rise in lipid peroxidation levels. Thus the hippocampus region was found most vulnerable to hypoxia. Among the three enzymes, most conspicuous decrease was shown by superoxide dismutase. The present study revealed that 3 hours of hypoxia followed by reoxygenation increased lipid peroxidation levels in the rat brain.
Article Information
11
67-75
406 kB
998
English
IJPSR
Manju Antony* and T. J. James
Department of Life sciences, Kristu Jayanti College, Bangalore (Karnataka), India
manju_antony@hotmail.com
25 May, 2010
31 July, 2010
13 August, 2010
http://dx.doi.org/10.13040/IJPSR.0975-8232.1(9-S).67-75
15 September, 2010