STUDY OF ANTIOXIDANT EFFECTS OF CERTAIN SUBSTANCES ON ISCHAEMIC RAT BRAIN

Abstract

It is believed that ischaemia/reperfusion-mediated brain injury results, at least in part, from the oxidation of cellular macromolecules and micromolecules. Because of the brain's high consumption of oxygen, high concentration of polyunsaturated fatty acids and essential metals (e.g., iron and copper), and low concentrations of antioxidants, the brain is vulnerable to ischaemia-induced injury caused by reactive oxygen species. Within seconds of the onset of ischaemia, the decline in blood flow and the accompanying loss of oxygen supply result in a reduction of high-energy metabolites such as ATP and triphosphocreatine. The combination of ATP breakdown and compensatory activation of anaerobic glycolysis during ischaemia leads to an increase in levels of inorganic phosphate, in addition to lactate and I-t formation causing cellular acidification. Among the most discussed factors involved in pathogenesis of cerebral ischaemia/reperfusion are energy failure, disturbed calcium homoeostasis, glutamate receptor-mediated excitotoxicity, enhanced formation of free radicals, and acidosis. In the present study, we give emphasis on the pathological role of free radicals in participating in neuronal cell death and the response of neuronal cell toward free radical insuJts. Many experimental models are used to study cerebral ischaemic damage. Three main classes of in-vivo models are global ischaemia, focal ischaemia and hypoxial ischaemia. Throughout the present i nvestigation, global cerebral ischaemia has been induced in Wistar rats by occlusion of the two main carotid arteries. In the present study, parameters markering oxidative damage such as brain cytosolic activities of LDH and SOD enzymes and brain content of MDA and GSH have been assessed.