Microchromatographic analysis of lipids, protein, and occurrence of lipid peroxidation in various brain areas of vanadium exposed rats: a possible mechanism of vanadium neurotoxicity.

Administration of sodium metavanadate (3 mg/kg) to adult female Sprague Dawley rats for 5 consecutive days by intraperitoneal route resulted in major alterations in lipid profiles and protein concentration in all the brain regions. Sodium metavanadate exposure displayed significant decrease in the levels of total lipids, phospholipids, cholesterol and cerebrosides, and protein, but ganglioside concentration was significantly increased in various areas of the brain. Loss of body weight observed in this study could be attributed to the loss of appetite; loss of nutrients and wasting of tissues. It is likely that large amount of body water was lost through diarrhoea. Gas liquid chromatography has revealed that oleic acid, linoleic acid, linolenic acid, and arachidonic acid were preferentially lost in the brain of vanadium-exposed rats. Thin layer chromatography further proved degradation of individual lipids. Sphingomyelin was substantially decreased followed by phosphatidyl choline and phosphatidyl ethanolamine, but phosphatidyl serine and phosphatidyl inositol were slightly affected. Our recent work has demonstrated vanadium-induced stimulation of lipid peroxidation in the various regions of the rat brain. It is speculative that deterioration of myelin sheath by vanadium exposure contributed to preferential lipid loss but lesser loss of protein. These studies also indicate that vanadium-induced stimulation of lipid peroxidation is characterized by a selective loss of brain polyunsaturated fatty acids and thus comprehensive degradation of lipids in the different regions of the rat brain. However, the mechanism involved in the elevation of ganglioside levels is not yet fully understood. It is concluded that these perturbations produced damage to the associated physiological functions leading to CNS functions.