MICROCHROMATOGRAPHIC ANALYSIS OF LIPIDS, PROTEIN, AND OCCURRENCE OF LIPID-PEROXIDATION IN VARIOUS BRAIN-AREAS OF VANADIUM EXPOSED RATS - A POSSIBLE MECHANISM OF VANADIUM NEUROTOXICITY (VOL 14, PG 57, 1993)

Administration of sodium metavanadate (3 mg/kg) to adult female Spragu e Dawley rats for 5 consecutive days by intraperitoneal route resulted in major alterations in lipid profiles and protein concentration in a ll the brain regions. Sodium metavanadate exposure displayed significa nt decrease in the levels of total lipids, phospholipids, cholesterol and cerebrosides, and protein, but ganglioside concentration was signi ficantly increased in various areas of the brain. Loss of body weight observed in this study could be attributed to the loss of appetite; lo ss of nutrients and wasting of tissues. It is likely that large amount of body water was lost through diarrhoea. Gas liquid chromatography h as revealed that oleic acid, linoleic acid, linolenic acid, and archid onic acid were perferentially lost in the brain of vanadium-exoposed r ats. Thin layer chromatography further proved degradation of individua l lipids. Sphingomyelin was substantially decreased followed by phosph atidyl 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 deterioratio n of myelin sheath by vanadium exposure contributed to preferential li pid 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 compre hensive degradation of lipids in the different regions of the rat brai n. However, the mechanism involved in the elevation of ganglioside lev els is not yet fully understood. It is concluded that these perturbati ons produced damage to the associated physiological functions leading to CNS dysfunctions. (C) 1994 Intox Press, Inc.