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 Spragu e Dawley rats for 5 consecutive days by intreaeritoneal route resulted in major alterations in lipid profiles and protein concentration in a ll the brain regions. Sodium metavanadate exposure displayed phospholi pids, cholesterol and cerebrosides, and protein, but ganglioside conce ntration was significantly increased in various areas of the brain. Lo ss of body weight observed in this study could be attributed to the lo ss of appetite; loss of nutrients and wasting of tissues. It is likely that large amount of body water was lost through diarrhoea. Gas liqui d chromatography has revealed that oleic acid, linoleic acid, linoleni c acid, and archidonic acid were perferentially lost in the brain of v anadium-exoposed rats. Thin layer chromatography further proved degrad ation of individual lipids. Sphingomyelin was substantially decreased followed by phosphatidyl choline and phosphatidyl ethanolamine, but ph osphatidyl serine and phosphatidyl inositol were slightly affected. Ou r recent work has demonstrated vanadium-induced stimulation of lipid p eroxidation 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 a lso indicate that vanadium-induced stimulation of lipid peroxidation i s characterized by a selective loss of brain polyunsaturated fatty aci ds and thus comprehensive degradation of lipids in the different regio ns of the rat brain. However, the mechanism involved in the elevation of ganglioside levels is not yet fully understood. It is concluded tha t these perturbations produced damage to the associated physiological functions leading to CNS dysfunctions. (C) 1993 Intox Press, Inc.