Vanadium exposure enhances lipid peroxidation in the kidney of rats and mice.
Vanadium (V) as sodium orthovanadate induces an increase in lipid peroxidation in the kidneys after a single subcutaneous or intraperitoneal injection to rats or mice. The rate of malondialdehyde (MDA) formation, an index of lipid peroxidation, by kidney homogenates increased by more than 100% 1 h after injection. Chronic exposure of rats to vanadium sulfate, initially through maternal milk and later in the drinking water, resulted after 10 weeks in a significant increase in MDA formation by kidney but not by other tissues. In both acute and chronic studies in rats and mice, no significant increase in lipid peroxidation by V treatment was detected in brain, heart, lung, spleen, or liver. In mice, administration of ascorbate prior to acute exposure to V diminished both toxicity, i.e., respiratory depression and limb paralysis, and the formation of MDA in kidney.
D000818:Animals; D001205:Ascorbic Acid / Q000494:pharmacology; D004032:Diet; D007668:Kidney / Q000378:metabolism*; D008054:Lipid Peroxides / Q000378:metabolism*; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D051379:Mice; D008815:Mice, Inbred Strains; D051381:Rats; D011919:Rats, Inbred Strains; D013997:Time Factors; D014638:Vanadates; D014639:Vanadium / Q000494:pharmacology* / Q000633:toxicity; D017968:Vanadium Compounds
D008054:Lipid Peroxides; D017968:Vanadium Compounds; D014639:Vanadium; D014638:Vanadates; D008315:Malondialdehyde; C034028:vanadyl sulfate; D001205:Ascorbic Acid