Vitamin-E reduces the oxidative damage on δ-aminolevulinic dehydratase induced by lead intoxication in rat erythrocytes

• Published in: Toxicology in vitro 2007-09, Vol.21 (6), p.1121-1126
• Main Authors: Rendón-Ramirez, A., Cerbón-Solórzano, J., Maldonado-Vega, M., Quintanar-Escorza, M.A., Calderón-Salinas, J.V.
• Format: Article
• Language: English
• Subjects: Animals; Antioxidants - pharmacology; Chromans - pharmacology; Erythrocyte Count; Erythrocytes - drug effects; Erythrocytes - metabolism; Lead - blood; Lead - pharmacokinetics; Lead - toxicity; Lipid Peroxidation - drug effects; Oxidative damage; Oxidative Stress - drug effects; Porphobilinogen Synthase - metabolism; Protoporphyrins - blood; Rats; Rats, Wistar; Thiobarbituric Acid Reactive Substances - metabolism; Vitamin E - pharmacology; Vitamin-E; Vitamins - pharmacology; δ-aminolevulinic dehydratase activity
• ISSN: 0887-2333; 1879-3177
• DOI: 10.1016/j.tiv.2007.04.019

Lead intoxication induces oxidative damage on lipids and proteins. In the present paper we study in vivo and in vitro the antioxidant effect of vitamin-E and trolox, on the oxidative effects of lead intoxication in rat erythrocytes. Vitamin-E simultaneously administered to erythrocytes treated with lead was capable to prevent the inhibition of δ-aminolevulinic dehydratase activity and lipid oxidation. Partial but important protective effects were found when vitamin-E was administered either after or before lead exposure in rats. In vitro, the antioxidant trolox protected δ-ALA-D activity against damage induced by lead or menadione. These results indicate that vitamin-E could be useful in order to protect membrane-lipids and, notably, to prevent protein oxidation produced by lead intoxication.