The ability of vitamin E to prevent or treat experimental lead intoxication was investigatedin rats.Lead ingestion(10 mg/kg,lead as lead acetate,orally fbr 6 weeks)significantly inhibitedthe activity of blood δ-aminolevulinic acid dehydratase(ALAD),reduced the brain dopamine(DA)contents,enhanced the blood zinc protoporphyrin,and enhanced the urinary excretion ofδ-aminolevulinic acid(ALA).Lead exposure also elevated brain norepinephrine,homovanillicacid,and 5-hydroxyindole acetic acid(5-HIAA)levels and concentration of lead in blood andtissue.Simultaneous supplementation of vitamin E along with lead significantly reduced theinhibition of blood ALAD activity,brain DA and 5-HIAA levels,and elevation of urinary ALAexcretion.Blood and liver lead concentrations were also significantly reduced by simultaneoussupplementation with vitamin E.Postlead exposure treatment with vitamin E was ineffective inreducing the lead-induced effects,except that the inhibition of blood ALAD activity was slightlyreduced.The present results suggest that vitamin E given simultaneously with lead is effectivein reducing the severity of lead intoxication.1989 Academic Press.Inc.
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