Selenium and lead: Mutual detoxifying effects

Antagonistic toxic effects of selenium and lead were studied in growing rats. Chronic lead intoxication was produced by cutaneous application of lead naphthenate solution (80–200 mg Pb/kg body weight) for a period of 8 weeks and chronic selenium intoxication was induced by giving 5 ppm, 10 ppm and 15 ppm selenium in drinking water. The growth rate and food consumption of rats receiving selenium in addition to lead approached normal rate while animals treated with only one of them showed hampered growth rate and lower food consumption. The enzymatic activity of δ-aminolevulinic acid dehydrase (ALA-D) in whole blood, liver and kidney and liver P-450 enzyme activity were normal in rats receiving both selenium and lead. The enzymic activities assayed were, however, depressed in the animals receiving either lead or selenium.Assay of lead and selenium in liver, brain, kidney and blood was carried out. Rats receiving both metals and higher concentrations of these metals in the organs studied, as compared to those only receiving one component. The data seem to indicate that the effect of selenium on the toxic effects of lead is similar to its protective role against methylmercury intoxication.     

Brain microsomal enzyme mediated covalent binding of benzo[a]pyrene to DNA

The covalent binding of benzo[a]pyrene (BP) to calf thymus DNA by brain microsomes isolated from control and 3-methylcholanthrene (3-MC) treated rats was investigated. The influence of incubation time, pH, and concentrations of protein, BP and NADPH on covalent binding was investigated to obtain optimum conditions for the in vitro binding of [3H]BP to DNA. Treatment of rats to 3-MC resulted in a 1.53-fold increase in the brain microsomal mediated covalent binding of [3H]BP to DNA. Inhibitors of monooxygenase enzyme activity such as alpha-naphthoflavone, metyrapone, 1-benzylimidazole and ellagic acid significantly inhibited the binding of [3H]BP to DNA from control and 3-MC stimulated brain microsomes. Our results indicate that inhibitors and inducers of monooxygenases may modulate brain enzyme-mediated binding of polycyclic aromatic hydrocarbons (PAHs) to DNA.