Intake of Magnesium and Toxicity of Lead: An Experimental Model

Groups of ten male Wistar rats were fed 100 mg lead/kg body wt . day, or 100 mg lead plus 250 mg Mg . kg body wt . day mixed in the powdered diet as chlorides. Blood and urine were monitored for lead-related enzymes and lead concentrations. Compared to the lead-treated, blood lead and urinary aminolevulinic acid were much lower and blood aminolevulinic acid dehydratase and urinary lead were higher at 30, 45, and 62 days in the lead-magnesium-treated animals. At 45 and 62 days, blood lead was higher in the lead-magnesium group even though the urinary excretion of lead was significantly higher (P less than .01). At 62 days, the lead feeding was discontinued to both groups, but magnesium administration was continued. Both groups of rats were then monitored for urinary excretion of lead and this was significantly higher (P less than .01) in the rats fed magnesium suggesting that magnesium intake helped mobilize lead from bone, thus increasing the blood lead level and subsequent urine excretion. Enzyme levels approached normal values at 106 days only in the lead-magnesium group, thereby indicating low levels of lead toxicity. Lead levels of bones in rats of the lead-magnesium group, when sacrificed at 106 days, were significantly lower (P less than .01) than among those given lead alone, another indication that magnesium helped mobilize lead from bone. The results, therefore, clearly show that feeding magnesium leads to lower retention and increased excretion of lead under the experimental conditions outlined.