Abstract
The influence of milk in the diet on the toxicity of orally ingested lead was investigated in male weanling Wistar rats. Three groups of 20 rats were fed diets based on soya protein, whole milk or lactose-hydrolysed milk, and half of the animals in each group were given 20 μg lead (as lead acetate)/g diet. After 8 wk, biochemical tests for lead toxicity were carried out and tissue-lead levels were measured. While all of the rats given lead-supplemented diets had higher concentrations of lead in bone, brain, blood, kidney and liver than those given diets without added lead, the increase was significantly greater in all tissues in the group given lead in milk. Lead-treated animals fed a milk diet from which lactose had been removed by hydrolysis had tissue-lead concentrations similar to those of rats fed the lead-containing soya diet. Lead supplementation did not increase levels of urinary δ-aminolaevulinic acid (ALA) or free erythrocyte protoporphyrin, but did cause inhibition of erythrocyte ALA dehydratase activity. ALA dehydratase inhibition was not greater in the group given lead in milk despite the fact that tissue lead concentrations were 30–60% higher in these rats, compared to those given lead in soya or in lactose-hydrolysed milk. In a second experiment two groups of rats were fed two meals per day. Both groups were given 5 g soya-based diet containing 60 μg lead/g in the morning. In the evening one group was given, ad lib., the milk diet without added lead, while the other was given, ad lib., the soya diet without added lead. There was no difference in tissue-lead concentrations between the two groups, indicating that milk must be present in the gastro-intestinal tract at the same time as lead in order to increase the levels of lead in the tissues. These studies show that milk consumption increases tissue-lead concentrations in rats fed low concentrations of lead and milk simultaneously. Lactose appears to be the factor in milk responsible for this increase. These studies indicate the need for further research on interactions of diet and lead toxicity and the need for more sensitive methods for assessing the health effects of chronic exposure to low levels of lead.
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