Abstract

Mothers were fed a diet containing 2% lead acetate acording to the Pentschew-Garro model for inducing lead encephalopathy in young rats. At 20-22 days of age the young lead-treated rats had a mean brain Pb of 2.8 microgram/g and liver Pb of 11 microgram/g. The ALA dehydratase activity decreased 29% in brain and 69% in liver compared to controls, suggesting that the enzyme activity is related to the tissue lead level. Mothers that had received lead prior to conception gave birth to pups with a significantly raised mean blood lead level (44 microgram %). The ALA dehydratase activity in brain and liver was unchanged, suggesting that low blood lead levels may be insufficient to inhibit this enzyme in the rat. Focal haemorrhages were present, however, in the cerebral cortex of some of the pups from the lead-treated mothers. It is concluded that damage to the rat brain vascular system is a better index of lead toxicity than measurement of the lead sensitive enzyme ALA dehydratase.

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