Abstract

Suckling mice were found to absorb and retain a greater fraction of an oral lead dose than did adult mice. Pinocytotic activity and lead uptake (in vivo) were found to be greatest in the distal small intestinal tissue. Cortisone pretreatment results in precocious cessation of pinocytotic activity in the intestine of suckling mice. Cortisone pretreatment of adult mice had no effect on whole body lead retention or intestinal tissue content of lead following an oral dose. The data indicate that the distal small intestine is the site of active pinocytosis of lead, and that pinocytosis is the major mechanism involved in lead absorption in suckling mice. Developmental differences were also observed in the percentage of lead retained in the whole body. Both groups exhibited dose-independent lead retention, indicating a first-order absorption process for each age group. Lead distribution and elimination from organs also differed between suckling and adult mice. Developmental differences were observed in organ lead concentration for kidneys and brain following oral doses. Relative distribution of lead to the brains of suckling mice were greater than to adult brains. Whole body and bone lead elimination rates were reduced in suckling compared to adult mice. Brain lead elimination rates did not differ in suckling and adult mice. A lactating mouse model was developed to study lead transfer to suckling offspring. Lead was transferred in milk to suckling offspring from mothers which had previously ingested lead in the drinking water. Relative lead transfer to suckled offspring during lactation greatly exceeded transfer to fetuses during gestation. Lactation resulted in an increased rate of maternal lead elimination. Lead concentration in milk exceeded plasma concentration by a factor of approximately 25. (ERB)

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