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Lead: intestinal absorption and bone mobilization during lactation

Department of Biochemistry, CINVESTAV-IPN, Department of Pharmacology and Toxicology, CINVESTAV-IPN, México City

J. Cerbón-Solorzano

Department of Biochemistry, CINVESTAV-IPN

A. Albores-Medina

Department of Pharmacology and Toxicology, CINVESTAV-IPN, México City

C. Hernández-Luna

Department of Biochemistry, Faculty of Biological Sciences, UANL, San Nicolas de los Garza, NL, Mexico

JV Calderón-Salinas

Department of Biochemistry, CINVESTAV-IPN

The aim of this study was to examine lead (Pb) intestinal absorption, its mobilization and redistribution during lactation in rats chronically exposed to lead. Lead and calcium (Ca) concentrations were measured in blood, milk, femurs, liver and kidney samples obtained from pregnant and lactating mother rats which were subjected to different schedules of exposure to Pb: 158 days before and during lactation (group A), 144 days before lactation (group B) and 14 days only during lactation (group C). Results were compared to those of non-pregnant but Pb- exposed matched rats and non-exposed control rats. In groups A and B during lactation, Pb in blood (PbB), liver and kidney increased while Pb in bone decreased. Since there was not an external source of Pb in group B during lactation, the results indicate resorption of Pb in bone as the main source of Pb in the organism. In group A, there was an additional increase of PbB when compared to group B as a result of Pb intestinal absorption. In group C a significant increase in PbB due to intestinal absorption and deposit in bone was found when compared to non- pregnant 144 days old rats, suggesting that the three processes intestinal absorption, bone resorption and bone absorption were taking place. These data indicate that Pb stored in bone as a result of prior maternal exposure, should be considered as a major source of self intoxication and of Pb in milk available to suckling pups.

Key Words: bone resorption • lactancy • lead • intestinal absorption • lead distribution

Human & Experimental Toxicology, Vol. 15, No. 11, 872-877 (1996)
DOI: 10.1177/096032719601501102


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