EFFECT OF LOW-DOSE LEAD ACETATE EXPOSURE ON THE METABOLISM OF NUCLEIC-ACIDS AND LIPIDS IN CEREBELLUM AND HIPPOCAMPUS OF RAT DURING POSTNATAL-DEVELOPMENT

Postnatal exposure (from the second day after birth to 30 days) of rat pups to low levels of lead acetate (50 mg/kg body weight/day), administered by gastric intubation, yielded a maximum blood level of 76.1μg/100 ml, at day 15 of age. Cerebellar and hippocampal lead contents were 8.67μg/100 mg and 11.7μg/100 mg, respectively, at day 30 of age. This lead exposure has been shown to elicit little change in some biochemical parameters in cerebellum and hippocampus. At the three ages investigated (5,15, and 30 days after birth) there were no alterations of body weight; brain, cerebellum, and hippocampus wet weight; and DNA, RNA, protein and phospholipid content, either in total tissue or in mitochondria. A similar invariance following lead exposure was observed in mitochondrial succinate dehydrogenase and cytochrome oxidase activities. After intraperitoneal administration, the incorporation of [methyl‐14C]thymidine into DNA and [5,6‐3H]uridine into RNA of cerebellum and hippocampus showed a significant decrease only at day 5, reaching the control value at 15 and 30 days of age. After intraperitoneal injection, [2‐3H]glycerol incorporation into total lipids and phospholipids of cerebellum and hippocampus also showed no significant changes in Pb‐treated pups compared to controls at all three postnatal ages. We concluded that subclinical lead administration exerts its effect by slowing cell proliferation in the very early growth phase of the brain. It is likely that a metabolic compensative response to subtoxic effect of lead acetate may be brought about in cerebellum and hippocampus during critical phases of nervous system development between days 15 and 30. Copyright © 1990 Wiley‐Liss, Inc.