Abstract

Adult female rats were chronically treated with nicotine administered via the drinking water during pregnancy and/or lactation. The approximate doses of nicotine consumed per day were 2.4 mg/kg and 4.5 mg/kg of body weight. The pups were weaned at 20 days of age. The pups were killed by decapitation on postnatal days 20, 30, or 40 and plasma from heparinized trunk blood was assayed for luteinizing hormone (LH). At 30 days of age untreated male and female offspring had the highest levels of plasma LH compared to 20 and 40 days of age. This level was not affected by any subsequent dose or treatment. Prepubertal females exposed to nicotine during pregnancy failed to exhibit the pattern of LH levels seen in control animals, whereas those exposed during lactation or throughout the perinatal period showed a distinctive pattern of plasma LH. Chronic exposure of female offspring to the low dose of nicotine during lactation tended to increase plasma LH levels at 20 and 40 days. Female offspring exposed to nicotine during pregnancy or to the low dose during lactation showed significant deficits in body weight at 40 days of age which appeared to correlate with a delay in vaginal opening. The results suggest that perinatal exposure to maternally administered nicotine may disrupt normal patterns of LH release in the offspring of both sexes and alter sexual development in female offspring.

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