Effect of prenatal and neonatal exposure to lead on the affinity and number of estradiol receptors in the uterus.
Female Sprague-Dawley rats were treated with lead chloride (20 ppm or 200 ppm Pb) or sodium chloride (controls) in their drinking water. Three treatment regimens were employed: (I) rats were treated prior to mating and uteri were removed from 21-d-old offspring, (II) treatments were begun when females were in d 7 of pregnancy and continued on the dams until the pups were 21 d old, and half of these offspring were continued on the Pb treatments and half on saline, with uteri removed during diestrus when female offspring were approximately 150 d old; (III) female rats were treated from d 21 to d 35 and then uteri were removed. Estradiol-receptor binding and affinity were determined on the uterine tissues. Treatment with lead prior to mating (group I) resulted in a significant increase in estradiol-receptor affinity (Ka) in 21-d-old offspring without a change in estradiol receptor number (N). Treatment from d 7 of pregnancy until weaning of the pups resulted in approximately 35% decrease (p less than 0.05) in estradiol receptors per milligram uterine protein when these offspring reached 150 d of age (group II). Similarly, treatment with Pb from d 21 until d 35 or until d 150 resulted in a significant decrease in uterine estradiol receptor number at 35 and 150 d, respectively, while the Ka was significantly (p less than 0.01) increased by the exposure to Pb. The results demonstrate that prenatal and/or postnatal exposure to Pb alters the number and affinity of estradiol receptors in the prepubertal and adult rat uterus.[1]References
- Effect of prenatal and neonatal exposure to lead on the affinity and number of estradiol receptors in the uterus. Wiebe, J.P., Barr, K.J. Journal of toxicology and environmental health. (1988) [Pubmed]
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