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Tchernitchin AN, Gaete L, Bustamante R, et al. Effect of prenatal exposure to lead on estrogen action in the prepubertal rat uterus. ISRN Obstet Gynecol. 2012;2011:329692doi: 10.5402/2011/329692.
Tchernitchin, A. N., Gaete, L., Bustamante, R., & Báez, A. (2011). Effect of prenatal exposure to lead on estrogen action in the prepubertal rat uterus. ISRN obstetrics and gynecology, 2011329692. https://doi.org/10.5402/2011/329692
Tchernitchin, Andrei N, et al. "Effect of prenatal exposure to lead on estrogen action in the prepubertal rat uterus." ISRN obstetrics and gynecology vol. 2011 (2011): 329692. doi: https://doi.org/10.5402/2011/329692
Tchernitchin AN, Gaete L, Bustamante R, Báez A. Effect of prenatal exposure to lead on estrogen action in the prepubertal rat uterus. ISRN Obstet Gynecol. 2011;2011:329692. doi: 10.5402/2011/329692. Epub 2012 Jan 02. PMID: 22263113; PMCID: PMC3255308.
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ISRN Obstet Gynecol. 2011;2011:329692. doi: 10.5402/2011/329692. Epub 2012 Jan 02.

Effect of prenatal exposure to lead on estrogen action in the prepubertal rat uterus.

ISRN obstetrics and gynecology

Andrei N Tchernitchin, Leonardo Gaete, Rodrigo Bustamante, Aracelly Báez

Affiliations

  1. Laboratory of Experimental Endocrinology and Environmental Pathology (LEEPA), Institute of Biomedical Sciences (ICBM), University of Chile Medical School, P.O. Box 21104, Santiago 21, Chile.

PMID: 22263113 PMCID: PMC3255308 DOI: 10.5402/2011/329692

Abstract

Lead is a widely spread environmental pollutant known to affect both male and female reproductive systems in humans and experimental animals and causes infertility and other adverse effects. The present paper investigated the effects of prenatal exposure to lead on different parameters of estrogen stimulation in the uterus of the prepubertal rat. In prenatally and perinatally exposed rats, estrogen-induced endometrial eosinophilia, endometrial stroma edema, and eosinophil migration towards the endometrium, and uterine luminal epithelial hypertrophy are enhanced while several other responses to estrogen appear unchanged. These effects may contribute to decrease in fertility following prenatal exposure to lead. The striking difference between most of these effects of prenatal exposure and the previously reported effects of chronic exposure to lead suggests that prenatal exposure to lead may neutralize the effects of chronic exposure to lead, providing partial protection of cell function against the adverse effects of chronic exposure to lead. We propose that the mechanism involved, named imprinting or cell programming, persisted through evolution as a nongenetic adaptive mechanism to provide protection against long-term environmental variations that otherwise may cause the extinction of species not displaying this kind of adaptation.

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