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GESTATIONAL EXPOSURE TO NONYLPHENOL CAUSES PRECOCIOUS MAMMARY GLAND DEVELOPMENT IN FEMALE RAT OFFSPRING
Citation:
MOON, H. J., S. HAN, J. H. SHIN, I. H. KANG, T. S. KIM, J. H. HONG, S. H. KIM, AND S. E. FENTON. GESTATIONAL EXPOSURE TO NONYLPHENOL CAUSES PRECOCIOUS MAMMARY GLAND DEVELOPMENT IN FEMALE RAT OFFSPRING. Journal of Reproduction and Development. Japanese Society of Animal Reproduction, Tokyo, Japan, 53(2):333-344, (2007).
Impact/Purpose:
Late pregnancy and puberty are critical periods of mammary development that can be altered by hormones, growth factors, and environmental agents. This study examined whether or not in utero nonylphenol exposure can induce changes in mammary gland and reproductive development in female rat offspring. Nonylphenol induced precocious development of the gland, an effect that is similar to estradiol or other estrogenic endocrine disruptors. In addition, the relationships between nonylphenol (precocious)- and atrazine (delays)-induced mammary development and expression of hormone receptors, such as estrogen receptor (ER), progesterone receptor (PR), and prolactin receptor (PRLR), were investigated using immunohistochemical staining. This information will be used to better understand the impact that developmental exposure has on common receptor populations of the mammary gland in the adult animal.
Description:
This study examined whether or not exposure to 4-nonylphenol (NP) during late gestation affects reproductive and mammary development in the offspring of female rats. Time pregnant Long Evans rats were gavaged with NP (10 or 100 mg/kg), atrazine (ATR, 100 mg/kg), or corn oil on gestation days 15-19. The uterus weights of the NP (100 mg/kg/d)-exposed pups were higher than those of the controls but the weights of the other organs were unchanged. Delayed mammary gland (MG) development was detected in the ATR pups on PND 4 and persisted through to PND 66. The high dose NP pups had advanced lobular development of their MG on PND 22, while the glands from the low dose NP pups were no different morphologically from the controls. Immunohistochemical comparisons of the mammary sections from PND 41 demonstrated low levels of estrogen receptor (ER) staining in the control gland stroma and epithelium but higher levels in the tissue of the pups exposed to NP and ATR. ATR also elevated ER in the stroma surrounding the epithelial layer of the terminal end buds. The level of progesterone receptor (PR) staining was markedly lower in the epithelium of the 100 mg/kg NP glands vs. the control glands. However, PR was present at high levels in the epithelium of the 10 mg/kg NP glands and was even more prominent in the ATR-exposed ductal epithelium and fat cell nuclei. The level of prolactin staining was only elevated in glands containing lobule areas (NP-exposed) compared with the control levels. These results suggest that NP and ATR have opposite effects on the development of MG after gestational exposure. Exposure to them during the critical period of epithelial outgrowth altered the receptor levels of mammary progesterone and prolactin and might contribute to the differences in the mammary morphology at PND 41.
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GESTATIONAL EXPOSURE TO NONYLPHENOL CAUSES PRECOCIOUS MAMMARY GLAND DEVELOPMENT IN FEMALE RAT OFFSPRING