期刊
TOXICOLOGICAL SCIENCES
卷 133, 期 1, 页码 157-173出版社
OXFORD UNIV PRESS
DOI: 10.1093/toxsci/kft035
关键词
brain; endocrine disruptor; endocrine disruption; hypothalamus; development; sexually dimorphic; ethinyl estradiol
类别
资金
- National Institutes of Health [R01-16001-04S1]
Bisphenol A (BPA) exposure is ubiquitous, and in laboratory animals, early-life BPA exposure has been shown to alter sex-specific neural organization, neuroendocrine physiology, and behavior. The specific mechanisms underlying these brain-related outcomes, however, remain largely unknown, constraining the capacity to ascertain the potential human relevance of neural effects observed in animal models. In the perinatal rat brain, estrogen is masculinizing, suggesting that BPA-induced perturbation of estrogen receptor (ESR) expression may underpin later in-life neuroendocrine effects. We hypothesized that prenatal BPA exposure alters sex-specific ESR1 (ER alpha) and ESR2 (ER beta) expression in postnatal limbic nuclei. Sprague Dawley rats were mated and gavaged on gestational days (GDs) 6-21 with vehicle, 2.5 or 25 mu g/kg bw/day BPA, or 5 or 10 mu g/kg bw/day ethinyl estradiol. An additional group was restrained but not gavaged (naive control). Offspring were sacrificed the day after birth to quantify ESR gene expression throughout the hypothalamus and amygdala by in situ hybridization. Relative to the vehicle group, significant effects of BPA were observed on ESR1 and ESR2 expression throughout the mediobasal hypothalamus and amygdala in both sexes. Significant differences in ESR expression were also observed in the mediobasal hypothalamus and amygdala of the naive control group compared with the vehicle group, highlighting the potential for gavage to influence gene expression in the developing brain. These results indicate that ESR expression in the neonatal brain of both sexes can be altered by low-dose prenatal BPA exposure.
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