美国一项新研究成果显示，受孕小鼠在孕期过多接触双酚A，会导致其后代出现永久性的生理缺陷。
美国耶鲁大学医学院研究人员在新一期《美国实验生物学联合会会刊》（The FASEB Journal）上报告说，他们让两组受孕小鼠中的一组接触双酚A，另一组接触安慰剂。结果发现，接触双酚A的受孕小鼠其后代成年后对雌激素的反应也异常强烈。
该研究项目负责人休泰勒解释说，这是因为受孕小鼠后代在胎儿时期DNA(脱氧核糖核酸)就遭到修改，甲基化出现问题，因而造成其成年后对雌激素高度敏感。新研究对人类同样有借鉴意义，孕妇应该避免在孕期接触双酚A，否则有可能对后代造成永久性不良影响。
双酚A是一种广泛用于塑料产品的化学物质，婴儿奶瓶、饮料瓶等塑料容器及包装物中大多含有该物质。双酚A是否危害健康尤其是儿童健康的争论由来已久。一些研究认为，双酚A可能会发挥类似雌激素的作用，使人体代谢紊乱，引发一些疾病。
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《美国实验生物学联合会会刊》发表论文摘要（英文）
Published online before print February 24, 2010 as doi: 10.1096/fj.09-140533.
Bisphenol-A exposure in utero leads to epigenetic alterations in the developmental programming of uterine estrogen response
Jason G. Bromer, Yuping Zhou, Melissa B. Taylor, Leo Doherty, and Hugh S. Taylor
E-mail contact: hugh.taylor@yale.edu
Bisphenol-A (BPA) is a nonsteroidal estrogen that is ubiquitous in the environment. The homeobox gene Hoxa10 controls uterine organogenesis, and its expression is affected by in utero BPA exposure. We hypothesized that an epigenetic mechanism underlies BPA-mediated alterations in Hoxa10 expression. We analyzed the expression pattern and methylation profile of Hoxa10 after in utero BPA exposure. Pregnant CD-1 mice were treated with BPA (5 mg/kg IP) or vehicle control on d 9–16 of pregnancy. Hoxa10 mRNA and protein expression were increased by 25% in the reproductive tract of mice exposed in utero. Bisulfite sequencing revealed that cytosine-guanine dinucleotide methylation was decreased from 67 to 14% in the promoter and from 71 to 3% in the intron of Hoxa10 after in utero BPA exposure. Decreased DNA methylation led to an increase in binding of ER- to the Hoxa10 ERE both in vitro as and in vivo as determined by EMSA and chromatin immunoprecipitation, respectively. Diminished methylation of the ERE-containing promoter sequence resulted in an increase in ERE-driven gene expression in reporter assays. We identify altered methylation as a novel mechanism of BPA-induced altered developmental programming. Permanent epigenetic alteration of ERE sensitivity to estrogen may be a general mechanism through which endocrine disruptors exert their action.—Bromer, J. G., Zhou, Y., Taylor, M. B., Doherty, L., Taylor, H. S.. Bisphenol-A exposure in utero leads to epigenetic alterations in the developmental programming of uterine estrogen response.
