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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Maternal nutrient supplementation counteracts bisphenol A-induced DNA hypomethylation in early development
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Maternal nutrient supplementation counteracts bisphenol A-induced DNA hypomethylation in early development

机译：母体营养补充剂可抵消双酚A诱导的早期发育中DNA甲基化不足

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摘要

The hypothesis of fetal origins of adult disease posits that early developmental exposures involve epigenetic modifications, such as DNA methylation, that influence adult disease susceptibility. In utero or neonatal exposure to bisphenol A (BPA), a high-production-volume chemical used in the manufacture of polycarbonate plastic, is associated with higher body weight, increased breast and prostate cancer, and altered reproductive function. This study shows that maternal exposure to this endocrine-active compound shifted the coat color distribution of viable yellow agouti (A~(vy)) mouse offspring toward yellow by decreasing CpG (cytosine-guanine dinucleotide) methylation in an intracisternal A particle retrotransposon upstream of the Agouti gene. CpG methylation also was, decreased at another metastable locus, the CDK5 activator-binding protein (Cabp~(IAP)). DNA methylation at the A~(vy) locus was similar in tissues from the three germ layers, providing evidence that epigenetic patterning during early stem cell development is sensitive to BPA exposure. Moreover, maternal dietary supplementation, with either methyl donors like folic acid or the phytoestrogen genistein, negated the DNA hypomethylating effect of BPA. Thus, we present compelling evidence that early developmental exposure to BPA can change offspring phenotype by stably altering the epigenome, an effect that can be counteracted by maternal dietary supplements.
机译：成人疾病的胎儿起源的假设认为，早期发育暴露涉及表观遗传修饰，例如DNA甲基化，会影响成人疾病的易感性。在子宫内或新生儿接触双酚A（BPA）时，制造聚碳酸酯塑料的高产量化学品与体重增加，乳腺癌和前列腺癌增加以及生殖功能改变有关。这项研究表明，母体暴露于这种内分泌活性化合物会通过减少在其上游的脑池内A颗粒逆转录转座子中的CpG（胞嘧啶-鸟嘌呤二核苷酸）甲基化来使有活力的黄色刺鼠（A〜（vy））小鼠后代的外壳颜色分布向黄色移动。 Agouti基因。 CpG甲基化在另一个亚稳位点CDK5激活物结合蛋白（Cabp〜（IAP））也降低。在三个胚层的组织中，A〜（vy）位点的DNA甲基化相似，这提供了证据，表明干细胞早期发育过程中的表观遗传模式对BPA暴露敏感。此外，孕妇的膳食补充剂，无论是叶酸这样的甲基供体还是植物雌激素染料木黄酮，都可以消除BPA的DNA低甲基化作用。因此，我们提供了令人信服的证据，表明BPA的早期发育暴露可以通过稳定地改变表观基因组来改变后代的表型，而母体膳食补充剂可以抵消这种影响。

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