Abstract：
Earlier research has demonstrated that developmental exposure to bisphenol A (BPA) has persistent impacts on both adult brain growth and actions. It has been suggested that BPA might obstruct the methylation coding of the genes in the brain. In this study, the methylation changes in the hippocampus tissue of male rat pups were examined following prenatal BPA exposure. Pregnant Sprague-Dawley rats were treated with either vehicle (tocopherol-stripped corn oil) or BPA (4, 40, or 400 μg/kg·body weight/day) throughout the entire duration of gestation and lactation. At 3 weeks of age, the male rat offspring were euthanized, and the hippocampus were dissected out for analysis. The expression levels of DNA methyltransferases (DNMT1, DNMT3A, and DNMT3B) and DNA demethylases (TET1, Gadd45a, Gadd45b, and Apobec1) were analyzed in the hippocampus by means of quantitative real-time polymerase chain reaction and Western blotting, respectively. The results showed that prenatal exposure to BPA upregulated the expression of enzymes associated with DNA methylation and demethylation processes in the hippocampus of male rat offspring. These findings suggest that prenatal exposure to a low dose of BPA could potentially disrupt the balance of methylation and demethylation in the hippocampus, thereby perturbing epigenetic modifications. This may represent a neurotoxicity mechanism of BPA.
摘要：
早期的研究表明，双酚A（BPA）的发育暴露对成人的大脑生长和行为都有持续的影响。有人认为，BPA可能会阻碍大脑中基因的甲基化编码。在这项研究中,产前BPA暴露后，检测雄性幼鼠海马组织的甲基化变化。在妊娠和哺乳的整个过程中，用媒介物（生育酚剥离的玉米油）或BPA（4、40或400μg/kg·体重/天）处理怀孕的Sprague-Dawley大鼠。在3周龄时，雄性大鼠的后代被安乐死，解剖海马体进行分析。DNA甲基转移酶的表达水平（DNMT1，DNMT3A，和DNMT3B）和DNA去甲基酶（TET1，Gadd45a，Gadd45b,和Apobec1）通过定量实时聚合酶链反应和蛋白质印迹在海马中进行分析，分别。结果表明，产前暴露于BPA上调了雄性大鼠后代海马中与DNA甲基化和去甲基化过程相关的酶的表达。这些结果表明，产前暴露于低剂量的BPA可能潜在地破坏海马中甲基化和去甲基化的平衡。从而扰乱表观遗传修饰。这可能代表了BPA的神经毒性机制。
