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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Bisphenol A prevents the synaptogenic response to estradiol in hippocampus and prefrontal cortex of ovariectomized nonhuman primates
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Bisphenol A prevents the synaptogenic response to estradiol in hippocampus and prefrontal cortex of ovariectomized nonhuman primates

机译：双酚A可防止卵巢切除的非人类灵长类动物对海马和前额叶皮层对雌二醇的突触反应。

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Exposure measurements from several countries indicate that humans are routinely exposed to low levels of bisphenol A (BPA), a synthetic xenoestrogen widely used in the production of polycarbonate plastics. There is considerable debate about whether this exposure represents an environmental risk, based on reports that BPA interferes with the development of many organs and that it may alter cognitive functions and mood. Consistent with these reports, we have previously demonstrated that BPA antagonizes spine synapse formation induced by estrogens and testosterone in limbic brain areas of gonadectomized female and male rats. An important limitation of these studies, however, is that they were based on rodent animal models, which may not be representative of the effects of human BPA exposure. To address this issue, we examined the influence of continuous BPA administration, at a daily dose equal to the current U.S. Environmental Protection Agency's reference safe daily limit, on estradiol-induced spine synapse formation in the hippocampus and prefrontal cortex of a nonhuman primate model. Our data indicate that even at this relatively low exposure level, BPA completely abolishes the synaptogenic response to estradiol. Because remodeling of spine synapses may play a critical role in cognition and mood, the ability of BPA to interfere with spine synapse formation has profound implications. This study is the first to demonstrate an adverse effect of BPA on the brain in a nonhuman primate model and further amplifies concerns about the widespread use of BPA in medical equipment, and in food preparation and storage.
机译：来自多个国家的暴露测量表明，人类通常会暴露于低含量的双酚A（BPA）中，双酚A是一种广泛用于生产聚碳酸酯塑料的合成异雌激素。关于双酚A会干扰许多器官的发育以及可能改变认知功能和情绪的报道，关于这种暴露是否构成环境风险存在很多争议。与这些报告一致，我们以前已经证明了BPA可以拮抗雌雄同体大鼠角膜缘大脑区域中的雌激素和睾丸激素诱导的脊柱突触形成。但是，这些研究的一个重要局限性是它们是基于啮齿动物模型的，这可能不能代表人类BPA暴露的影响。为了解决这个问题，我们研究了以每日剂量等于当前美国环境保护局参考安全每日限量的连续BPA给药对非人灵长类动物模型海马和前额叶皮质中雌二醇诱导的脊柱突触形成的影响。我们的数据表明，即使在相对较低的暴露水平下，BPA也完全消除了对雌二醇的突触反应。由于脊柱突触的重塑可能在认知和情绪中起关键作用，因此BPA干扰脊柱突触形成的能力具有深远的意义。这项研究是首次在非人类灵长类动物模型中证明BPA对大脑的不利影响，并进一步放大了人们对BPA在医疗设备以及食品制备和储存中的广泛使用的担忧。

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