Park Min-Ah, Hwang Kyung-A, Choi Kyung-Chul
Laboratory of Veterinary Biochemistry and Immunology, College of Veterinary Medicine, Chungbuk National University, Cheongju, Korea.
Lab Anim Res. 2011 Dec;27(4):265-73. doi: 10.5625/lar.2011.27.4.265. Epub 2011 Dec 19.
Acting as hormone mimics or antagonists in the interaction with hormone receptors, endocrine disrupting chemicals (EDCs) have the potentials of disturbing the endocrine system in sex steroid hormone-controlled organs and tissues. These effects may lead to the disruption of major regulatory mechanisms, the onset of developmental disorders, and carcinogenesis. Especially, among diverse EDCs, xenoestrogens such as bisphenol A, dioxins, and di(2-ethylhexyl)phthalate, have been shown to activate estrogen receptors (ERs) and to modulate cellular functions induced by ERs. Furthermore, they appear to be closely related with carcinogenicity in estrogen-dependant cancers, including breast, ovary, and prostate cancers. In in vivo animal models, prenatal exposure to xenoestrogens changed the development of the mouse reproductive organs and increased the susceptibility to further carcinogenic exposure and tumor occurence in adults. Unlike EDCs, which are chemically synthesized, several phytoestrogens such as genistein and resveratrol showed chemopreventive effects on specific cancers by contending with ER binding and regulating normal ER action in target tissues of mice. These results support the notion that a diet containing high levels of phytoestrogens can have protective effects on estrogen-related diseases. In spite of the diverse evidences of EDCs and phytoestrogens on causation and prevention of estrogen-dependant cancers provided in this article, there are still disputable questions about the dose-response effect of EDCs or chemopreventive potentials of phytoestrogens. As a wide range of EDCs including phytoestrogens have been remarkably increasing in the environment with the rapid growth in our industrial society and more closely affecting human and wildlife, the potential risks of EDCs in endocrine disruption and carcinogenesis are important issues and needed to be verified in detail.
内分泌干扰化学物质(EDCs)在与激素受体相互作用时充当激素模拟物或拮抗剂,有可能扰乱性类固醇激素控制的器官和组织中的内分泌系统。这些影响可能导致主要调节机制的破坏、发育障碍的发生和致癌作用。特别是,在各种EDCs中,双酚A、二恶英和邻苯二甲酸二(2-乙基己基)酯等外源性雌激素已被证明可激活雌激素受体(ERs)并调节由ERs诱导的细胞功能。此外,它们似乎与雌激素依赖性癌症(包括乳腺癌、卵巢癌和前列腺癌)的致癌性密切相关。在体内动物模型中,产前暴露于外源性雌激素会改变小鼠生殖器官的发育,并增加成年后对进一步致癌暴露和肿瘤发生的易感性。与化学合成的EDCs不同,染料木黄酮和白藜芦醇等几种植物雌激素通过竞争ER结合并调节小鼠靶组织中的正常ER作用,对特定癌症显示出化学预防作用。这些结果支持了这样一种观点,即含有高水平植物雌激素的饮食对雌激素相关疾病具有保护作用。尽管本文提供了关于EDCs和植物雌激素在雌激素依赖性癌症的病因和预防方面的各种证据,但关于EDCs的剂量反应效应或植物雌激素的化学预防潜力仍存在有争议的问题。随着包括植物雌激素在内的各种EDCs在我们工业社会快速发展的环境中显著增加,并对人类和野生动物产生更密切的影响,EDCs在内分泌干扰和致癌方面的潜在风险是重要问题,需要详细验证。