Department of Clinical and Experimental Endocrinology, Medical University of Gdansk, Gdansk, Poland.
Department of Endocrinology and Diabetes Center of Excellence, Medical School University of Athens, EUROCLINIC, Athens, Greece.
Fertil Steril. 2016 Sep 15;106(4):948-58. doi: 10.1016/j.fertnstert.2016.08.031. Epub 2016 Aug 22.
Polycystic ovary syndrome (PCOS) is the most common, heterogeneous, and multifactorial endocrine disorder in premenopausal women. The pathophysiology of this endocrinopathy is still unclear; however, the heterogeneity of its features within ethnic races, geographic location, and families suggests that environment and lifestyle are of prime importance. This work is mainly focused on the possible role of the most common and studied environmental toxins for this syndrome in the pathogenesis of PCOS. Plasticizers, such as bisphenol A (BPA) or phthalates, which belong to the categories of endocrine disrupting chemicals (EDCs) and advanced glycation end products (AGEs), affect humans' health in everyday, industrialized life; therefore special attention should be paid to such exposure. Timing of exposure to EDCs is crucial for the intensity of adverse health effects. It is now evident that fetuses, infants, and/or young children are the most susceptible groups, especially in the early development periods. Prenatal exposure to EDCs that mimic endogenous hormones may contribute to the altered fetal programming and in consequence lead to PCOS and other adverse health effects, potentially transgenerationally. Acute or prolonged exposure to EDCs and AGEs through different life cycle stages may result in destabilization of the hormonal homeostasis and lead to disruption of reproductive functions. They may also interfere with metabolic alterations such as obesity, insulin resistance, and compensatory hyperinsulinemia that can exacerbate the PCOS phenotype and contribute to PCOS consequences such as type 2 diabetes and cardiovascular disease. Since wide exposure to environmental toxins and their role in the pathophysiology of PCOS are supported by extensive data derived from diverse scientific models, protective strategies and strong recommendations should be considered to reduce human exposure to protect present and future generations from their adverse health effects.
多囊卵巢综合征（PCOS）是绝经前妇女最常见、最具异质性和多因素的内分泌疾病。这种内分泌疾病的病理生理学仍不清楚；然而，其在不同种族、地理位置和家族中的特征的异质性表明，环境和生活方式至关重要。这项工作主要集中在最常见和研究最多的环境毒素对这种综合征在 PCOS 发病机制中的可能作用。增塑剂，如双酚 A（BPA）或邻苯二甲酸酯，属于内分泌干扰化学物质（EDCs）和晚期糖基化终产物（AGEs）的类别，在日常工业化生活中影响人类健康；因此，应特别注意这种暴露。接触 EDCs 的时间对不良健康影响的强度至关重要。现在很明显，胎儿、婴儿和/或幼儿是最易受影响的群体，尤其是在早期发育阶段。胎儿期暴露于模拟内源性激素的 EDCs 可能导致胎儿编程改变，并因此导致 PCOS 和其他不良健康影响，可能具有代际效应。通过不同的生命周期阶段急性或长期接触 EDCs 和 AGEs 可能导致激素内稳态不稳定，并导致生殖功能障碍。它们还可能干扰代谢改变，如肥胖、胰岛素抵抗和代偿性高胰岛素血症，这些改变可能会加重 PCOS 表型，并导致 PCOS 的后果，如 2 型糖尿病和心血管疾病。由于广泛接触环境毒素及其在 PCOS 病理生理学中的作用得到了来自不同科学模型的广泛数据的支持，应该考虑采取保护策略和强烈建议，以减少人类接触，保护现在和未来的几代人免受其不良健康影响。
