Many environmental chemicals have been found to exert estrogenic effects in cells and experimental animals by activating nuclear receptors such as estrogen receptors and estrogen-related receptors. These compounds include bisphenols, pesticides, polybrominated diphenyl ethers (PBDEs), organophosphate flame retardants, phthalates and metalloestrogens. G protein-coupled estrogen receptor (GPER) exists widely in numerous cells/tissues of human and other vertebrates. A number of studies have demonstrated that GPER plays a vital role in mediating the estrogenic effects of environmental pollutants. Even at very low concentrations, these chemicals may activate GPER pathways, thus affect many aspects of cellular functions including proliferation, metastasis and apoptosis, resulting in cancer progression, cardiovascular disorders, and reproductive dysfunction. This review summarized the environmental occurrence and human exposure levels of these pollutants, and integrated current experimental evidence toward revealing the underlying mechanisms of pollutant-induced cellular dysfunction via GPER. The GPER mediated rapid non-genomic actions play an important role in the process leading to the adverse effects observed in experimental animals and even in human beings.

已经发现许多环境化学物质通过激活核受体如雌激素受体和雌激素相关受体而在细胞和实验动物中发挥雌激素作用。这些化合物包括双酚，农药，多溴联苯醚（PBDEs），有机磷酸酯阻燃剂，邻苯二甲酸酯和金属雌激素。G蛋白偶联雌激素受体（GPER）广泛存在于人类和其他脊椎动物的许多细胞/组织中。大量研究表明，GPER在介导环境污染物的雌激素作用中起着至关重要的作用。即使浓度很低，这些化学物质也可能激活GPER途径，从而影响细胞功能的许多方面，包括增殖，转移和凋亡，导致癌症进展，心血管疾病，和生殖功能障碍。这篇综述总结了这些污染物在环境中的发生和人体暴露水平，并综合了当前的实验证据，以揭示通过GPER引起的污染物诱导的细胞功能障碍的潜在机制。GPER介导的快速非基因组作用在导致实验动物乃至人类所观察到的不利影响的过程中起着重要作用。