环境重金属暴露与子宫内膜异位症

子宫内膜异位症（EMs）发生发展机制包括内分泌、遗传、免疫和环境因素。环境污染会导致水源、土壤以及空气中积累大量重金属,如铁、镍和镉等元素。妇女暴露于这些重金属,大量重金属进入体内,在其体内与某些有机成分结合形成金属络合物或金属整合物,后者促进活性氧（ROS）的产生。ROS通过激活丝裂原活化蛋白激酶（MAPK）途径,加重机体氧化应激,进而促进内膜细胞的增殖和对异位病灶的侵袭。部分重金属如镉、镍等,在体内能与雌激素受体（ER）特异性结合,产生类雌激素效应,干扰内分泌代谢,增加女性罹患EMs的风险。综述妇女暴露于环境重金属与EMs的相关性及研究进展,为探讨EMs发生发展机制积累新的资料。

Environmental Heavy Metal Exposure and Endometriosis

The etiological and pathophysiological mechanisms of endometriosis (EMs) include endocrine, genetic, immune and environmental factors. Environmental pollution can lead to the accumulation of a large number of heavy metal elements, such as iron, nickel and cadmium, in water, soil and air. If women were exposed to this kind of environment, a lot of these heavy metals could enter into their bodies. After that, these heavy metals were combined with some organic compounds in body to form the metallic integration or metal-protein complex that promote the production of harmful reactive oxygen species (ROS). Many studies have showed that ROS promotes the proliferation of endometrial cells and the invasion of ectopic lesions by activating the mitogen-activated protein kinase (MAPK) pathway and aggravating oxidative stress. Some heavy metals, such as cadmium and nickel, can specifically bind with estrogen receptor (ER) in the body, by which the estrogen-like effects were induced so as to interfere with endocrine and metabolism, and to increase the risk of EMs in women. This paper reviews the correlation between the environmental heavy metal exposure and the pathophysiological mechanism of EMs, as well as the research progress, as to add a new reference for us to explore the etiology and pathophysiology of EMs.