The rapid development of urbanization results to concentrated outbreak of pollution. The impact of organic compounds pollution on human health has become increasingly serious. The high incidence of many diseases is considered to be related to pollutant. Endometriosis (EM) belongs one of them. The incidence of this estrogen- dependent disease is up to 5~10% in women of childbearing age, which brings severe health outcomes to women and society. Epidemiological studies have shown the effects of polychlorinated biphenyls (PCBs) exposure on the morbidity of EM. However, little evidence is available from the toxicology. Molecular toxicology research team (Sijun Dong’s group), IUE, CAS in cooperation with The the obstetrics and gynecology of The First Affiliated Hospital of Xiamen University, collected clinical samples, cultured the original generation endometrial cells and found that PCBs in occupational exposures crowd concentrations, PCB126 significantly enhanced 17β-estradiol (E2) biosynthesis and decreased the methylation of the 17β-hydroxysteroid dehydrogenase 7 (HSD17B7) promoter, futther enhanced the expression of the mRNA and protein of HSD17B7 so that to stimulate estrogen biosynthesis. In addition, PCB126 triggered the inflammatory response by restraining the biosynthesis of endogenous inhibitory lipid medium, lipoxin A4 (LXA4). Both the PCB-treated EM mouse model and the results of the clinical sample level confirmed that PCB126 promotes the development of the disease. The aryl hydrocarbon receptor (AhR) mediated the toxicity of dioxin-like PCB126. Non-dioxin-like PCB153 doesn’t bind with AhR. so it doesn’t have these effects.

The research results (Dioxin-like, rather than non dioxin-like PCBs promote the development of endometriosis through stimulation of endocrine-inflammation interactions, DOI: 10.1007/s00204-016-1854-0) has published on the toxicology mainstream magazine: Archives of Toxicology (IF = 6.6). The first author is Associate Researcher, Qiansheng Huang. The research is funded by the National Natural Science Foundation of China (21477123, 41390240), and Youth Foundation (21107107).

Figure Molecular mechanisms of promoting incidence of endometriosis.