| The ubiquitously distribution of endocrine disrupting chemicals (EDCs) arecausing an increasingly serious pollution problem to the human and wildlife all overthe world. These chemicals have the ability to mimic or resist the action ofendogenous hormones, and affect sex differentiation and gonad development of fishand other wildlife. In this paper, molecular toxicology of abnormal gonadaldevelopment and sex differentiation caused by EDCs were studied by comparingexpression levels of the sex related genes in medaka (Oryzias latipes).In this paper, the medaka were exposed to different concentrations ofenvironmental estrogens: simazine (CAT) and atrazine. The environmentalmolecular toxicology was carried out on the topic of how the EDCs disrupt thegonad development by quantifying genes expression. Results demonstrated thatenvironmental estrogen exposed male medaka developed testicular oocytes andretarded testes development. In the course, the marker genes (VTG-I) were inducedhighly expression. Above all, estrogen receptor α (ER-α) mRNA level increasedsignificantly, and the increased ER-α level would make more opportunity forestrogen to be combined by ER-α, and this would obviously accelerate thefeminization. By extrinsic estrogen exposure, the varieties of some genes expression thatproved to take action in mammal sex differentiation have been detected in medaka.CYP19B, WNT4, GATA4 and STAR are induced in male embryos by CAT andatrazion, but these genes expression doesn't increased significantly. These genes toextrinsic estrogen exposure aren't promising to be new markers for detection ofEDCs.In addition, based on the foregoing methods and results, the effects of simazineand atrazion on Chinese sturgeon were also primary studied in this paper. |