低浓度二噁英抑制青鳉幼鱼耳泡生成与SOX9b相关联  

The Relation Between SOX9b and TCDD Inhibited Development of Otic Vesicle in Medaka Embryos

作　　者：于永利[1,2] 王丰[1] 陈形[1] 于华荣[3] 赵宝全[4] 东彦新[1] 杨景峰[1] 董武[1] 

机构地区：[1]内蒙古民族大学动物科技学院\内蒙古自治区高等学校毒物与动物疾病监控重点实验室,通辽市028042 [2]内蒙古民族大学生命科学学院,通辽市028042 [3]内蒙古民族大学农学院,通辽市028042 [4]军事医学科学院毒物药物研究所,北京100850

出　　处：《生态毒理学报》2014年第6期1141-1145,共5页Asian Journal of Ecotoxicology

基　　金：内蒙古自治区自然科学基金(Nos.2012MS1203);国家自然科学基金项目(Nos.30360090;21267015);教育部新世纪优秀人才支持计划项目(Nos.NCET-04-0262);内蒙古自治区"草原英才"工程(2014)

摘　　要：2,3,7,8-四氯二苯并对二恶英(2,3,7,8-Tetrachlorodibenzo-p-Dioxin,TCDD)是一种持久性环境有机污染物质,它在有机体内的蓄积性引起研究人员的重视。以青鳉胚胎作为实验动物模型,使用原位杂交和定量聚合酶链锁反应(Polymerase Chain Reaction,PCR)技术从分子水平探讨了TCDD对胚胎耳泡的发育及其毒性作用机制。结果表明,TCDD造成青鳉幼鱼耳泡生成障碍。通过原位杂交和q PCR分析表明,TCDD引起软骨发育的变化与SOX9b表达降低有密切的关联。研究认为青鳉胚胎是一种非常敏感的TCDD模式动物,其耳泡软骨发育以及SOX9b基因表达可能是一种二恶英发育毒性的效应标记物。2,3,7,8-tetrachlorodenzo-p-dioxin （TCDD） is one of persistent organic pollutants in the environment and have bioaccumulation. Medaka embryos were used as a testing platform, we explored the relationship between TC- DD exposure and development of the otic vesicle. In this study, we employed both in situ hybridization and RT-PCR techniques to investigate the relationship between SOX9b expression and TCDD exposure during development of otic vesicle in medaka embryos. Our results showed that exposure of TCDD caused suppression in formation of otic vesicle in medka embryos. By in situ hybridization and RT-PCR analyses, we can relate changes of cartilage development caused by TCDD with the reduced expression of SOX9b. These results indicated that otic vesicle carti lage development and SOXgb expression are potential biomarkers for TCDD toxicity.

关 键 词：青鳉胚胎 耳泡 毒性 

分 类 号：X171.5[环境科学与工程—环境科学]