Quizalofop-P-ethyl exposure increases estrogen axis activity in male and slightly decreases estrogen axis activity in female zebrafish (Danio rerio)

• Published in: Aquatic toxicology 2017-02, Vol.183, p.76-84
• Main Authors: Zhu, Li-Zhen, Qi, Su-Zhen, Cao, Fang-Jie, Mu, Xi-Yan, Yang, Yang, Wang, Chengju
• Format: Article
• Language: English
• Subjects: Adult zebrafish; Animals; Endocrine disruption; Endocrine Disruptors - toxicity; Estradiol - blood; Estrogen receptors (ESRs); Estrogens - blood; Female; Gene Expression Regulation - drug effects; Gonads - drug effects; Gonads - pathology; Herbicides - toxicity; Liver - drug effects; Liver - metabolism; Male; Propionates - toxicity; Quinoxalines - toxicity; Quizalofop-P-ethyl; Receptors, Estrogen - genetics; Receptors, Estrogen - metabolism; Sex-specific; Up-Regulation; Vitellogenins - blood; Vitellogenins - genetics; Water Pollutants, Chemical - toxicity; Zebrafish - blood; Zebrafish - genetics
• ISSN: 0166-445X; 1879-1514
• DOI: 10.1016/j.aquatox.2016.12.011

•QpE disrupted the endocrine system of zebrafish in a sex-specific manner.•QpE increases estrogen axis activity in males and decreases estrogen axis activity in females.•The sex-specific manner may be explained by QpE regulating steroidogenesis or activating ESRs. The herbicide Quizalofop-P-ethyl (QpE) exerts toxic effects in fish, but limited information is currently available on its effects on the endocrine system. In the current study, adult zebrafish (Danio rerio) were exposed to different concentrations (0, 2, 20, 200μg/L) of QpE for 30days. In males, QpE exposure significantly increased plasma estradiol (E2) and vitellogenin (VTG) levels, concomitant with up-regulation of hepatic esr1 and vtg gene expression. In females, plasma sex hormone levels and VTG concentrations were not altered significantly, but an increased expression of hepatic esr1 in addition to decreased expression of hepatic vtg, esr2a and esr2b was observed. Marked histological lesions were also observed in the gonads of both males and females. Moreover, QpE exposure significantly increased transcriptional profiles of some genes in the HPG axis and liver in males, while the majority of these genes were down-regulated in females. Docking studies showed QpE forming stable interactions with the ligand-binding domain (LBD) of zebrafish ESR1 and ESR2a, suggesting QpE may bind to estrogen receptors (ESRs). This study for the first time reveals QpE as an endocrine-disrupting chemical (EDC) disrupting the zebrafish endocrine system in a sex-specific manner, whereby it increases estrogen axis activity in males and slightly decreases estrogen axis activity in females, which may be accounted for by QpE regulating steroidogenesis and/or activating ESR(s).