Display Settings:

Format

Send to:

Choose Destination
See comment in PubMed Commons below
Environ Toxicol Pharmacol. 2014 May;37(3):1194-201. doi: 10.1016/j.etap.2014.04.018. Epub 2014 Apr 20.

Endocrine disrupting effects of dichlorodiphenyltrichloroethane analogues on gonadotropin hormones in pituitary gonadotrope cells.

Author information

  • 1MOE Key Lab of Environmental Remediation and Ecosystem Health, Institute of Environmental Science, Zhejiang University, Hangzhou 310058, China.
  • 2MOE Key Lab of Environmental Remediation and Ecosystem Health, Institute of Environmental Science, Zhejiang University, Hangzhou 310058, China. Electronic address: jliue@zju.edu.cn.

Abstract

It has been shown that exposure to dichlorodiphenyltrichloroethane (DDT) analogues leads to disharmony of follicle-stimulating hormone (FSH) and luteinizing hormone (LH). However, the effects and mechanisms of DDT analogues on the expression of gonadotropin genes (FSHβ, LHβ and Cgα), which is the rate-limiting step of FSH and LH biosynthesis, remain unknown. In this study, we assessed the effects of p,p'-DDT, o,p'-DDT, p,p'-dichlorodiphenyldichloroethylene (p,p'-DDE) and methoxychlor (MXC) on gonadotropin genes expression and hormones synthesis in gonadotrope cells. p,p'-DDT and MXC at test concentrations ranging from 10(-9) to 10(-7)mol/L, stimulated gonadotropin genes expression and hormones synthesis in a dose-dependent manner. The activation of extracellular signal-regulated kinase (ERK) was required for the induction of gonadotropin genes expression and hormones synthesis by p,p'-DDT or MXC exposure. This study showed for the first time that p,p'-DDT and MXC regulated gonadotropin genes expression and hormones synthesis through ERK pathway in gonadotrope cells.

Copyright © 2014 Elsevier B.V. All rights reserved.

KEYWORDS:

Dichlorodiphenyltrichloroethane; Follicle-stimulating hormone; Luteinizing hormone; Methoxychlor; Pituitary

PMID:
24814263
[PubMed - in process]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Icon for Elsevier Science
    Loading ...
    Write to the Help Desk