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

- p,p′-DDT and MXC stimulated gonadotropin subunit genes expression in LβT2 cells.
- p,p′-DDT and MXC stimulated gonadotropin hormones synthesis in LβT2 cells.
- ERK inhibitor suppressed p,p′-DDT- or MXC-induced gonadotropin subunit genes expression.
- ERK pathway was activated in response to p,p′-DDT and MXC exposure.

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.