Effects of Wnt/β-catenin signaling on bisphenol A exposure in male mouse reproductive cells.

Bisphenol A (BPA) is a chemical used in numerous consumer products that is able to interfere with the mammalian endocrine system. The aim of the present study was to investigate the effects of BPA on male mouse reproductive cells following prenatal to postnatal exposure. In addition, the influence of BPA was detected on the expression levels of β‑catenin and dickkopf WNT signaling pathway inhibitor 1 (DKK‑1) during the differentiation of spermatogenic cells in the mouse testes. β‑catenin and DKK‑1 are two important proteins of the Wnt/β‑catenin signaling pathway. On gestational day 1, pregnant ICR mice were randomly divided into four groups: A dimethyl sulfoxide group, and three groups treated with various concentrations of BPA (0.5, 10, and 50 µg/kg). BPA was administered from gestational day 1 to weaning on postnatal day (PND) 42. The number of murine pups and the male:female ratio was recorded for each group. On PND 42, the male pups were sacrificed and their wet weights and testicular coefficients were measured. Immunohistochemical and western blot analyses were used to detect the protein expression of β‑catenin and DKK‑1 in the testicular tissue samples of the six‑week‑old male mice. The results indicated that the number of murine pups, as well as the testicular viscera coefficient of the male mice, significantly decreased in the BPA‑treated groups, as compared with the control group (P<0.05, P<0.01); however, no significant difference was observed in the male/female ratio in the BPA‑treated groups, as compared with the control group (P>0.05). The results from the immunohistochemical and western blot analyses indicated that the protein expression of β‑catenin and DKK‑1 were significantly increased in the BPA‑treated groups, as compared with the control group, and the distribution of spermospore and Leydig cells also increased in the testes. These results suggest that high expression levels of β‑catenin and DKK‑1 may participate in BPA‑induced pathogenesis in male mouse reproductive cells.