Disruption of spermatogenesis and differential regulation of testicular estrogen receptor expression in mice after polychlorinated biphenyl exposure

The testicular toxicity of polychlorinated biphenyls (PCBs) has been extensively studied. However, the detailed mechanism is still obscure. In the present study, male C57 mice were treated with different doses of Aroclor 1254 (a commercial PCB mixture) once every 3 days by oral gavage. After exposure to Aroclor 1254 for 50 days, the sperm count decreased in a dose-dependent manner. Cell proliferation and apoptosis are key processes regulating development of the testis, and alterations in these processes may underlie testicular dysgenesis. Our results showed that the germ cell proliferation was inhibited and the apoptosis of the germ cell was induced in a dose-dependent manner after treatment with Aroclor 1254. Although there was no significant change in serum testosterone levels and androgen receptor expression levels after treatment with different dosages of Aroclor 1254, the estradiol levels decreased and the expression of estrogen receptor (ER) β increased in a dose-dependent manner, whereas an elevation of the expression of ERα was only observed in the 50 μg/kg group. The data as a whole suggested that inhibited proliferation and induced apoptosis in germ cells, and a differential regulation of ER, may be involved in the testicular toxicity of PCBs.

► Testicular effects of PCBs at low doses which have not been reported before.
► PCNA is used as a marker of testicular effect of PCBs.
► Differential expression of ERs is correlated with germ cell apoptosis in PCB exposure.