Perfluorooctane sulfonate-induced testicular toxicity and differential testicular expression of estrogen receptor in male mice

- PFOS inhibited sperm production in mice which might be associated with the decreased proliferation and increased apoptosis of germ cells.
- Expression levels of testicular bax, cleaved caspase-9 and cleaved caspase-3 elevated after PFOS treatment.
- Alteration in ERs expression might be an important reason for PFOS-induced spermatogenesis failure.

Perfluorooctane sulfonate (PFOS, CAS#1763-23-1) causes male reproductive toxicities, but the underlying mechanisms are still unclear. In this study, 0, 0.5 and 10 mg/kg/day PFOS were given by oral gavage to adult mice for 5 weeks. In the 10 mg/kg group, serum testosterone levels decreased significantly. Sperm counts declined which might be associated with the decreased proliferation and increased apoptosis of germ cells. In relation to increased apoptosis, bax, cleaved caspase-9 and cleaved caspase-3 levels elevated significantly, indicating that PFOS induced germ cell apoptosis by activating the mitochondrial pathway. In addition, the increase in levels of testicular estrogen receptor (ER) β was observed in both 0.5 and 10 mg/kg group, whereas a decrease in ERα expression was only observed in 10 mg/kg group. These results suggested that the alterations in testicular ERs expression, together with decreased proliferation and increased apoptosis of germ cells, might be involved in PFOS-induced testicular toxicity.