Sulphur dioxide and arsenic affect male reproduction via interfering with spermatogenesis in mice

Abstract As two potential environmental hazards, sulphur dioxide (SO 2 ) and arsenic have adverse effects on male reproduction, but the mechanism of which and their combined toxicity are not clear. In this study, we investigate male reproductive toxicity with a focus on spermatogenesis by treating mice with 5 mg/m 3 SO 2 and/or 5 mg/L arsenic. Our results showed that arsenic exposure caused significant decreases in water and food consumption and body weight in mice, whereas these changes were not observed in the SO 2 -only group. Both SO 2 and arsenic reduced sperm counts, increased the percentage of sperm malformation, and induced abnormal testicular pathological changes. Elevated H 2 O 2 and MDA contents, declined T-SOD activity, decreased spermatogenic cell counts, enhanced caspase-3 activity, and increased TUNEL-positive cells were also observed in mice exposed to SO 2 and/or arsenic. Moreover, SO 2 and arsenic co-exposure changed the mRNA levels of Bax and Bcl-2, decreased serum testosterone levels, and downregulated the expression of steroidogenic-related genes (LHR, StAR, and ABP) in mice. These findings provide a new theoretical basis for understanding how SO 2 and arsenic interfere with spermatogenesis leading to infertility. These results also suggest that SO 2 and arsenic co-exposure likely result in an additive effect on male reproductive toxicity in mice.