Journal
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
Volume 165, Issue -, Pages 164-173Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ecoenv.2018.08.109
Keywords
Sulphur dioxide; Arsenic; Spermatogenesis; Apoptosis; Steroidogenesis
Categories
Funding
- National Natural Science Foundation of China [31371868, 31500504]
- Hundred Talent Project of Shanxi Province in 2015
- Science and Technology Innovation Talent Project of Shanxi Province [201605D211031]
- Key Research and Development Plan of Shanxi Province (Social Development) [201703D321026-4]
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As two potential environmental hazards, sulphur dioxide (SO2) 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) SO2 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 SO2-only group. Both SO2 and arsenic reduced sperm counts, increased the percentage of sperm malformation, and induced abnormal testicular pathological changes. Elevated H2O2 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 SO2 and/or arsenic. Moreover, SO2 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 SO2 and arsenic interfere with spermatogenesis leading to infertility. These results also suggest that SO2 and arsenic co-exposure likely result in an additive effect on male reproductive toxicity in mice.
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