Deoxynivalenol induced spermatogenesis disorder by blood-testis barrier disruption associated with testosterone deficiency and inflammation in mice.

Abstract Deoxynivalenol (DON) is an unavoidable cereal crops contaminants and environmental pollutants, which seriously threated the health of human and animal. DON has been reported to exert significant toxicity effects on spermatogenesis, but the underlying mechanisms remain largely inconclusive. The blood-testis barrier (BTB) provides a specialized biochemical microenvironment for maintaining spermatogenesis. Thus, we hypothesized that DON could impair BTB and lead to spermatogenesis disorder. To confirm this hypothesis, sixty male mice were intragastrically administered with 0, 1.2, 2.4 and 4.8 mg/kg body weight DON for 28 days, and several important observations were obtained in present study. First, we found that DON induced spermatogenesis disorder, reflected by the declines of sperm concentration and quality, sperm ultrastructural damage as well as seminiferous tubular damage. Then, we first proved that DON induced BTB disruption as well as decreased the expressions of BTB junction proteins, including Occludin, Connexin 43 and N-cadherin. Finally, the present study the present study showed that DON induced inflammation and inhibited T biosynthesis in testis of mice. These results revealed that DON induced spermatogenesis disorder by BTB disruption associated with testosterone deficiency and inflammation in mice, which shed a new light on the potential mechanisms of reproductive toxicity induced by DON.