Retrotransposons, as vital regulator of male fertility, are essential for spermatogenesis. Cadmium (Cd) is an environmental toxicant and endocrine disruptor, targeting the reproductive system. Growing evidence shows that Cd exposure can induce male infertility in mammals. In this study, we generated a male C57BL/6 J mice model with consecutive 35 days cadmium chloride (CdCl2) in different concentrations of 0, 0.25, 0.5, 1.0, and 2.0 mg/kg. The results indicated that 1.0 and 2.0 mg/kg CdCl2 significantly affected the body weight. Meanwhile, the highest dose group with 2.0 mg/kg CdCl2 presented low fertility. Furthermore, the expression of retrotransposon mRNA was markedly increased in the higher doses group. We examined methylcytosine (mC) levels of the three active LINE-1 subfamilies TfI, A, and GfII in testis. Conclusively, Cd exposure probably undermines the male mice fertility by disrupting DNA methylation to regulate the retrotransposons. Further studies are required for identifying whether retrotransposon activation has any significant impacts on genome structure, stability, and expression in Cd-induced testicular injury, laying foundation for the treatment for male infertility.
Keywords: Cadmium; DNA methylation; LINE-1; Retrotransposons; Testis.