Pubertal exposure to acrylamide disrupts spermatogenesis by interfering with meiotic progression in male mice.

[Display omitted] • Pubertal acrylamide exposure decrease sperm concentration by interfering spermatogenesis in male mice. • Pubertal acrylamide exposure induces apoptosis of germ cells in the testes. • Pubertal acrylamide exposure delays the meiotic prophase I progression. • Pubertal acrylamide exposure disrupts H2AX phosphorylation pattern of meiotic prophase I. Teenagers are a major group likely to love junk foods, such as potato chips and bread items, which contain high levels of acrylamide (AA). The increasing evidence suggests that AA exposure may be associated with decreased reproductive capacity in humans and animals. However, the reproductive toxicity of AA in pubertal males has not been fully elucidated. In this study, we evaluated the effects of pubertal AA exposure on adult spermatogenesis in male mice. Mice were exposed to AA at 0, 5, 10, 20, and 40 mg/kg/day by gavage from postnatal day 28 (PND28) to PND56. Our results showed that pubertal AA exposure increased apoptosis of germ cells in seminiferous tubules, decreased sperm concentration, and caused defects in sperm of adult mice. To explore the possible mechanisms of AA on spermatogenesis, the meiotic process was analyzed. The ratio of leptotene and zygotene spermatocytes increased, while the pachytene and diplotene spermatocytes decreased in AA-treated mice. Further analysis revealed that AA exposure disrupted the pattern of H2AX phosphorylation expansion, synapsis, and the crossover formation during meiotic prophase I (MPI). Taken together, these results indicate that pubertal AA exposure affects the spermatogenesis may be by disrupting the MPI progression of male mice. [ABSTRACT FROM AUTHOR]