Paternal chronic exposure to copper nanoparticles (CuNPs) impairs testicular androgen and estrogen signalling in adult male offspring in mice

At present, the use of copper nanoparticles (CuNPs) is very common for various human applications. Despite its uses to improve human welfare, the toxicity of CuNPs is well documented. It can cause toxicity to different vital organs, including the male reproductive organs, or testes. Whether the offspring of CuNP-treated males show testicular impairment has not been well documented. The present study investigated the effects of paternal exposure to CuNPs on the testes of male offspring (Swiss Albino mice) divided into the following four groups: a control group and 10 mg/kg, 100 mg/kg and 200 mg/kg exposure groups, whose only male parent was exposed to CuNPs at 0, 10, 100 and 200 mg/kg, respectively, for 70 days, which covered two spermatogenic cycles. The findings reveal that exposure of male parents to CuNPs at higher doses, 100 and 200 mg/kg, compromises spermatogenesis in the testes of male offspring due to decreased germ cell proliferation. Our results showed that oxidative stress was also elevated in the male offspring of male parents treated with a higher dose of CuNPs. However, elevated apoptosis (increased caspase3) was noted in the male offspring of all treated male parental groups. Circulating testosterone and estrogen levels were elevated in the F1 males of higher dose CuNP-treated male paternal groups; however, the expression of androgen receptor (AR), apelin receptor (APJ) and estrogen receptor-β (Erβ) was decreased in the male offspring from all treated parental groups. In conclusion, paternal exposure to CuNPs was found to disrupt spermatogenesis and steroid signalling function in the offspring of F1 males.