Mitochondrial damage are involved in Aflatoxin B₁-induced testicular damage and spermatogenesis disorder in mice

Aflatoxin B₁ (AFB₁) is an unavoidable environmental pollutants, which seriously endangers human and animal health. AFB₁ has male reproductive toxicity, yet the underlying mechanisms remain inconclusive. Mitochondra are a kind of crucial organelle for maintaining spermatogenesis in testis. Thus, we hypothesized that AFB₁ can impair mitochondria to aggravate testicular damage and spermatogenesis disorder. To verify this hypothesis, 48 male mice were intragastrically administered with 0, 0.375, 0.75 or 1.5 mg/kg body weight AFB₁ for 30 days, respectively. In this study, we found AFB₁ caused testicular histopathological lesions and spermatogenesis abnormalities, with the elevation of oxidative stress (increased H₂O₂, whereas decreased SOD and GSH). Significant mitochondria structure damage of germ cells and Leydig cells, MMP loss, ATP contents reduction, and inhibited activities of mitochondrial complexes I-IV in mice testis were found in AFB₁ treatment groups. Besides, AFB₁ inhibited mitochondrial biogenesis and mitochondrial dynamics, presenting as the decreased mRNA and protein expressions of PGC-1α, Nrf1, Tfam, Drp1, Fis1, Mfn1 and Opa1. The results revealed that the mitochondrial damage were involved in AFB₁-induced testicular damage and spermatogenesis disorder, providing a considerable direction to clarify potential mechanisms of AFB₁ reproductive toxicity.