Lycopene ameliorates aflatoxin B1-induced testicular lesion by attenuating oxidative stress and mitochondrial damage with Nrf2 activation in mice

Abstract

Aflatoxin B₁ (AFB₁) is an extremely hazardous and unavoidable pollutant for cereals and feedstuff. AFB₁ can cause testicular lesion, and how to alleviate its testicular toxicity has received much attention in recent years. Lycopene (LYC), a foodborne nutrient derived from red fruits and vegetables, has protective effects against sperm abnormality and testicular lesions. To confirm the beneficial effects and mechanisms of LYC on AFB₁-induced testicular lesion, 48 male mice were exposed to 0.75 mg/kg AFB₁ or/and 5 mg/kg LYC for consecutive 30 days. Results demonstrated the LYC significantly restored the lesions of testicular microstructure and ultrastructure, and sperm abnormalities in AFB₁-exposed mice. Furthermore, LYC effectively attenuated AFB₁-induced oxidative stress and mitochondrial damage, including ameliorative mitochondrial structural, and elevated mitochondrial biogenesis for maintaining mitochondrial function. Meanwhile, LYC resisted AFB₁-induced mitochondrial-dependent apoptosis. In addition, LYC promoted nuclear factor erythroid 2-related factor 2 (Nrf2) nuclear translocation, and upregulated the Nrf2 signaling pathway. Collectively, our findings demonstrate LYC ameliorates AFB₁-induced testicular lesion by attenuating oxidative stress and mitochondrial damage, which is related to the activation of Nrf2.

Keywords: Aflatoxin B(1); Lycopene; Mitochondria; Nrf2; Oxidative stress; Testicular toxicity.