Abstract
Aflatoxin B1 (AFB1) can cause oxidative stress leading to mitochondrial damage and subsequent liver injury. Although it is well-known that damaged mitochondria are eliminated by PINK1/Parkin-mediated mitophagy, this mechanism has not yet been characterized in the context of AFB1-induced liver injury. In this study, male wild-type C57BL/6N mice were divided into groups 1–4, which were then orally administered 0, 0.5, 0.75, and 1 mg/kg body weight AFB1 for 28 d, respectively. Our results demonstrated that oxidative stress, NLRP3-inflammasome activation, and mitochondrial damage were dose-dependently augmented in AFB1-induced liver injury. Additionally, PINK1/Parkin-mediated mitophagy peaked in the groups that had received a mid-dose of AFB1 (0.75 mg/kg), which was attenuated slightly in high-dose groups. Afterward, we further characterized AFB1-induced liver injury by comparing wild-type C57BL/6N mice with Parkin knockout (Parkin-/-) mice. We found that the restricted mitophagy in Parkin-/- mice was associated with increased oxidative stress, NLRP3-inflammasome activation, mitochondrial damage, and liver injury. Taken together, these results indicate that PINK1/Parkin-mediated mitophagy plays an important role in attenuating AFB1-induced liver injury in mice.
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