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Fluorochloridone induces mitochondrial dysfunction and apoptosis in primary goat Sertoli cells
Yuan Li1, Lishu Li1, Wenjie Xiong1
1Key Laboratory of Applied Technology on Green-Eco-Healthy Animal Husbandry of Zhejiang Province, Zhejiang Provincial Engineering Laboratory for Animal Health Inspection & Internet Technology, Zhejiang International Science and Technology Cooperation Base for Veterinary Medicine and Health Management, China-Australia Joint Laboratory for Animal Health Big Data Analytics, College of Animal Science and Technology & College of Veterinary Medicine of Zhejiang A&F University, Hangzhou, 311300, People's Republic of China.
Abstract:
Fluorochloridone (FLC), a pyrrolidone herbicide, has been recognized as a hazardous chemical. The in vitro adverse effects of FLC on the reproduction of livestock have not been assessed. This study was conducted to explore the cytotoxicity and toxicological mechanisms of FLC on cultured goat Sertoli cells. The results showed that FLC exposure significantly decreased goat Sertoli cell viability (p < 0.05) and induced oxidative stress. And FLC treatment promoted apoptosis and initiation of autophagy. Interestingly, FLC inhibited lysosomal biogenesis and blocked autophagic flux in goat Sertoli cells. The expression levels of autophagy-related proteins Atg5, LC3II, and p62 were significantly increased (p < 0.05) in FLC-treated goat Sertoli cells compared with the control. Importantly, FLC-induced ROS accumulation further causes mitochondrial dysfunction and disturbs mitophagy. FLC significantly decreased (p < 0.05) the expression levels of OPA1, MFN2, p-Drp1, FIS1, PINK1, and Parkin in goat Sertoli cells. Moreover, pretreatment with N-acetyl-l-cysteine (NAC, an antioxidant) significantly reduced (p < 0.01) FLC-induced ROS accumulation and reversed the disorder of autophagy levels. Our results indicated that FLC-induced toxicity in primary goat Sertoli cells was characterized by ROS accumulation, inducing oxidative stress, inhibiting lysosomal biogenesis, blocking autophagic flux, and promoting mitochondrial dysfunction, resulting in apoptosis via the mitochondrial pathway.
