Autophagy and PPARs/NF-κB-associated inflammation are involved in hepatotoxicity induced by the synthetic phenolic antioxidant 2,4-di-tert-butylphenol in common carp (Cyprinus carpio)

鲤鱼 抗氧化剂 超氧化物歧化酶 炎症 鲤鱼 谷胱甘肽 促炎细胞因子 碱性磷酸酶 化学 药理学 谷胱甘肽过氧化物酶 过氧化氢酶 分子生物学 生物 生物化学 免疫学 渔业
作者
Jiaqi Xie,Yuxiang Yin,Bixiao Lin,Xinlian Li,Qiuyue Li,Xiao‐Qing Tang,Lingai Pan,Xuan Xiong
出处
期刊:Ecotoxicology and Environmental Safety [Elsevier BV]
卷期号:284: 116937-116937
标识
DOI:10.1016/j.ecoenv.2024.116937
摘要

The synthetic phenolic antioxidant 2,4-di-tert-butylphenol (2,4-DTBP) is an emergent contaminant and can disrupt the delicate balance of aquatic ecosystems. This study aimed to investigate 2,4-DTBP-induced hepatotoxicity in common carp and the underlying mechanisms involved. Sixty common carp were divided into four groups and exposed to 0 mg/L, 0.01 mg/L, 0.1 mg/L or 1 mg/L 2,4-DTBP for 30 days. Here, we first demonstrated that 2,4-DTBP exposure caused liver damage, manifested as hepatocyte nuclear pyknosis, inflammatory cell infiltration and apoptosis. Moreover, 2,4-DTBP exposure induced hepatic reactive oxygen species (ROS) overload and disrupted antioxidant capacity, as indicated by the reduced activity of the antioxidant enzymes superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px). In addition, transmission electron microscopy revealed that 2,4-DTBP exposure induced autophagosome accumulation in the liver of common carp. Western blot analysis further revealed that 2,4-DTBP exposure significantly decreased the protein levels of mTOR and increased the LC3II/LC3I ratio. Furthermore, 2,4-DTBP exposure inhibited lysozyme (LZM) and alkaline phosphatase (AKP) activity; decreased immunoglobulin M (IgM), complement 3 (C3), and complement 4 (C4) levels in the serum; increased the mRNA levels of proinflammatory cytokines (NF-κB, TNF-α, IL-1β and IL-6); and increased the mRNA levels of three types of proliferator-activated receptors (PPARs) (α, β/δ and γ). Molecular docking revealed that 2,4-DTBP directly binds to the internal active pocket of PPARs. Overall, we concluded that 2,4-DTBP exposure in aquatic systems could induce hepatotoxicity in common carp by regulating autophagy and controlling inflammatory responses. The present study provides new insights into the hepatotoxicity mechanism induced by 2,4-DTBP in aquatic organisms and furthers our understanding of the effects of 2,4-DTBP on public health and ecotoxicology.
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