Zhang Huanxin, Zhang Yu, Cui Shixuan, Cui Lihua, Li Jiaxin, Chu Jizhuang, Zhou Yumiao, Zhang Youru, Kong Qiang
College of Geography and Environment, Shandong Normal University, Jinan 250000, PR China.
College of Geography and Environment, Shandong Normal University, Jinan 250000, PR China.
J Hazard Mater. 2025 Aug 15;494:138469. doi: 10.1016/j.jhazmat.2025.138469. Epub 2025 May 7.
Pentachlorophenol (PCP) is widely distributed in marine environments and poses a threat to the health of marine organisms. Recent studies have demonstrated that PCP induces energy deficiency in marine organisms. However, the underlying toxification mechanism and the resulting adverse outcomes remain unclear. This study analyzed the energy metabolism of marine medaka (Oryzias melastigma) exposed to PCP at environmentally relevant concentrations via proteomic analysis and multiple physiological assessments. The results showed that PCP disrupted mitochondrial morphology, reduced mitochondrial membrane potential (MMP), and decreased adenosine triphosphate (ATP) levels in marine medaka. Proteomic analysis revealed that PCP induced oxidative stress, cytoskeletal disruption, and inhibition of the cytochrome bc1 complex and ATP synthase. These effects culminated in structural and functional impairments to mitochondria, which in turn inhibited ATP synthesis. Chronic PCP exposure led to enhanced glycolytic activity, the accumulation of liver lipids, and reduced liver function. The present study has deepened our understanding of the mechanism of PCP-induced energy production deficiency in marine fish and provides new insights into ecological risk assessment for PCP.
五氯苯酚（PCP）广泛分布于海洋环境中，对海洋生物的健康构成威胁。最近的研究表明，PCP会导致海洋生物能量缺乏。然而，其潜在的毒性作用机制以及由此产生的不良后果仍不清楚。本研究通过蛋白质组学分析和多项生理学评估，分析了暴露于环境相关浓度PCP下的海洋青鳉（Oryzias melastigma）的能量代谢。结果表明，PCP破坏了海洋青鳉的线粒体形态，降低了线粒体膜电位（MMP），并降低了三磷酸腺苷（ATP）水平。蛋白质组学分析显示，PCP诱导氧化应激、细胞骨架破坏以及对细胞色素bc1复合体和ATP合酶的抑制。这些影响最终导致线粒体的结构和功能受损，进而抑制ATP合成。长期暴露于PCP会导致糖酵解活性增强、肝脏脂质积累以及肝功能下降。本研究加深了我们对PCP诱导海洋鱼类能量产生缺乏机制的理解，并为PCP的生态风险评估提供了新的见解。
