Pentachlorophenol causes energy deficiency and liver injury in marine medaka (Oryzias melastigma) through damaging mitochondria and inducing oxidative stress.

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.