Coenzyme Q10 mitigates high-fat-induced mitochondrial damage in spotted seabass (Lateolabrax maculatus) hepatocytes by promoting mitophagy

Coenzyme Q10 (COQ10), a natural fat-soluble compound, is known to protect mitochondria, though the exact mechanism remains unclear. Here, we explored the mechanism through which COQ10 enhances mitochondrial function using hepatocytes from spotted seabass ( Lateolabrax maculatus ). Three experimental groups were established: a normal medium control group, a fatty acid (FA) group containing 100 μM FA, and a group containing100 μM FA plus 5 μM COQ10 (FA + COQ10). After incubation, the results showed that FA treatment significantly increased triglyceride content in the cells, while COQ10 treatment reduced triglycerides content ( P  < 0.05). Additionally, COQ10 alleviated FA-induced hepatocyte damage, restored mitochondrial membrane potential and increased ATP content ( P  < 0.05). Further analysis showed that FA downregulated key mitophagy genes ( PINK1 , PARKIN , and LC3B ) while upregulating P62 ( P  < 0.05). To investigate whether the enhancement of mitochondrial function by COQ10 is dependent on mitophagy activation, we used the mitophagy inhibitor Mdivi-1 and set it to FA + COQ10 + Mdivi-1 group. After mtphagy Dye staining, the number of autophagosomes in the FA + COQ10 + Mdivi-1 group was lower than in the FA + COQ10 group, indicating that the mitophagy activation by COQ10 was inhibited. Overall, these results demonstrated that COQ10 enhances mitochondrial function and alleviates excessive fat deposition in hepatocytes via PINK1-mediated mitophagy. This also indicates that COQ10 can be potentially applied to improve the metabolic disorders of fish in aquaculture.