La coexposición a cobre y PFOS induce neurotoxicidad sinérgica a través de la mitofagia mediada por ROS en C. elegans

excessive oxidative stress induced by co-exposure aberrantly and persistently activated the ROS-mediated mitophagy pathway, thereby impairing mitochondrial quality control. Critically, intervention with N-acetylcysteine (NAC), an antioxidant, effectively mitigated the co-exposure-induced deficits, identifying oxidative stress as the central driver of the synergistic toxicity. Our findings reveal a novel mechanism by which Cu and PFOS exert synergistic neurotoxicity via the oxidative-stress-mitophagy axis, providing key scientific evidence for refining the assessment of their combined environmental pollution risks.