The plastic threat to marine gastropods: Oxidative stress, energy metabolism and impaired recovery in juvenile abalone (Haliotis discus hannai) exposed to polystyrene microplastics

Microplastic (MP) pollution challenges marine ecosystems, with gastropods like Haliotis discus hannai being potentially vulnerable. However, the reversibility of MP-induced physiological damage in gastropods remains poorly understood. This study investigated the effects of polystyrene microplastics (PS-MPs; 0, 100, and 1000 μg/L) on H. discus hannai in a 14-day exposure followed by a 7-day recovery experimental design. The analysis focused on antioxidant status, energy metabolism, and immune pathways. Results showed dose-dependent oxidative stress during PS-MPs exposure, indicated by significantly (P < 0.05) elevated antioxidant enzyme activities (Superoxide dismutase, Catalase and Glutathione peroxidase), which decreased but did not normalize during recovery. Exposure to a low concentration of PS-MPs (100 μg/L) resulted in metabolic adjustments consistent with homeostatic maintenance, whereas a high concentration (1000 μg/L) significantly increased lactate dehydrogenase and Na/K-ATPase activities, suggesting metabolic disruption. These energy metabolism alterations persisted, showing incomplete recovery. Immune pathway analysis revealed minimal changes at low PS-MPs concentrations but significant enrichment of pathways like IL-17 and Fc-Epsilon-RI signaling at high concentrations during exposure. Notably, sustained activation of immune pathways, including NOD-like receptor, Toll-like receptor, and IL-17 signaling (particularly in the high-concentration group), persisted during recovery, potentially indicating prolonged cellular stress or links to apoptosis. Furthermore, Integrated Biomarker Response (IBR) analysis confirmed that H. discus hannai remained severely impacted even after the recovery period. This study provides crucial evidence on the complex toxicodynamics of PS-MPs in H. discus hannai, highlighting incomplete physiological recovery and significant damage during the recovery period following exposure, especially at high concentrations.