Abstract

The rapid expansion of offshore wind energy, driven by the global demand for clean energy, has raised concerns about the release of erosion particles (EPs) from turbine blade erosion and their potential impacts on marine benthic organisms. In this study, the Pacific oyster ( Magallana gigas ) was used as a model organism to investigate the toxicological mechanisms of EPs. Organisms were subjected to exposure experiments at different concentrations, combined with analyses of superoxide dismutase (SOD), catalase (CAT), and acid phosphatase (ACP) activities, malondialdehyde (MDA) content, transcriptomics, and metabolomics. Results showed that EP exposure induced significant oxidative stress, as evidenced by elevated lipid peroxidation and activation of the antioxidant enzyme defense system. Additionally, based on transcriptomic and metabolomic data, EPs may disrupt cytoskeletal integrity and endocytic function, thereby impairing membrane structural stability and substance transport capacity. Furthermore, EPs may disrupt the energy metabolism network: low-concentration exposure primarily suppresses the tricarboxylic acid (TCA) cycle and glycolysis, potentially leading to insufficient energy production, while high-concentration exposure may further diminish lipid reserves and inhibit gluconeogenesis, exacerbating metabolic imbalance. Moreover, EPs exposure activates the cGAS-STING and NF-κB signaling pathways, triggering innate immune responses and interfering with apoptosis. This study demonstrates that EPs are biologically active; they not only elicit antioxidant defense responses at the physiological and biochemical levels but also disrupt key metabolic and immune pathways at the molecular level. This research provides novel insights into the ecological risk assessment of this emerging pollutant from offshore wind farms and highlights the importance of incorporating EPs in marine ecological safety evaluations.