太平洋牡蛎（Magallana gigas）对近海风电场低频噪音的生理和分子反应

Abstract

A 250-Hz noise exposure elicited sublethal responses in Magallana gigas . • Noise induced oxidative stress and immune suppression. • ECM-related signaling and the PI3K/Akt pathway were disrupted. • Metabolic strategy shifted to anaerobic glycolysis to cope with noise exposure. The mechanisms by which low-frequency noise from operational offshore wind farms (OWFs) affects marine benthic invertebrates remain poorly understood. This study used the Pacific oyster ( Magallana gigas ) as a model species and integrated physiological and biochemical endpoints with transcriptomic and metabolomic approaches to characterize intensity-dependent biological responses to low-frequency noise exposure. The results showed that noise exposure induced oxidative stress, as evidenced by elevated superoxide dismutase (SOD) and catalase (CAT) activities and decreased antioxidant metabolites. The immune response was intensity-dependent: low-intensity exposure activated complement-mediated innate immunity, whereas high-intensity exposure triggered inflammatory responses mediated by the COX-2 pathway and promoted DNA damage repair. In terms of energy metabolism, the downregulation of key glycolytic genes ( Akr1b8 and Pck1 ), accumulation of free amino acids, and depletion of membrane lipids collectively indicated suppressed aerobic metabolism, with compensatory enhancement of anaerobic glycolysis and amino acid oxidation. Moreover, extracellular matrix (ECM) remodeling and alterations in ECM-associated focal adhesion and PI3K-Akt signaling pathways suggested impaired structural integrity and intercellular communication in the digestive gland. This study established for the first time in bivalves a multilevel response network linking enzyme activities, gene expression profiles, and metabolite levels, revealing distinct molecular response patterns under low- and high-intensity noise exposure. These findings provide a mechanistic basis for the ecological risk assessment of OWF noise and for