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Revealing the effects of polystyrene microplastics and di(2-ethylhexyl) phthalate on mussels:An evidence chain of gill-intestine-hemolymph

Environmental Research 2025 1 citation ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 53 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Yiming Gao, Xiaopeng Pang, James Kar‐Hei Fang, Zhen Zhong, Menghong Hu, Youji Wang

Summary

Researchers exposed mussels to polystyrene microplastics combined with the plasticizer DEHP for 30 days and found a cascade of harmful effects across gill, intestine, and blood systems. The combination caused gill damage, disrupted energy metabolism, triggered oxidative stress, altered gut microbiota, and suppressed immune function. The study establishes a pollutant cascade mechanism linking tissue damage, metabolic changes, and microbial imbalance in marine organisms.

Polystyrene microplastics (PS-MPs) and di(2-ethylhexyl) phthalate (DEHP) are widespread contaminants in marine ecosystems, posing significant risks to marine life due to their toxicity and interactions with other pollutants. This study evaluates the combined effects of PS-MPs and DEHP on Mytilus coruscus, focusing on physiological and immune responses over a 30-day exposure. Results showed significant morphological changes in gill structures, including reduced lamella dimensions and thinner stromal tissue, impairing gas exchange. Key enzymatic activities related to energy metabolism were altered, with LDH, SDH, and HK activities suppressed and PK activity increased, indicating a shift in energy regulation. ATPase activity decreased while ROS activity rose, suggesting oxidative stress. Changes in digestive enzyme lipase activity were noted alongside modifications in gut microbiota under high pollutant concentrations. Immune markers showed decreased THC, PHA, and EA levels, with increased HM, indicating immune disruption. Antioxidant defenses were activated, evidenced by elevated SOD, CAT, GPX, and GSH activities, yet increased MDA levels indicated lipid peroxidation. These findings establish a pollutant cascade mechanism linking tissue damage, metabolic reprogramming, and microbial imbalance, providing critical data for marine risk assessment.

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