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Microplastics disrupt energy metabolism and intestinal integrity in juvenile Chinese horseshoe crabs

Water Biology and Security 2026
Yi Jiang, Yue Wang, Wenbo Guo, Waiho Khor, Zhi Chen, James Kar-Hei Fang, Xiaowan Ma, Jae-Seong Lee, Cheong‐Meng Chong, Peiwen Yang, Yiran Mao, Menghong Hu

Summary

Scientists exposed young horseshoe crabs (an ancient marine species) to microplastics and found real damage: the plastic particles built up in their gills and gut, weakened digestion, thinned their intestinal walls, and messed up how they process fats and energy—and these problems didn't fully go away even after the plastic exposure stopped. This matters because it shows microplastics can cause lasting harm to marine life that filters or lives in polluted waters, a warning sign for the broader food chain and ecosystems humans depend on, including the seafood we eat.

Polymers

As an endangered marine living fossil, the Chinese horseshoe crab ( Tachypleus tridentatus ) inhabits microplastics (MPs) pollution hotspots. This study assessed the toxicity of different concentrations of 5 μm fluorescent polystyrene MPs on two-year-old horseshoe crab through a 14-day exposure and 7-day recovery experiment. The results showed that, (1) MPs accumulated concentration dependently, primarily in gills and intestine. High exposure (200 μg/L) resulted in significant residual burden (0.2109 μg/g), indicating inefficient excretion. (2) Respiratory metabolism was significantly inhibited (decreased oxygen consumption, P < 0.05), impacting energy metabolism and survival. (3) Digestive enzyme activity (lipase, trypsin) was dose-dependently suppressed ( P < 0.05), accompanied by intestinal wall thinning ( P < 0.05) and down-regulation of lipid metabolism genes ( Amy1 , PNLIP ). (4) Lipid metabolism disruption manifested as elevated triglycerides/cholesterol ( P < 0.05), inhibited total lipase ( P < 0.05), and low regulated lipolysis genes ( Mgll-2 , PLD1 ). MPs induced complex toxicity via a “physical damage–metabolic interference–gene regulation” triad. Short-term low-dose exposure triggered compensation, while long-term high-dose exposure caused intestinal damage and metabolic disorder. Incomplete recovery post-exposure to MPs demonstrates cumulative and persistent ecological risks to endangered intertidal species, providing crucial insights for assessing MP impacts on living fossils.

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