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生物微塑料与抗生素:海洋青鳉鱼脂肪肝疾病的毒性混合物

Biomicroplastics and Antibiotics: A Toxic Cocktail for Fatty Liver Disease in Marine Medaka.

作者信息

Zhang Yu Ting, Gouveia Ana, Chen Ruanni, Xing Daochao, Wang Juying, Mu Jingli

机构信息

Fujian Key Laboratory on Conservation and Sustainable Utilization of Marine Biodiversity, College of Geography and Oceanography, Minjiang University, Fuzhou 350108, China.

Institute of Environment and Ecology, Shenzhen International Graduate School, Tsinghua University, Shenzhen 518055, China.

出版信息

Environ Sci Technol. 2025 Jul 1;59(25):12485-12494. doi: 10.1021/acs.est.4c13931. Epub 2025 Jun 18.

Abstract

The increasing production and use of bioplastics contribute to the accumulation of bioplastic debris in marine environments. The impact of such debris, particularly when combined with co-occurring pollutants like antibiotics, on marine life remains largely unexplored. In this study, we demonstrate that coexposure to aged polylactic acid (PLA) biomicroplastics and the antibiotic sulfamethazine (SMZ) induces overweight (an increase of 20.9-26.2%) and fatty liver-like disease in juvenile marine medaka (). We investigated the underlying mechanism involving the orchestration of physiological processes between the host and its gut microbiota. We found that SMZ acted as a precondition or driver, while PLA acted as an environmental selective pressure, directionally shaping the gut microbiota communities. This altered microbiota demonstrated an increased ability to break down PLA into lactic acid, activating intestinal gluconeogenesis and consequently generating glucose. Excessive glucose shifted the hepatic glucose-fat balance toward fat accumulation, resulting in triglyceride and lipid droplet accumulation and overweight in the fish. Given the prevalent co-occurrence and interaction of PLA and antibiotics in the real-world environment, the combined ecological risk posed by these pollutants requires further investigation.

摘要

生物塑料产量和使用量的不断增加导致海洋环境中生物塑料碎片的积累。此类碎片,尤其是与抗生素等同时存在的污染物相结合时,对海洋生物的影响在很大程度上仍未得到探索。在本研究中,我们证明,幼年海洋青鳉同时暴露于老化的聚乳酸(PLA)生物微塑料和抗生素磺胺二甲嘧啶(SMZ)会导致超重(增加20.9 - 26.2%)和类似脂肪肝的疾病。我们研究了宿主与其肠道微生物群之间生理过程协调的潜在机制。我们发现,SMZ起到了前提条件或驱动因素的作用,而PLA则作为一种环境选择压力,定向塑造肠道微生物群群落。这种改变后的微生物群分解PLA生成乳酸的能力增强,激活肠道糖异生,从而产生葡萄糖。过量的葡萄糖使肝脏葡萄糖 - 脂肪平衡向脂肪积累方向转变,导致甘油三酯和脂滴积累以及鱼超重。鉴于在现实环境中PLA和抗生素普遍同时存在且相互作用,这些污染物共同构成的生态风险需要进一步研究。

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