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Behavioral impairments and disrupted mitochondrial energy metabolism induced by polypropylene microplastics in zebrafish larvae

The Science of The Total Environment 2024 22 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 65 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Biran Zhu, Jianghuan Hua, Jianghuan Hua, Xianglin Chen, Taotao Zhang, Xianglin Chen, Biran Zhu, Min Zhao, Kaiyu Fu, Min Zhao Kaiyu Fu, Bingsheng Zhou, Kaiyu Fu, Kaiyu Fu, Jianghuan Hua, Jianghuan Hua, Bingsheng Zhou, Yindan Zhang, Yindan Zhang, Hao Pang, Bingsheng Zhou, Bingsheng Zhou, Huijia Tang, Huijia Tang, Hao Pang, Yongyong Guo, Yongyong Guo, Jian Han, Jian Han, Bingsheng Zhou, Lihua Yang, Lihua Yang, Bingsheng Zhou, Min Zhao Min Zhao

Summary

Zebrafish embryos exposed to polypropylene microplastics at environmentally relevant levels showed behavioral changes and disrupted energy production in their cells. The microplastics impaired the mitochondria -- the energy-producing structures inside cells -- in both intestinal and liver tissue, while also causing oxidative stress. These findings suggest that even at concentrations found in the environment, common polypropylene microplastics can interfere with basic cellular energy processes.

Polypropylene microplastics (PP-MPs) are emerging pollutant commonly detected in various environmental matrices and organisms, while their adverse effects and mechanisms are not well known. Here, zebrafish embryos were exposed to environmentally relevant concentrations of PP-MPs (0.08-50 mg/L) from 2 h post-fertilization (hpf) until 120 hpf. The results showed that the body weight was increased at 2 mg/L, heart rate was reduced at 0.08 and 10 mg/L, and behaviors were impaired at 0.4, 10 or 50 mg/L. Subsequently, transcriptomic analysis in the 0.4 and 50 mg/L PP-MPs treatment groups indicated potential inhibition on the glycolysis/gluconeogenesis and oxidative phosphorylation pathways. These findings were validated through alterations in multiple biomarkers related to glucose metabolism. Moreover, abnormal mitochondrial ultrastructures were observed in the intestine and liver in 0.4 and 50 mg/L PP-MPs treatment groups, accompanied by significant decreases in the activities of four mitochondrial electron transport chain complexes and ATP contents. Oxidative stress was also induced, as indicated by significantly increased ROS levels and significant reduced activities of CAT and SOD and GSH contents. All the results suggested that environmentally relevant concentrations of PP-MPs could induce disrupted mitochondrial energy metabolism in zebrafish, which may be associated with the observed behavioral impairments. This study will provide novel insights into PP-MPs-induced adverse effects and highlight need for further research.

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