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The presence of polystyrene nanoplastics enhances the MCLR uptake in zebrafish leading to the exacerbation of oxidative liver damage

The Science of The Total Environment 2021 40 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 50 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Qing Yang, Xiaodong Ling, Junli Zuo, Guangyu Li Junli Zuo, Meiqi Pan, Qing Yang, Hongyan Nie, Qing Yang, Hongyan Nie, Qing Yang, Qing Yang, Qing Yang, Qing Yang, Qing Yang, Jianzhong Shen, Qing Yang, Qing Yang, Guangyu Li Qing Yang, Qing Yang, Qing Yang, Qing Yang, Qing Yang, Qing Yang, Guangyu Li Jianzhong Shen, Tien‐Chieh Hung, Qing Yang, Qing Yang, Qing Yang, Tien‐Chieh Hung, Tien‐Chieh Hung, Guangyu Li Guangyu Li

Summary

Researchers found that polystyrene nanoplastics enhanced the uptake of the toxin microcystin-LR in zebrafish liver over three months of co-exposure, exacerbating oxidative damage and cellular swelling compared to microcystin exposure alone.

Polymers
Body Systems

The accumulation of diminutive plastic waste in the environment, including microplastics and nanoplastics, has threatened the health of multiple species. Nanoplastics can adsorb the pollutants from the immediate environment, and may be used as carriers for pollutants to enter organisms and bring serious ecological risk. To evaluate the toxic effects of microcystin-LR (MCLR) on the liver of adult zebrafish (Danio rerio) in the presence of 70 nm polystyrene nanoplastics (PSNPs), zebrafish were exposed to MCLR alone (0, 0.9, 4.5 and 22.5 μg/L) and a mixture of MCLR + PSNPs (100 μg/L) for three months. The results indicated that groups with combined exposure to MCLR and PSNPs further enhanced the accumulation of MCLR in the liver when compared to groups only exposed to MCLR. Cellular swelling, fat vacuolation, and cytoarchitectonic damage were observed in zebrafish livers after exposure to MCLR, and the presence of PSNPs exacerbated these adverse effects. The results of biochemical tests showed the combined effect of MCLR + PSNPs enhanced MCLR-induced hepatotoxicity, which could be attributed to the altered levels of reactive oxygen species, malondialdehyde and glutathione, and activities of catalase. The expression of genes related to antioxidant responses (p38a, p38b, ERK2, ERK3, Nrf2, HO-1, cat1, sod1, gax, JINK1, and gstr1) was further performed to study the mechanisms of MCLR combined with PSNPs aggravated oxidative stress of zebrafish. The results showed that PSNPs could improve the bioavailability of MCLR in the zebrafish liver by acting as a carrier and accelerate MCLR-induced oxidative stress by regulating the levels of corresponding enzymes and genes.

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