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

微塑料 氧化应激 斑马鱼 化学 过氧化氢酶 生物累积 谷胱甘肽 活性氧 达尼奥 丙二醛 污染物 毒理 药理学 生物化学 男科 环境化学 生物 医学 基因 有机化学
作者
Xiaodong Ling,Junli Zuo,Meiqi Pan,Hongyan Nie,Jianzhong Shen,Qing Yang,Tien‐Chieh Hung,Guangyu Li
出处
期刊:Science of The Total Environment [Elsevier]
卷期号:818: 151749-151749 被引量:14
标识
DOI:10.1016/j.scitotenv.2021.151749
摘要

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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