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Microcystin-LR and polystyrene microplastics jointly lead to hepatic histopathological damage and antioxidant dysfunction in male zebrafish

Environmental Pollution 2024 24 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.

Wang Lin, Wang Lin, Wang Lin, Wang Lin, Wang Lin, Ling Ling, Ling Ling, Fen Hu, Ling Liao, Pinhong Yang, Fen Hu, Pinhong Yang, Ling Ling, Ling Ling, Fang Liu Ling Ling, Ling Liao, Ling Ling, Ling Ling, Ling Ling, Li Li, Li Li, Li Li, Li Li, Li Li, Jifeng Yang, Wang Lin, Jifeng Yang, Pinhong Yang, Pinhong Yang, Pinhong Yang, Pinhong Yang, Ling Liao, Jifeng Yang, Pinhong Yang, Fang Liu Pinhong Yang, Pinhong Yang, Pinhong Yang, Li Li, Li Li, Fang Liu

Summary

This study exposed zebrafish to a common water toxin (microcystin-LR) both alone and combined with polystyrene microplastics, and found that the microplastics made the liver damage significantly worse. The microplastics acted as carriers, increasing how much toxin accumulated in the fish liver and amplifying oxidative stress. This is relevant to human health because it shows microplastics can boost the harmful effects of other pollutants commonly found in drinking water sources.

Polymers

Body Systems

Hepatic

Models

Zebrafish

The co-occurrence of cyanobacterial blooms and nano-microplastic pollution in the water is becoming an emerging risk. To assess the combined hepatotoxicity of microcystin-LR (MC-LR) and polystyrene microplastics (PSMPs) on zebrafish (Danio rerio), male adult zebrafish were exposed to single MC-LR (0, 1, 5, 25 μg/L) and a mixture of MC-LR and PSMPs (100 μg/L). After 60 d exposure, the results indicated that PSMPs significantly increased the MC-LR bioaccumulation in the livers in contrast to the single 25 μg/L MC-LR treatment group. Moreover, the severity of hepatic pathological lesions was aggravated in the MC-LR + PSMPs treatment groups, which were mainly characterized by cellular vacuolar degeneration, swollen hepatocytes, and pyknotic nucleus. The ultrastructural changes also proved that PSMPs combined with MC-LR could enhance the swollen mitochondria and dilated endoplasmic reticulum. The biochemical results, including increased malondialdehyde (MDA) and decreased glutathione (GSH), indicated that PSMPs intensified the MC-LR-induced oxidative damage in the combined treatment groups. Concurrently, alterations of sod1 and keap1a mRNA levels also confirmed that PSMPs together with MC-LR jointly lead to enhanced oxidative injury. Our findings demonstrated that PSMPs enhanced the MC-LR bioavailability by acting as a vector and exacerbating the hepatic injuries and antioxidant dysfunction in zebrafish.

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