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The presence of polystyrene nanoplastics enhances the MCLR uptake in zebrafish leading to the exacerbation of oxidative liver damage
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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.
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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Mechanisms of parental co-exposure to polystyrene nanoplastics and microcystin-LR aggravated hatching inhibition of zebrafish offspring
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Zebrafish parents co-exposed to microcystin-LR and polystyrene nanoplastics produced offspring with greater MCLR accumulation and more severe hatching inhibition than MCLR alone, with nanoplastics acting as a carrier that enhanced toxin transfer to embryos.
Microcystin-LR and polystyrene microplastics jointly lead to hepatic histopathological damage and antioxidant dysfunction in male zebrafish
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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.
The joint effect of parental exposure to microcystin-LR and polystyrene nanoplastics on the growth of zebrafish offspring
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Adult zebrafish co-exposed to polystyrene nanoplastics and microcystin-LR (MCLR) for 21 days transferred more MCLR to their offspring than MCLR alone, and the nanoplastic-enhanced MCLR parental load correlated with greater growth inhibition and developmental defects in F1 larvae.
Microplastics as vectors for microcystin-LR: Enhanced bioavailability, oxidative damage, and immune dysregulation in zebrafish spleen
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Researchers studied the combined effects of the algal toxin microcystin-LR and polystyrene microplastics on zebrafish spleen over 60 days. They found that microplastics enhanced the bioavailability of the toxin, worsening oxidative damage and suppressing immune function beyond what either pollutant caused alone. The study suggests that microplastics can act as vectors for harmful algal toxins, amplifying their biological impact in aquatic organisms.
Polystyrene microplastics enhance microcystin-LR-induced cardiovascular toxicity and oxidative stress in zebrafish embryos
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Zebrafish embryos exposed to both microplastics and microcystin-LR (a toxin produced by algal blooms) developed significantly worse heart and blood vessel damage than those exposed to the toxin alone. The microplastics amplified oxidative stress and cell death, suggesting that in polluted waterways where both contaminants coexist, the combined health risks may be greater than either one individually.
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