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Embryotoxicity of microplastics, isolated and associated with copper, in zebrafish (Danio rerio)
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Zebrafish embryo experiments showed that microplastics strongly adhere to the embryonic chorion and, when combined with copper, cause significant delays in hatching and reduced heart rate in developing larvae. These results demonstrate that microplastics act as vectors enhancing metal co-exposure during critical developmental windows, raising concerns about synergistic toxic effects in vertebrates from combined microplastic and heavy metal exposure.
Microplastics (MPs) can adsorb metals like copper (Cu), raising concerns about their combined presence in freshwater environments and the acute effects of this mixture on fish during their embryonic development. Thus, this study aimed to evaluate the effects of acute exposure to MP (20 µg l−1) and Cu (10 µg l−1), isolated and mixed (MP + Cu), in embryos of Danio rerio, up to 96 h post-fertilization (hpf). The results showed a high affinity of MPs for the embryonic chorion. When compared to the control, embryos from the Cu (72 hpf) and MP + Cu (72 and 96 hpf) groups showed a significant delay in the hatching rate. Larvae exposed to MP alone and MP + Cu, exhibited a significant decrease in heart rate (96 hpf). Cu accumulation was found to be similar in larvae exposed to Cu and MP + Cu. There was no increase in DNA damage following the exposures. This study highlights that MPs not only have a strong affinity for the embryonic chorion but also adversely affects the development of D. rerio embryos, both isolated and in combination with Cu. Delays in hatching and bradycardia following exposure to MP + Cu reduce larvae's ecological fitness in the wild, impacting their long-term viability.
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Researchers exposed zebrafish to microplastics and copper individually and in combination over 14 days, finding that combined exposure caused the most severe histological damage across multiple organ systems including skin, gills, intestine, liver, and kidneys, while microplastic excretion rates declined over time and copper tissue levels were unaffected by co-exposure.
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This review synthesizes evidence on how micro- and nanoplastics cause developmental, reproductive, gastrointestinal, and oxidative stress toxicity in zebrafish, positioning the species as a valuable vertebrate model for understanding plastic pollutant effects across trophic levels. Zebrafish research is accelerating mechanistic understanding of how microplastics harm vertebrate biology, providing insights relevant to assessing risks for fish-eating wildlife and humans.
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Co-exposure of zebrafish larvae to polystyrene microplastics combined with bisphenol A or F increased larval lethality by 7–51% compared to either pollutant alone, while also causing stronger behavioral effects including reduced movement and activity. This synergistic toxicity — not seen in embryos — highlights the danger of treating microplastics and chemical contaminants as independent hazards, since real-world exposures are always mixed.
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Researchers comprehensively reviewed micro- and nanoplastic bioaccumulation and toxicity in zebrafish, finding that these particles accumulate in digestive organs, gills, liver, and brain, inducing oxidative stress, developmental delays, neurotoxicity, and transgenerational reproductive impairments that highlight broad ecological risks.
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