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Combined Toxicities of Di-Butyl Phthalate and Polyethylene Terephthalate to Zebrafish Embryos
Summary
Researchers exposed zebrafish embryos to polyethylene terephthalate microplastics and the plasticizer di-butyl phthalate, both alone and in combination. While the microplastics alone mainly delayed hatching, the plasticizer caused severe developmental abnormalities and death. The study found that the microplastics actually reduced the toxicity of the plasticizer by adsorbing it, though they also slowed its breakdown, creating a more persistent exposure risk.
The increasing concern for the ecological risks of microplastics (MPs) as carriers of hydrophobic organic contaminants is evident. Di-butyl phthalate (DBP) is extensively utilized as an additive in plastic products, and both DBP and MPs are widespread in the environment. However, the combined toxicity of these substances remains uncertain. In this study, zebrafish embryos were employed to assess the toxic effects of polyethylene terephthalate (PET, MPs) and DBP, with a focus on the DBP toxicities influenced by PET. The embryonic chorion was partially covered by PET particles, and PET led to a delayed hatching of zebrafish embryos without inducing death or teratogenesis. On the other hand, exposure to DBP considerably inhibited the hatching of embryos, leading to severe lethal and teratogenic effects. The most common phenotypes induced by DBP exposure were delayed yolk sac absorption and pericardial edema. The mortality increased in co-treatment with 100 particles/mL PET and 2 mg/L DBP at 24 hpf and 48 hpf. The malformation phenotype, bent notochord, and delayed yolk sac absorption became more severe in 1 mg/L DBP exposition with the co-exposure of 100 particles/mL PET at 72 hpf. PET might act as a carrier that enhances the bioavailability of ambient DBP.
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