Combined Toxicities of Di-Butyl Phthalate and Polyethylene Terephthalate to Zebrafish Embryos.

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.

The developmental toxicity and transcriptome analyses of zebrafish (Danio rerio) embryos exposed to carbon nanoparticles.

Long-term and short-term exposure to carbon nanoparticles (CNPs) can affect fetal development and subsequent adverse outcomes including preterm delivery, intrauterine growth restriction, low birth weight, increased health risk linked to cardiovascular, respiratory and nervous systems in adulthood. The adverse developmental outcomes of CNPs were well known, but the underlying mechanisms remain unresolved. In this study, zebrafish embryos were treated with CNPs of 50,100,200 µg/mL and the toxic effects were observed. Using the RNA-seq analysis approach, we examined the effects of CNPs (200 µg/mL) on gene expression in zebrafish embryos exposed from 4 to 96 h-post-fertilization (hpf). We observed that CNPs-treated embryos exhibited increased malformations and decreased hatching. A total of 236 differentially expressed genes were detected by transcriptome analyses, which were associated with phototransduction, amino acid metabolism, steroid and steroid hormone biosynthesis. Transcriptome results were verified by real-time fluorescence quantitative PCR (RT-qPCR). Our results indicated that CNPs exposure was most likely to lead to differential gene changes in steroid and hormone biosynthesis pathways, thus inducing developmental toxicity such as delayed incubation of zebrafish embryos, increased malformation rate and multiple malformation phenotypes.