Triphenyltin (TPT) is known to be an environmental endocrine disruptor and has adverse effects on aquatic animals. In this study, zebrafish embryos were treated with three different concentrations (12.5, 25, 50 nmol/L) based on the LC50 value at 96 h post fertilization (96 hpf), after TPT exposure. The developmental phenotype and hatchability were observed and recorded. Reactive oxygen species (ROS) levels in zebrafish were detected at 72 hpf and 96 hpf using 2',7'-dichlorodihydrofluorescein diacetate (DCFH-DA) as a probe. The number of neutrophils after exposure was observed using transgenic zebrafish Tg (lyz: DsRed). RNA-seq analysis was used to compare the gene expression changes in zebrafish embryos at 96 hpf in the control group and 50 nmol/L TPT exposure group. The data revealed that TPT caused a delay in hatching of zebrafish embryos in a time- and dose-dependent manner, as well as causing pericardial edema, spinal curvature and melanin reduction. ROS levels in embryos exposed to TPT increased, and the number of neutrophils increased after TPT exposure to Tg (lyz: DsRed) in transgenic zebrafish. RNA-seq results were also analyzed, and KEGG enrichment analysis showed that significant differential genes were enriched in the PPAR signaling pathway (P < 0.05), and the PPAR signaling pathway mainly affected genes related to lipid metabolism. The RNA-seq results were verified using real-time fluorescence quantitative PCR (RT-qPCR). Oil red O and Nile red staining showed increased lipid accumulation after TPT exposure. These findings suggest that TPT affects the development of zebrafish embryos even at relatively low concentrations.
Keywords: Developmental toxicity; RNA-seq; TPT; Zebrafish.
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