Zinc pyrithione (ZPT) is a frequently used organometallic biocide, carrying potentially adverse consequences to multiple species in the environment. Previously we have demonstrated its embryonic, organ developmental and liver metabolic toxicity of zebrafish. However, details of ZPT toxicity during embryogenesis are still limited. The present study was designed to evaluate the effects and possible mechanisms of ZPT-induced embryonic toxicogenomic responses by morphological investigations, transcriptome and gene quantitative analysis, as well as biochemical assays. The results revealed that treatment with ZPT caused embryogenesis toxicity, specifically in irregular cell division and rearrangement, delayed differentiations of eyes and notochords, the epiboly and germ ring formation and somite segmentation defects. In addition, ZPT exposure altered gene expression during early embryonic development, especially related with morphological abnormities and metabolic dysfunctions including reduction of oxidoreductase activity. Activities of antioxidants and caspases examinations showed inductions of oxidative stress and apoptosis by ZPT and quantitative analysis of marker genes further indicated that ZPT also triggered endoplasmic reticulum (ER) stress and autophagy. Thus, we deduce here that ZPT-induced embryonic toxicogenomic responses reveal involvement of oxidative damage, apoptosis, endoplasmic reticulum (ER) stress and autophagy.

吡啶硫酮锌 (ZPT) 是一种常用的有机金属杀菌剂，对环境中的多种物种具有潜在的不利影响。以前我们已经证明了斑马鱼的胚胎、器官发育和肝脏代谢毒性。然而，胚胎发生过程中 ZPT 毒性的细节仍然有限。本研究旨在通过形态学研究、转录组和基因定量分析以及生化分析来评估 ZPT 诱导的胚胎毒理学反应的影响和可能的机制。结果表明，用 ZPT 处理会导致胚胎发生毒性，特别是不规则的细胞分裂和重排、眼睛和脊索的延迟分化、外胚层和胚环的形成以及体节分割缺陷。此外，ZPT 暴露在早期胚胎发育过程中改变了基因表达，特别是与形态异常和代谢功能障碍有关，包括氧化还原酶活性降低。抗氧化剂活性和半胱天冬酶检测显示 ZPT 诱导氧化应激和细胞凋亡，标记基因的定量分析进一步表明 ZPT 还引发内质网 (ER) 应激和自噬。因此，我们在此推断 ZPT 诱导的胚胎毒理学反应揭示了氧化损伤、细胞凋亡、内质网 (ER) 应激和自噬的参与。抗氧化剂活性和半胱天冬酶检测显示 ZPT 诱导氧化应激和细胞凋亡，标记基因的定量分析进一步表明 ZPT 还引发内质网 (ER) 应激和自噬。因此，我们在此推断 ZPT 诱导的胚胎毒理学反应揭示了氧化损伤、细胞凋亡、内质网 (ER) 应激和自噬的参与。抗氧化剂活性和半胱天冬酶检测显示 ZPT 诱导氧化应激和细胞凋亡，标记基因的定量分析进一步表明 ZPT 还引发内质网 (ER) 应激和自噬。因此，我们在此推断 ZPT 诱导的胚胎毒理学反应揭示了氧化损伤、细胞凋亡、内质网 (ER) 应激和自噬的参与。