Zinc pyrithione (ZPT) -induced embryonic toxicogenomic responses reveal involvement of oxidative damage, apoptosis, endoplasmic reticulum (ER) stress and autophagy.

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.