Pretilachlor has the potential to induce endocrine disruption, oxidative stress, apoptosis and immunotoxicity during zebrafish embryo development

The objectives of the present study were to investigate the toxic effects of pretilachlor on zebrafish during its embryo development. The results demonstrated that the transcription of genes involved in the hypothalamic-pituitary-gonadal/thyroid (HPG/HPT) axis was increased after exposure to 50, 100, 200 μg/L pretilachlor for 96 h, the aromatase activity, vitellogenin (VTG) and thyroid Hormones T3 and T4 levels in zebrafish were also up-regulated simultaneously. Pretilachlor exposure induced a noticeable increase in ROS level, increased the transcription and level of antioxidant proteins (e.g., CAT, SOD and GPX). Moreover, the up-regulation of P53, MDM2, Bbc3 expression and Caspase3 and Caspase9 activities in the Apoptosis pathway suggested pretilachlor might trigger cell Apoptosis in zebrafish. In addition, the transcription of CXCL-C1C, IL-1β and IL-8 related to the innate immunity was down-regulated after pretilachlor exposure. These data suggested that pretilachlor could simultaneously induce endocrine disruption, Apoptosis, oxidative stress and immunotoxicity during zebrafish embryo development.

Apoptosis; Endocrine disruption; Immunotoxicity; Oxidative stress; Pretilachlor; Zebrafish.