Bifenazate Induces Developmental And Immunotoxicity In Zebrafish

Bifenazate is a new acaricide widely used in the control of mites in fruit trees and ornamental plants,but its biosafety is not clear yet.In order to assess the potential health risks of bifenazate to environmental ecosystems,zebrafish were selected as model animals to evaluate the toxicity of bifenazate to animals and its mechanism of action.Due to its unique advantages,zebrafish has been widely used as a model animal for evaluating drugs and environmental toxicants.This study is the first to evaluate the effects of bifenazate on the development and immune system of zebrafish embryos.After exposure to different concentrations of bifenazate,zebrafish embryos showed shorter body length and swelling of yolk sac,indicating the developmental toxicity of bifenazate to zebrafish.At the same time,the neutrophils,macrophages and thymus T cells of zebrafish after exposure to bifenazate gradually decreased with the increase of bifenazate exposure concentration.After exposure to bifenazate,ROS staining showed that the level of oxidative stress was significantly increased,the activities of antioxidant enzymes CAT and SOD were significantly inhibited,and the content of ROS metabolite MDA was decreased.The expression of gclm,prdxl,serpinel and gss genes in antioxidant enzymes related signaling pathways,such as glutathione metabolism pathway,significantly changed.Bifenazate exposure also resulted in abnormal expression of inflammatory factors such as CXCL-clc,IFN-y,iL-8,iL-6,and MyD88,suggesting that bifenazate exposure could cause inflammation in vivo.These results suggest that oxidative stress induced by bifenazate exposure is an important cause of developmental and immunotoxicity in zebrafish.Astaxanthin is an effective antioxidant that can effectively reduce the accumulation of oxidative stress in zebrafish caused by bifenazate exposure.In addition,it can effectively reverse the developmental toxicity phenotypes such as enlarged yolk and shortened body length caused by bifenazate exposure,as well as the immunotoxic phenotypes such as neutropenia and thymus T cell reduction caused by bifenazate exposure.In conclusion,bifenazate exposure can increase the level of oxidative stress in zebrafish embryos,leading to developmental and immunotoxicity in zebrafish.Astaxanthin can effectively counteract the toxicity caused by bifenazate exposure.