| Pyrethroid is a kind of insecticide synthesized based on the chemical structure of pyrethrin.According to whether pyrethroids contain cyanogroup or not,pyrethroids can be divided into two types: type I and type II.Type I molecular configuration contains no cyanogroup,while type II contains cyanogroup.Deltamethrin(DM)is a type II pyrethroid widely used for its low persistence,high efficacy and low toxicity towards mammals and birds.DM is one of the common pollutants in water ecosystem,and the current research focuses on the acute toxicity and other aspects,and there are few studies on the mechanism and mechanism of its action.Zebrafish,as an ideal animal model of adversity developmental biology,has many advantages,such as high homology with human genes,small size,easy breeding,rapid development,large number of eggs,transparent embryos and easy to observe phenotypes after drug administration.Therefore,this study took zebrafish as the research object and selected DM as the test object to investigate the effect of low-dose DM on the embryonic development of zebrafish,providing a basis for further confirmation of its developmental toxicity.The experimental results show that:1.After 20 ?g/L and 40 ?g/L DM treatment,the zebrafish embryonic swim bladder decreased in size and failed to inflate.Compared with the control group,the expression levels of pbx1,foxA3,mnx1,has2,anxa5 b,hprt1l and elovl1 a,the key genes regulating the development of swim bladder,were significantly reduced in the DM treatment group.It is suggested that DM may cause the failure of bladder inflation by inhibiting the formation of tissue in zebrafish embryonic swim bladder.It has been reported that the Wnt and Hedgehog signal pathways play an important role in the development of swim bladder.Compared with the control group,the transcription levels of Wnt pathway marker genes wnt5 b,tcf3a,wnt1,wnt9 b,fzd1,fzd3 and fzd5 and Hedgehog pathway marker genes ihhb,ptc1 and ptc2 were significantly reduced in the DM treatment group.The Wnt pathway was rescued by its agonist(2'Z,3'E)-6-bromoindirubin-3'-oxime(BIO),but the size of embryonic swim bladder treated with BIO and DM was not significantly different from that treated with DM alone,suggesting that there might be other molecular mechanisms underlying DM-induced abnormal swim bladder development.2.Spontaneous swimming of zebrafish embryos at 48,72,and 96 hpf in DM-treated groups was significantly hyperactive than the control group.GO functional classification on DEGs for zebrafish embryos shows that a large number of DEGs in the DM-treated group and the control group were mainly concentrated in the pathways of neurogenesis,negative regulation of movement,and negative regulation of cell component movement.Compared with the control group,the expression levels of mylz3,ckmb,mybphb,mylz3,myhz2,ckmb,pvalb1 and smyd1 b related to fast muscle,myotme,cardiac muscle cell embryos in the DM treatment group of embryos at 48 hpf were significantly reduced.The expression of neurotoxicity-related genes plxna3,gap43 and elavl3 in 60 hpf embryos were significantly decreased.In summary,when DM concentrations is greater than 20 ?g/L,locomotor behavior and the development of swim baldder will be impaired.At the same time,this study made a preliminary exploration of the molecular mechanism leading to the abnormal development of swim baldder,which laid the foundation for further research on the toxic effects of DM on early embryos of zebrafish. |
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