The impacts of triphenyltin (TPT) on ecological health are of particular concern due to the unexpectedly high levels found in wild fish around the world. Here, zebrafish embryos were exposed to TPT via in ovo nano-injection to study its toxicity on the development of retinal axons in fish. Lipophilic dye labeling revealed obvious defects in retinal axon development in larvae with normally shaped eyes, with incidences of 0, 1.08%, 2.66%, 4.26%, and 6.85% observed in the control, 0.8, 4.0, 20.0, and 100ng TPT-Cl/g wet weight (ww) exposure groups, respectively, showing a dose-dependent increase. Since the lowest observable effective concentration of TPT to induce retinal axon development defects was 0.8ng TPT-Cl/g ww, which is lower than the concentrations in wild fish eggs, this defect would occur in wild fish larvae. Alterations in the expressions of pax6 and ephrinBs, which regulate the establishment of retinal polarity, were correlated with defect incidence. Expression levels of the CYP26A1 gene and protein were significantly up-regulated in all exposure groups compared with the control, which may lead to significant decreases in concentrations of all-trans retinoic acid (atRA). Such a disruption of RA metabolism would, at least partly, contribute to the incidence of developmental defects in retinal axons. This study is the first to report that TPT can interfere with development of retinal axons in fish at low dose.
Keywords: Dark pigmentation; Retinal ganglion cell axons; Retinoic acid; Teratogenicity; Vision defect.
Copyright © 2017. Published by Elsevier B.V.