Silica Nanoparticles Induced Embryonic Dysplasia and Apoptosis Via Endoplasmic Reticulum Stress in Zebrafish(Danio Rerio)

Abstract The possible detrimental effects of nanomaterials on organisms have become a public concern because of the wide applications of nanomaterials in modern society. This study investigates the effects of silica nanoparticles (nano‐SiO 2 ) on zebrafish development. Fluorescent nano‐SiO 2 (FITC‐nano‐SiO 2 ) is synthesized with an emission wavelength of 517 nm. Due to similar hydrodynamic size, FITC‐nano‐SiO 2 is used to simulate the distribution of nano‐SiO 2 in zebrafish. Nano‐SiO 2 regulated col2a1a , col9a2 , lect1 , and her12 to delay liver development and regulated prox , wnt2bb , mypt1 , and hhex caused spinal curvature. The hand2 , mef2a , nkx2.5 , and atp1a2a are significantly down‐regulated. The whole embryo in situ hybridization revealed amhc and flk1 are also down‐regulated. This suggests that nano‐SiO 2 affected heart and blood vessels development of zebrafish. Furthermore, it is found that cell apoptosis occurred in the heart. The proapoptotic genes ( bax , bid ) are upregulated, and the antiapoptotic genes ( bcl‐2 , mcl‐1b ) are down‐regulated. Nano‐SiO 2 increases the endoplasmic reticulum (ER) stress‐related genes ( chop , bip , perk, elF2α ), indicating that the ER stress is involved in cell apoptosis. This study provides a toxicological basis for evaluating the possible hazards of nano‐SiO 2 to aquatic organisms.