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

Abstract

AbstractThe 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‐SiO2) on zebrafish development. Fluorescent nano‐SiO2 (FITC‐nano‐SiO2) is synthesized with an emission wavelength of 517 nm. Due to similar hydrodynamic size, FITC‐nano‐SiO2 is used to simulate the distribution of nano‐SiO2 in zebrafish. Nano‐SiO2 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‐SiO2 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‐SiO2 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‐SiO2 to aquatic organisms.