Influences of Co-Exposure to Fatty Acids and SiO2 Nanoparticles on Gene Expression in Zebrafish Intestines and Livers and Si Accumulation and Lipid Staining in Caco-2 and HepG2 Cells.

The interaction between fatty acids and nanoparticles (NPs) is increasingly recognized. This study investigated how stearic acid (SA)/linolenic acid (LNA) and SiO2 NPs co-exposure affects mRNA abundance of efflux, autophagy, fatty acid metabolism, and synthesis genes in adult zebrafish, and Si concentrations and lipid accumulation in Caco-2 and HepG2 cells. In vivo, SA or LNA inhibited SiO2 NPs from inducing abcg1 expression, and SiO2 NPs and SA/LNA co-exposure decreased agap1 expression in intestines. In livers, SiO2 NPs and SA co-exposure increased abcg1 expression. SiO2 NPs increased autophagic gene expression (map 1lc3b, atg7, and becn1) in intestines but not in livers. In contrast, SiO2 NPs + LNA increased map 1lc3b and atg7 expression, and SiO2 NPs + SA increased atg5 and becn1 expression in livers. For fatty acid β-oxidation genes, SiO2 NPs increased acox1 expression but decreased pparaa expression in intestines, an effect altered by SA or LNA. In livers, SiO2 NPs decreased acox1, cpt1aa, and pparaa but increased pnpla2 expression, which was also changed by SA. For fatty acid synthesis genes, LNA increased acaca and fasn expression in SiO2 NP-exposed intestines. In livers, SiO2 NPs decreased acaca, fasn, and scd expression, which was increased by LNA. In vitro, LNA increased Si accumulation in SiO2 NP-exposed Caco-2 cells, whereas both fatty acids reduced Si levels in HepG2 cells. Lipid accumulation was enhanced in HepG2 cells exposed to LNA and SiO2 NPs + LNA. Overall, our findings highlighted the complex interplay between SiO2 NPs and fatty acids, with outcomes dependent on fatty acid structure and cell/tissue type.