Zinc oxide (ZnO) nanoparticles (NPs) are used as a food additive Zn supplement due to the role of Zn in biological functions. They are directly added to complex processed foods or Zn-fortified functional foods. Hence, the interactions between ZnO NPs and nutritional or functional components can occur. In this study, the effects of ZnO NP interactions with two polyphenols (quercetin and rutin) on cytotoxicity, antioxidant activity, ex vivo intestinal absorption, and solubility were evaluated. Moreover, the characterization on the interactions was carried out by analyzing crystallinity, surface chemical bonding, chemical composition, and surface chemistry. The results demonstrate that the interactions caused higher cytotoxicity, ex vivo intestinal transport, and solubility of ZnO NPs than pristine ZnO NPs but did not affect antioxidant activity nor intestinal absorption of the polyphenols. The interaction effects were more evident by ZnO NPs interacted with quercetin than with rutin. The crystallinity of ZnO NPs was not influenced, but the degree of exposure of the chemical bondings, elemental compositions, and chemical group intensities on the surface of ZnO NPs, quercetin, or rutin were quenched or decreased to some extent by the interactions, especially by ZnO NPs interacted with quercetin. It is, therefore, concluded that the interactions affect chemical characteristics and surface chemical sates of ZnO NPs, quercetin, or rutin, which can cause high cytotoxicity, intestinal absorption, and solubility of ZnO NPs. Further study is required to elucidate the mechanism of action of the interactions.

Titanium dioxide (TiO₂), widely recognized as a whitening food additive, has been extensively employed in food products such as confectionery, sauces, and coffee creamers. The potential genotoxicity of TiO₂ has recently raised increasing concern, especially after the European Union prohibited its use as a food additive due to genotoxicity risks. The contradictory outcomes of in vitro and in vivo studies emphasize the necessity for more rigorous and systematic evaluation. In this study, we assessed the potential genotoxicity of food-grade TiO₂ in human intestinal cell lines and intestinal barrier models. Three distinct genotoxicity assays were conducted: the comet assay (DNA tail formation), chromosomal aberration analysis, and the micronucleus assay. The results revealed that TiO₂ exposure led to DNA damage primarily associated with oxidative stress in various intestinal cell systems at actual intake levels, regardless of metabolic activation; however, it did not trigger chromosomal aberrations or micronucleus formation. Thus, TiO₂ appears to cause in vitro genotoxic damage at the DNA level, but not at macroscopic endpoints, such as chromosomal aberrations or micronucleus formation. Further in-depth in vivo study is required to definitively determine the potential genotoxicity of TiO₂ in the food industry.