Na-Kyung Yoo

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.

(1) Background: Synthetic amorphous silica (SAS) is widely used as a food additive and contains nano-sized particles. SAS can be produced by fumed and precipitated methods, which may possess different physiochemical properties, toxicokinetics, and oral toxicity. (2) Methods: The toxicokinetics of fumed SAS and precipitated SAS were evaluated following a single-dose oral administration in rats. The tissue distribution and fate of both SAS particles were assessed after repeated oral administration in rats for 28 d, followed by recovery period for 90 d. Their 28-d repeated oral toxicity was also evaluated. (3) Results: Precipitated SAS showed higher oral absorption than fumed SAS, but the oral absorption of both SAS particles was low (<4%), even at 2000 mg/kg. Our tissue-distribution study revealed that both SAS particles, at a high dose (2000 mg/kg), were accumulated in the liver after repeated administration for 28 d, but the increased concentrations returned to normal levels at 29 d, the first day of the recovery period. A higher distribution level of precipitated SAS than fumed SAS and decomposed particle fates of both SAS particles were found in the liver at 28 d. No significant toxicological findings were observed after 28-d oral administration, suggesting their low oral toxicity. (4) Conclusions: Different manufacturing methods of SAS can, therefore, affect its oral toxicokinetics and tissue distribution, but not oral toxicity.

Food additive amorphous silicon dioxide (SiO₂) particles are manufactured by two different methods—precipitated and fumed procedures—which can induce different physicochemical properties and biological fates. In this study, precipitated and fumed SiO₂ particles were characterized in terms of constituent particle size, hydrodynamic diameter, zeta potential, surface area, and solubility. Their fates in intestinal cells, intestinal barriers, and tissues after oral administration in rats were determined by optimizing Triton X-114-based cloud point extraction (CPE). The results demonstrate that the constituent particle sizes of precipitated and fumed SiO₂ particles were similar, but their aggregate states differed from biofluid types, which also affect dissolution properties. Significantly higher cellular uptake, intestinal transport amount, and tissue accumulation of precipitated SiO₂ than of fumed SiO₂ was found. The intracellular fates of both types of particles in intestinal cells were primarily particle forms, but slowly decomposed into ions during intestinal transport and after distribution in the liver, and completely dissolved in the bloodstream and kidneys. These findings will provide crucial information for understanding and predicting the potential toxicity of food additive SiO₂ after oral intake.