Background: The in vivo kinetics of nanoparticles is an essential to understand the hazard of nanoparticles. Here, the absorption, distribution, and excretion patterns of titanium dioxide (TiO₂) and zinc oxide (ZnO) nanoparticles following oral administration were evaluated. Methods: Nanoparticles were orally administered to rats for 13 weeks (7 days/week). Samples of blood, tissues (liver, kidneys, spleen, and brain), urine, and feces were obtained at necropsy. The level of Ti or Zn in each sample was measured using inductively coupled plasma-mass spectrometry. Results: TiO₂ nanoparticles had extremely low absorption, while ZnO nanoparticles had higher absorption and a clear dose-response curve. Tissue distribution data showed that TiO₂ nanoparticles were not significantly increased in sampled organs, even in the group receiving the highest dose (1041.5 mg/kg body weight). In contrast, Zn concentrations in the liver and kidney were significantly increased compared with the vehicle control. ZnO nanoparticles in the spleen and brain were minimally increased. Ti concentrations were not significantly increased in the urine, while Zn levels were significantly increased in the urine, again with a clear dose-response curve. Very high concentrations of Ti were detected in the feces, while much less Zn was detected in the feces. Conclusions: Compared with TiO₂ nanoparticles, ZnO nanoparticles demonstrated higher absorption and more extensive organ distribution when administered orally. The higher absorption of ZnO than TiO₂ nanoparticles might be due to the higher dissolution rate in acidic gastric fluid, although more thorough studies are needed.

Background: Hazard identification for risk assessment of nanoparticles (NPs) is mainly composed ofin vitrocell-based assays andin vivoanimal experimentation. The rapidly increasing number and functionalizations of NPs makesin vivotoxicity tests undesirable on both ethical and financial grounds, creating an urgent need for development ofin vitrocell-based assays that accurately predictin vivotoxicity and facilitate safe nanotechnology.Methods: In this study, we used 9 different NPs (CeO₂, TiO₂, carbon black, SiO₂, NiO, Co₃O₄, Cr₂O₃, CuO, and ZnO). As anin vivotoxicity endpoint, the acute lung inflammogenicity in a rat instillation model was compared with thein vitrotoxicity endpoints comprising cytotoxicity, pro-inflammatory cytokine expression, or haemolytic potential. Forin vitroassays, 8 different cell-based assays were used including epithelial cells, monocytic/macrophage cells, human erythrocytes, and combined culture.Results: ZnO and CuO NPs acting via soluble toxic ions showed positive results in most of assays and were consistent with the lung inflammation data. When compared inin vitroassays at the same surface area dose (30 cm²/mL), NPs that were low solubility and therefore acting via surface reactivity had no convincing activity, except for CeO₂NP. Cytotoxicity in differentiated peripheral blood mononuclear cells was the most accurate showing 89% accuracy and 11% false negativity in predicting acute lung inflammogenicity. However, the haemolysis assay showed 100% consistency with the lung inflammation if any dose, having statistical significance was considered positivity. Other cell-basedin vitroassays showed a poorer correlation within vivoinflammogenicity.Conclusions: Based on the toxicity mechanisms of NPs, two different approaches can be applied for prediction ofin vivolung inflammogenicity. Mostin vitroassays were good at detecting NPs that act via soluble ions (i.e., ZnO and CuO NP). However,in vitroassays were limited in detecting NPs acting via surface reactivity as their mechanism of toxicity, except for the haemolysis assay.

The compound 6:2 chlorinated polyfluorinated ether sulfonate (F-53B), a replacement for perfluorooctanesulfonate (PFOS) in the electroplating industry, has been widely detected in numerous environmental matrices, human sera, and organisms. Due to regulations that limit PFOS use, F-53B use is expected to increase. Therefore, in this study, we performed a subchronic oral toxicity study of F-53B in Sprague Dawley (SD) rats. F-53B was administered orally once daily to male and female rats for 28 days at doses of 5, 20, and 100 mg/kg/day. There were no toxicologically significant changes in F-53B-treated rats, except in the thyroid gland. However, F-53B slightly reduced the serum concentrations of thyroid hormones, including triiodothyronine and thyroxine, compared with their concentrations in the vehicle group. F-53B also induced follicular hyperplasia and was associated with increased thyroid hormone biosynthesis-associated protein expression. These results demonstrate that F-53B is a strong regulator of thyroid hormones in SD rats as it disrupts thyroid function. Thus, caution should be exercised in the industrial application of F-53B as an alternative for PFOS.