Titanium dioxide (TiO2), a commonly used food additive, contains an appreciable fraction of particles falling in nanoscale. There is increasing concern about the potential unintended health risks associated with foodborne engineered inorganic NPs in specific susceptible populations, such as the obese. Herein, we determined the possible adverse effects of orally administered two types of TiO2 (30 nm and E171-food grade TiO2) for 12 weeks on two populations of mice, i.e., high-fat diet-treated obese mice and low-fat diet-treated non-obese mice. The results showed that administration of E171 and TiO2 NPs led to the accumulation of TiO2 in mouse kidney and liver dose-dependently, accompanied by the damage to specific cellular organelles in the renal and liver tissues. Furthermore, the TiO2 NPs profoundly modulated the mRNA levels of genes involved in oxidative damage in the liver and kidney. The effects mentioned above were more pronounced in obese mice than in non-obese mice. Dietary intake of TiO2 NPs aggravated the obesity-induced abnormality in serum biochemical parameters related to liver function and lipid metabolism. Additionally, it exacerbated the obesity-induced low-grade colonic inflammation, such as increasing inflammation-related cytokines and losing healthy colonic morphology in the colon. TiO2 NPs further reduced obesity-induced decline in the cecal levels of short-chain fatty acids. The results showed that dietary TiO2 NPs led to a significant dysbiosis of gut microbiota with stronger alterations in the obese mice than the non-obese mice. On the other hand, E171 and TiO2 NPs caused adverse effects on the reproductive systems of both male and female mice, such as the sperm and oocytes number decrease, sperm abnormality, pathological change of testes and ovaries, and abnormalities in sex hormone secretion. It is worth noting that the severity of these adverse effects appeared to be greater in the obese mice than non-obese mice. Moreover, TiO2 NPs disordered the expression of genes and proteins related to spermatogenesis, oogenesis, apoptosis, oxidative stress, and steroidogenesis in the gonads of mice, causing reproductive toxicity, especially in the obese ones. Overall, these findings provided a valuable new perspective on the potential adverse effects of foodborne TiO2 engineered NPs among obese vs. non-obese populations.

Potential adverse effects induced by foodborne titanium dioxide engineered nanoparticles

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