Titanium Dioxide Nanoparticles Mitigated 2,4,6- Trinitrobenzenesulfonic (TNBS) Acid Solution Induced Colitis By Downregulating NF-κB Related Transcription

BackgroundTitanium dioxide (TiO2) with nanofractions is increasingly applied in food products as a food additive, which makes consumers under the health risks of titanium dioxide nanoparticles (TiO2-NPs) oral exposure. The recent ban of food additive TiO2 (E171) use in France aggravated public controversy on safety of orally ingesting TiO2-NPs. This work aimed to determine biological effects of TiO2-NPs (38.3 ± 9.3) oral consumption (100 mg/kg bw, 10 days) on TNBS-induced colitis mice and healthy mice, and the additional vitamin E administration was also conducted to explore the possible mechanism of TiO2-NPs on colitis development.ResultsOral consumption of TiO2-NPs exacerbated oxidative stress status in colitis mice by decreasing the colonic glutathione (GSH) and total glutathione (T-GSH) levels, however, TiO2-NPs administration repaired the dysbacteriosis of colitis mice, and downregulated the Toll-like receptors (TLRs), nuclear factor kappa-B (NF-κB) signal pathway and inflammatory factor (IL-1β and TNF-α) transcription levels in colon tissue, which finally decreased the TNF-α expression level and participated in the mitigation of colitis symptoms. Moreover, further vitamin E intervention after TiO2-NPs consumption could relieve the oxidative stress status (mainly by scavenging reactive oxygen species, ROS) and the inflammatory factor over-transcription in colonic epithelium of colitis mice, but the effect of TiO2-NPs on dysbacteriosis repair would not be further changed by Vitamin E. At last, TiO2-NPs induced oxidative stress status and increased NF-κB signal transcription level in colonic epithelium, which increased daily disease activity index (DAI) score and caused mild mucosal inflammatory cell infiltrate in healthy mice. ConclusionOur present work showed that oral TiO2-NPs administration indeed induced oxidative stress and made an adverse effect on the development of colitis, but TiO2-NPs could also downregulate the NF-κB signal transduction level by repairing gut dysbacteriosis, which made a predominant role in alleviating colitis. On the other hand, it should also be noticed that TiO2-NPs oral ingestion caused potential colonic inflammation risks in healthy mice.