Dietary exposure to titanium dioxide nanoparticles in rainbow trout, (Oncorhynchus mykiss): no effect on growth, but subtle biochemical disturbances in the brain

Our laboratory recently reported gut pathology following incidental ingestion of titanium dioxide nanoparticles (TiO₂ NPs) during aqueous exposures in trout, but there are almost no data on dietary exposure to TiO₂ NPs in fish. The aim of this experiment was to observe the sub-lethal effects of dietary exposure to TiO₂ NPs in juvenile rainbow trout (Oncorhynchus mykiss). Stock solutions of dispersed TiO₂ NPs were prepared by sonication without the use of solvents and applied to a commercial trout diet. Fish were exposed in triplicate to either, control (no added TiO₂), 10, or 100 mg kg⁻¹ TiO₂ NPs diets for 8 weeks followed by a 2 week recovery period where all fish were fed the control diet. TiO₂ NPs had no impact on growth or nutritional performance, and no major disturbances were observed in red or white blood cell counts, haematocrits, whole blood haemoglobin, or plasma Na⁺. Ti accumulation occurred in the gill, gut, liver, brain and spleen during dietary TiO₂ exposure. Notably, some of these organs, especially the brain, did not clear Ti after exposure. The brain also showed disturbances to Cu and Zn levels (statistically significant at weeks 4 and 6; ANOVA or Kruskal–Wallis, P < 0.05) and a 50% inhibition of Na⁺K⁺-ATPase activity during TiO₂ NP exposure. Na⁺K⁺-ATPase activity was unaffected in the gills and intestine. Total glutathione in the gills, intestine, liver and brain were not affected by dietary TiO₂ NPs, but thiobarbituric acid reactive substances (TBARS) showed up to 50% decreases in the gill and intestine. We conclude that TiO₂ NPs behave like other toxic dietary metals where growth rate and haematology can be protected during sub-lethal exposures, but in the case of TiO₂ NPs this may be at the expense of critical organs such as the brain and the spleen.