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 (TiO(2) NPs) during aqueous exposures in trout, but there are almost no data on dietary exposure to TiO(2) NPs in fish. The aim of this experiment was to observe the sub-lethal effects of dietary exposure to TiO(2) NPs in juvenile rainbow trout (Oncorhynchus mykiss). Stock solutions of dispersed TiO(2) 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 TiO(2)), 10, or 100 mg kg(-1) TiO(2) NPs diets for 8 weeks followed by a 2 week recovery period where all fish were fed the control diet. TiO(2) 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 TiO(2) 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 TiO(2) 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 TiO(2) NPs, but thiobarbituric acid reactive substances (TBARS) showed up to 50% decreases in the gill and intestine. We conclude that TiO(2) NPs behave like other toxic dietary metals where growth rate and haematology can be protected during sub-lethal exposures, but in the case of TiO(2) NPs this may be at the expense of critical organs such as the brain and the spleen.