Manufactured titanium dioxide nanoparticles (TiO2-NP) have been intensely applied in numerous industrial products and may be a risk for aquatic systems as they are not completely removed from domestic and industrial wastes after water treatment. This study evaluated the osmo- and ionic balance, Na+/K+-ATPase, H+-ATPase and carbonic anhydrase activities and the mitochondria-rich cells (MRC) in the gills and kidney of the Neotropical fish Prochilodus lineatus after 2 (acute) and 14 (subchronic) days of exposure to nominal 0, 1, 5, 10 and 50 mg L-1 TiO2-NP. The nominal concentrations corresponded to 0.0, 0.6, 1.6, 2.7 and 18.1 mg L-1 suspended TiO2-NP, respectively, in the water column one hour after NP introduction and were maintained for at least 24 h. Acute exposure to TiO2-NP decreased plasma osmolality and Ca2+ levels. Na+/K+-ATPase, H+-ATPase and carbonic anhydrase activities were inhibited in the gills, but not in the kidney. Total MRC density did not change in gills and kidneys. At gill surface, total MRC density decreased in fish exposed to 50 mg L-1 TiO2-NP and the total MRC fractional surface area unchanged although, there were some changes in the fractional area of MRC with apical microvilli (MRCm) and MRC with apical sponge-like structure (MRCs). MRCm was more abundant than MRCs. After subchronic exposure, there was no change in plasma osmolality, ionic balance and enzyme activities. Total gill MRC density increased in the filament epithelium and renal tubules. In the gills, MRC contacting water exhibited some adjustments. Total MRC and fractional surface area unchanged, but there was an increase of MRCs contacting water at gill surface after exposure to10 and 50 mg L-1 TiO2-NP. MRC proliferation in filament epithelium and in renal tubules as well as the increasing MRCs at gill surface may have contributed to avoid change in plasma osmolality, ionic balance and enzyme activities and suggested a cellular physiological and morphological response to restore and maintain osmotic and ionic homeostasis after subchronic exposure.
Keywords: Carbonic anhydrase; Gills; H(+)-ATPase; Kidney; Na(+)/K(+)-ATPase; Plasma ions.
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