Efeito da exposição a nanopartículas de dióxido de titânio (NP-TiO2) em curimbatá (Prochilodus lineatus, Teleostei): aspectos fisiológicos, bioquímicos e morfológicos

Abstract

This project aims to investigate the TiO2-NP toxicity after acute (48 h) and subchronic (14 d) exposure using hematology, biochemical and morphological biomarkers in P. lineatus. TiO2- NP only caused blood disorders after subchronic exposure and did not show geno- and neurotoxicity, but they affected the immunity of P. lineatus. In gills, acute exposure to TiO2- NP decreased reactive oxygen species (ROS) formation and increased glutathione (GSH) levels, while subchronic exposure increased ROS and GSH levels and inhibited superoxide dismutase (SOD) activity. In kidney, acute exposure to TiO2-NP did not cause ROS formation and changes in antioxidant enzymes activity, but increased GSH and lipid peroxidation (LPO) levels. Subchronic exposure inhibited catalase activity in kidney tissue, but redox balance was not impaired. In the liver, acute exposure to TiO2-NP did not alter the antioxidant enzymes activity and metallothionein levels, but ROS formation decreased and GSH levels increased. After subchronic exposure, SOD activity did not change, but GPx and GST activity and GSH levels increased in the liver. Additionally, morphological damage was found in gills, liver and kidneys. Gills showed slight changes after acute exposure and slight to moderate changes after subchronic exposure. In kidney and liver tissue, degenerative changes and necrosis occurred after TiO2-NP exposure. TiO2-NP also inhibited enzymes of osmoregulation activity in gills after acute exposure, but had no effect after subchronic exposure and in renal tissue. Mitochondria-rich cells (MRC) density increased in gill filaments and renal tissue after subchronic exposure, while plasma osmolality decreased and calcium ions (Ca2+) concentration increased after acute exposure. Osmolality, however, was restored after subchronic exposure. These results suggest that GSH played an important role in preventing ROS formation. In liver and kidneys, TiO2-NP can cause moderate to severe tissue damage the long term, may lead to organ dysfunction, as considerable portion of the organ was reduced due to necrosis and degenerative damage. Osmoregulatory system impairment was caused after acute exposure to TiO2-NP, but no after subchronic exposure, probably due to proliferation of new MRC and morphological changes in gills. However, these morphological changes may hinder gases exchange and osmotic and ionic balance in the long term.