Co-exposure to titanium dioxide nanoparticles (NpTiO(2)) and lead at environmentally relevant concentrations in the Neotropical fish species Hoplias intermedius

Growing production and utilization of titanium dioxide nanoparticles (NpTiO(2)) invariably lead to their accumulation in oceans, rivers and other water bodies, thus increasing the risk to the welfare of this ecosystem. The progressive launch of these nanoparticles in the environment has been accompanied by concern in understanding the dynamics and the toxic effect of these xenobiotic in different ecosystems, either on their own or in tandem with different contaminants (such as organic compounds and heavy metals), possibly altering their toxicity. Nevertheless, it remains unknown if these combined effects may induce damage in freshwater organisms. Therefore, this study aimed to analyze the consequences caused by NpTiO(2), after a waterborne exposure of 96 h to a Neotropical fish species Hoplias intermedius, as well as after a co-exposure with lead, whose effects for fish have already been well described in the literature. The characterization of NpTiO(2) stock suspension was carried out in order to provide additional information and revealed a stable colloidal suspension. As a result, NpTiO(2) showed some genotoxic effects which were observed by comet assay in gill, kidney and brain cells. Also, the activity of brain acetylcholinesterase (AChE) has not changed, but the activity of muscle AChE decreased in the group exposed only to PbII. Regarding the hepatic antioxidant system, catalase (CAT) did not show any change in its activity, whereas that of superoxide dismutase (SOD) intensified in the groups submitted only to PbII and NpTiO(2) alone. As for lipid peroxidation, there was a decrease in the group exposed to the NpTiO(2) alone and to the co-exposed group (NpTiO(2)+PbII). As far as metallothionein is concerned, its concentration rose for the co-exposed group (NpTiO(2)+PbII) and for the group exposed to PbII alone. Overall, we may conclude that NpTiO(2) alone caused DNA damage to vital tissues. Also, some impairment related to the antioxidant mechanism was described but it is probably not related to the DNA damage observed, suggesting that the genotoxic effect observed may be due to a different mechanism instead of ROS production.