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  • Polyunsaturated fatty acid components of


    Polyunsaturated fatty 5,7-dihydroxychromone components of brain are more prone to oxidative attack, an event called lipid peroxidation. Consistent with previous findings on neurotoxicity [58,59], colistin sulphate increased the level of MDA in the brain of rats. The elevated MDA, a consequence of overwhelmed antioxidants, could lead to distortion in membrane organization, functional loss and modification of proteins and DNA bases [60]. Furthermore, fragmented DNA (%) decreased significantly in the brain of colistin sulphate treated rats. This indicates oxidative damage of the nuclei and genetic material of brain cells.
    Declaration of conflicting interests
    Introduction Silver has been used as an antibiotic since the ancient time, and it has had greater applications in medicine, optics, sensing, paintings and cosmetics (Chen and Schluesener, 2008, McShan et al., 2014). The exceptional characteristics of nanosilver particles (AgNP) as biocide have made them the largest and fastest growing class of manufactured nanomaterials in commercial applications (Pinto et al., 2010). The Nanodatabase ( listed 353 consumer products containing AgNP in 2017. The use of AgNP is proliferating, and it is expected that the environment will be increasingly exposed to these materials. When AgNP arise the aquatic media, they release Ag+ that is one of the most toxic metal forms for organisms in natural water systems (Ratte, 1999). As well as most nanoparticles, AgNP physico-chemistry suggests they are likely to aggregate depending on concentration and type of organic matter, and solids in suspension (Handy et al., 2008). Unfortunately, precise estimations of the emissions from silver-containing materials are hampered by lack of available information about content and form of the silver in the products (Geranio et al., 2009). The release of AgNP can happen at any stage of the product life-cycle: production, transport, storage, usage and disposal (Ribeiro et al., 2014). The predicted environmental concentrations for AgNP in the aquatic environment are in the low µg L−1 or ng L−1 (Gottschalk et al., 2013). Therefore, environmental concerns have risen due to there is evidence that AgNP induce deleterious effects in aquatic systems as well in aquatic life (Choi et al., 2010). Many investigations have proved that fish are valuable organisms to asses toxicological effects caused by AgNP (Govindasamy and Rahuman, 2012, Lee et al., 2012; Wu and Zhou, 2012; Massarsky et al., 2013; Bacchetta et al., 2016; Martin et al., 2016). Particularly, the gills constitute a multifunctional organ (respiration, ionoregulation, acid-base regulation, nitrogenous waste excretion) accounting for well over 50 per cent of the total surface area of the animal. They are the major site of uptake for most waterbone toxicants and also the first, and most important, site of toxic impact for many of them. Essential physiologic processes are performed by the gills and they are sensitive to both structural and biochemical disturbance of the branchial epithelium (Schlenk and Benson, 2001). Nanosilver can be taken up by many different cells and become internalized inside the cell. High levels of Ag accumulation from AgNP has been reported in the liver, gills, kidney, intestine and muscle of fish (Scown et al., 2010; Wu and Zhou, 2012; Bacchetta et al., 2016; Martin et al., 2016). The main deleterious effect reported by AgNP is oxidative stress due to they enter the cell through diffusion or endocytosis and generate reactive oxygen species, leading to damages to proteins and acids inside the cell, and finally inhibition of cell proliferation (McShan et al., 2014). Lipid peroxidation, impairment of antioxidant enzyme system and glutathione depletion caused by AgNP has been reported in gills and liver of many fish species (Farmen et al., 2012; Govidasamy and Rahuman, 2012; Wu and Zhou, 2012; Griffitt et al., 2013; Martin et al., 2016). Regarding a higher level of damage, it has been demonstrated that AgNP caused histopathological alterations in liver, muscle and gills of fish (Wu et al., 2010, Govindasamy and Rahuman, 2012, Wu and Zhou, 2013), including mucus cells proliferation (Lee et al., 2012). Finally, other responses such as metallothioneins induction, DNA damage and gene expression have been associated with toxicity generated by AgNP (Choi et al., 2010, Gagné et al., 2012, Martin et al., 2016).