Nitric oxide-mediated induction of superoxide dismutase and catalase genes, and altered expression of glutathione-dependent genes to defend against the TiO2 NP-induced oxidative stress in primary hepatocytes of air-breathing catfish, Clarias magur

The main objectives of the present investigation were to elucidate the possible induction of antioxidant genes under the TiO2 NP-induced oxidative stress and the potential involvement of endogenously produced nitric oxide (NO) in its antioxidant strategies in primary hepatocytes of air-breathing magur catfish (Clarias magur). As expected, exposure to TiO2 NPs led to (1) more ROS production as evidenced by a sharp rise of hydrogen peroxide (H2O2) and malonaldehyde (MDA) associated with cellular damage as evidenced by the increase of lactate dehydrogenase (LDH) leakage from hepatocytes, (2) induction of superoxide dismutase (SOD), catalase (CAT), followed by induction of different glutathione-related genes such as glutathione peroxidase (GPx), glutathione-Stransferase (GST), and thioredoxin glutathione reductase (TGR) with the induction of activities of corresponding enzymes, and (3) more production of NO associated with induction of inducible nitric oxide synthase (iNOS) activity and its corresponding gene. However, inhibition of NO production in primary hepatocytes using certain inhibitors in the presence of TiO2 NPs, resulted in (1) more generation of H2O2 and MDA, (2) inhibition of SOD and CAT genes expression in primary hepatocytes with more leakage of LDH leakage into the culture media. Thus, it can be contemplated that stimulation NO production plays a vital role in inducing the SOD-CAT system to handle the problems associated with enhanced TiO2 NP-induced ROS production and subsequent oxidative stress in magur catfish as a unique adaptational strategy. However, the NO-mediated induction of glutathionerelated antioxidant genes under TiO2 NP-induced oxidative stress is yet to be established.