Role of Oxidative Stress and Inflammatory Response in Subchronic Pulmonary Toxicity Induced by Nano Nickel Oxide in Rats

The aim of present study was to investigate the subchronic pulmonary toxicity induced by nano nickel oxide (NiO) and its potential mechanism in rats. Male Wistar rats received intratracheally instilled nano NiO (0.015, 0.06 and 0.24 mg/kg b. w), micro NiO (0.24 mg/kg b. w) and normal saline (control) twice a week for 6 weeks. Serum and lung tissue were collected to quantify biomarkers of inflammatory response and oxidative stress as well as HO-1 and MT-1 mRNA expression. The general toxicity was assessed through slow increase of body weight and decreased food utilization efficiency. The levels of IL-6, TNF-alpha and cytokine-induced neutrophil chemoattractants (CINCs, including CINC-1, CINC-2 alpha beta and CINC-3) increased while the level of IL-10 decreased in serum. Results showed the increased levels of OH, LPO and 8-OHdG, the decreased levels of CAT, GSH-Px and T-AOC, consistent with the upregulation of HO-1 and downregulation of MT-1 mRNA expression in lung tissue. The lung coefficient to body weight increased in 0.24 mg/kg nano NiO group. Lung hematoxylin and eosin staining showed inflammatory infiltration and particles deposition in NiO treated rats. The results of this subchronic study indicated that the lung lesion induced by nano NiO could be related to oxidative stress and inflammatory response.