Studies on fate and toxicity of nanoalumina in male albino rats: Oxidative stress in the brain, liver and kidney

摘要

The present work aimed to evaluate the oxidative stress of nanoalumina (aluminium oxide nanoparticles, Al2O3-NPs) with a diameter < 13 nm (9.83 +/- 1.61 nm) as assessed by the perturbations in the enzymatic and non-enzymatic antioxidants as well as lipid peroxidation (LPO) in the brain, liver and kidney of male albino rats, after 2 days of single acute dose (3.9 or 6.4 or 8.5 g/kg) injection and a sublethal dose of 1.3 g/kg once in 2 days for a period of 28 days. According to two-way analysis of variance, superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) activities as well as the levels of glutathione (GSH) and LPO were significantly affected by the injected doses, organs and their interactions. On the other hand, in sublethal experiments, these parameters were affected by the experimental periods, organs and their interactions. Regression analysis confirmed that the activities of SOD, CAT, GPx and GSH levels in the brain, liver and kidney were inversely proportional with the acute doses, the experimental periods, and aluminium accumulated in these tissues, whereas the levels of LPO exhibited a positive relationship. Correlation coefficient indicated that oxidative stress mainly depends on aluminium accumulated in the studied organs, followed by injected doses and the experimental periods. In comparison with the corresponding controls, the acute and sublethal doses of Al2O3-NPs caused significant inhibition of the brain, hepatic and renal SOD, CAT, GPx activities and a severe marked reduction in the concentrations of GSH that were associated with a significant elevation in the levels of malondialdehyde (an indicator of LPO). In conclusion, our data indicated that rats injected with nanoalumina suffered from the oxidative stresses that were dose and time dependent. In addition, Al2O3-NPs released into the biospheres could be potentiating a risk to the environment and causing hazard effects on living organisms, including mammals.