Metallic Nanoantioxidants as Potential Therapeutics for Type 2 Diabetes: A Hypothetical Background and Translational Perspectives

Figure 1

NPs can prevent diabetes-induced oxidative stress by affecting different steps of free-radical metabolism. Many NPs including all of those presented in Table 1 are able to restore the activities of superoxide dismutase (SOD) and catalase (CAT) that are often decreased under diabetic conditions. Lower oxidative damages to cellular macromolecules are achieved by decreasing the levels of superoxide anion (O₂⁻) or preventing the generation of hydroxyl radical from hydrogen peroxide (H₂O₂). Additionally, the liposome-delivered selenium and zinc oxide NPs can affect the activities of glutathione peroxidase (GPx) and glutathione reductase (GR), thereby increasing the H₂O₂ detoxification by glutathione-dependent system. Decreased concentration of oxidized glutathione (GSH) and increased activity of GPx are also observed under treatment with the gold NPs.