Redox interactions and genotoxicity of metal-based nanoparticles: A comprehensive review

Nanotechnology is a growing science that may provide several new applications for medicine, food preservation, diagnostic technologies, and sanitation. Despite its beneficial applications, there are several questions related to the safety of nanomaterials for human use. The development of nanotechnology is associated with some concerns because of the increased risk of carcinogenesis following exposure to nanomaterials. The increased levels of reactive oxygen species (ROS) that are due to exposure to nanoparticles (NPs) are primarily responsible for the genotoxicity of metal NPs. Not all, but most metal NPs are able to directly produce free radicals through the release of metal ions and through interactions with water molecules. Furthermore, the increased production of free radicals and the cell death caused by metal NPs can stimulate reduction/oxidation (redox) reactions, leading to the continuous endogenous production of ROS in a positive feedback loop. The overexpression of inflammatory mediators, such as NF-kB and STATs, the mitochondrial malfunction and the increased intracellular calcium levels mediate the chronic oxidative stress that occurs after exposure to metal NPs. In this paper, we review the genotoxicity of different types of metal NPs and the redox mechanisms that amplify the toxicity of these NPs. [Display omitted] •MNPs can increase the risk of mutagenesis and carcinogenesis causing cell death.•MNPs are able to produce ROS and free radicals through the direct/indirect integrations.•The overexpression of inflammatory mediators by MNPs can mediates the chronic oxidative stress.•ROS generation and oxidative stress induced by MNPs can lead to genotoxicity and cell death.•MNP's composition, size, shape, and surface coating determine the genotoxicity.