There has been little focus on the promising ability of metal-based nanoparticles (NPs) to kill cancer cells while sparing normal cells. Many in vitro and in vivo reports suggest that certain metal-based NPs are able to induce apoptosis and autophagy in cancer cells at specific concentrations that are not significantly toxic to non-cancerous cells. Those NPs are thought to exploit the oxidative stress conditions that prevail in cancer cells, which are largely exhausted of antioxidant ability. This review considers the induction of reactive oxygen species (ROS) by metal-based NPs as a mechanism for the specific killing of cancer cells. The article concomitantly provides a comprehensive description of the important pathways and molecules leading to programmed cell death (PCD), which occurs mainly via apoptosis, autophagy, and necroptosis. The PCD pathways are followed as ROS-burdened cancer cells succumb to ROS-generating metal-based NPs. Exploration of nanotechnology interventions in anticancer therapy demands further research into the mechanism of intracellular induction of ROS by metal-based NPs. Furthermore, the induction of ROS by NPs should be strictly controlled if ROS-based therapy is to become a paradigm in cancer therapy.
Keywords: Antioxidants; Cancer therapy; Metal-based nanoparticles; Programmed cell death; Reactive oxygen species.