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.