neurological disorders and oxidative toxic stress: a role of metal nanoparticles

conclusions the nps-induced ots may increase the pro-inflammatory responses. on the other hand, administration of antioxidants such as nac and vitamin c and e prior to exposure to metal nps significantly decreases ots conditions. evidence acquisition here, a nanotechnology approach is evaluated using nps in human neuronal protection against ots. it may be wide therapeutic applications in the case of acute and/or chronic neurodegenerative disorders related to ots. results in the brain of mice treated with nanosize tio2, a significant association was found between the ability to induce the production of ros and metabolic stress in intracellular environments and inflammatory responses in mice brai. the large surface area of agnps may efficiently facilitate the radicals generation including ros in various organs. the production of ros may cause dna damage, cellular apoptosis, and activation of the mitogen activated protein kinase (mapk) pathways which is responsible for regulating many cellular processes. prolonged and excessive ots may contribute to the activation of transcription factors and genes responsible for inflammation responses such as nf-κb and ap-1. furthermore, ots may contribute to the onset of neurodegenerative diseases. the ability of cuonps to generate ots in vitro studies has been demonstrated; however, information on the neurotoxicity of the cuonps in vivo is low. context oxidative stress is a hallmark of many types of neuropathology disorders and underlying mechanism in several neurodegenerative diseases and brain injuries. the cns is particularly susceptible to oxidative toxic stress (ots). reactive oxygen spices are the basic inflammation and neurotoxicity mediators in ischemia/reperfusion injuries. the purpose of the present review is to provide an overview of some nanoparticles (nps) in developing ots conditions and neurological disorders.