Biochemical targets of drugs mitigating oxidative stress via redox-independent mechanisms.

摘要: Acute or chronic oxidative stress plays an important role in many pathologies. Two opposite approaches are typically used to prevent the damage induced by reactive oxygen and nitrogen species (RONS), namely treatment either with antioxidants weak oxidants that up-regulate endogenous antioxidant mechanisms. This review discusses options for third pharmacological approach, amelioration of ‘redox-inert’ compounds, which do not inactivate RONS but inhibit basic mechanisms leading their formation (i.e. inflammation) help cells cope toxic action. The present study describes biochemical targets drugs mitigating acute animal models ischemia–reperfusion injury N-acetyl-p-aminophenol overdose. In addition pro-inflammatory molecules, include protein kinases transcription factors involved regulation energy metabolism cell life/death balance, proteins regulating mitochondrial permeability transition, endoplasmic reticulum unfolded response, nuclear receptors such as peroxisome proliferator-activated receptors, isoprenoid synthesis. data may identification mitigators will be effective human disease on top current standard care.