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Reactive oxygen species (ROS) and cellular antioxidant systems represent a complex network of molecules and enzymes dedicated to maintaining redox homeostasis within the cell. ROS, including superoxide radicals and hydrogen peroxide, are generated primarily as byproducts of mitochondrial respiration and by specialized enzymes like NADPH oxidases (NOX) (PMID: 28249118). While low levels of ROS act as essential signaling molecules for cell growth and survival, an imbalance—termed oxidative stress—leads to the damage of DNA, proteins, and lipids, contributing to the pathogenesis of cancer, neurodegeneration, and cardiovascular diseases (NIH, National Institute on Aging). The cellular antioxidant system counteracts this through enzymatic components such as superoxide dismutase (SOD), catalase, and glutathione peroxidase, as well as non-enzymatic antioxidants like glutathione (GSH) and vitamins C and E (StatPearls, "Antioxidants"). Pharmacological intervention typically targets this system by either directly scavenging ROS or by activating master regulatory pathways like the Nrf2-Keap1 signaling axis to upregulate endogenous defenses (PubMed, PMID: 30731145). However, therapeutic challenges include the risk of "reductive stress" and the potential for antioxidants to interfere with necessary physiological signaling or even promote the survival of certain cancer cells.
Direct scavenging of reactive species, induction of endogenous antioxidant enzymes via Nrf2 activation, and replenishment of cellular thiol pools.
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