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Reactive oxygen species (ROS) and cellular antioxidant targets represent a broad functional category of molecules and enzymes that regulate the redox state of the cell. ROS, including superoxide, hydrogen peroxide, and hydroxyl radicals, are produced during normal aerobic metabolism and serve as signaling molecules; however, their overproduction leads to oxidative stress and damage to cellular components (Sies et al., 2017, Nature Reviews Molecular Cell Biology). The cellular antioxidant system, comprising enzymes like superoxide dismutase (SOD), catalase, and glutathione peroxidase, as well as the Nrf2 transcription factor, works to neutralize these species and maintain homeostasis (Halliwell & Gutteridge, 2015, Free Radicals in Biology and Medicine). Dysregulation of this balance is a key driver in the progression of cancer, neurodegenerative diseases, and cardiovascular disorders (Murphy et al., 2011, Chemical Reviews). Therapeutic approaches involve either direct scavenging of ROS or the pharmacological activation of endogenous defense mechanisms to mitigate tissue injury and disease progression (Liby & Sporn, 2012, Nature Reviews Cancer).
Drugs targeting this system act through several mechanisms: 1) Direct scavenging of ROS (e.g., N-acetylcysteine, Vitamin C); 2) Activation of the Nrf2-KEAP1 pathway to induce endogenous antioxidant enzymes like SOD and GPx (e.g., Dimethyl fumarate, Bardoxolone methyl); 3) Mimicking the activity of antioxidant enzymes (e.g., Ebselen as a GPx mimetic); and 4) Inhibition of ROS-generating enzymes such as NADPH oxidase or xanthine oxidase (Zhang, 2006, Archives of Pharmacal Research; Liby & Sporn, 2012, Nature Reviews Cancer).
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