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Reactive oxygen species (ROS) generation and scavenging systems represent a complex network of enzymes and molecules that maintain cellular redox homeostasis [1]. ROS, including superoxide anions, hydrogen peroxide, and hydroxyl radicals, are produced primarily as byproducts of mitochondrial respiration or by specific enzymes like NADPH oxidases (NOX) [2]. To prevent oxidative damage to lipids, proteins, and DNA, cells employ scavenging systems consisting of enzymatic antioxidants such as superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPX), as well as non-enzymatic antioxidants like glutathione [3]. While basal levels of ROS are essential for physiological signaling processes, an imbalance—termed oxidative stress—is a hallmark of numerous pathologies, including cancer, neurodegeneration, and cardiovascular diseases [4]. Therapeutic strategies often aim to either bolster scavenging capacity or selectively inhibit ROS-generating enzymes, though achieving precise control without disrupting vital signaling remains a significant challenge [5].
Neutralization of free radicals, induction of endogenous antioxidant enzymes via Nrf2 activation, and inhibition of pro-oxidant enzymes such as NADPH oxidase or xanthine oxidase [5].
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