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Reactive oxygen species (ROS) and DNA radicals are highly reactive chemical entities that play dual roles in biological systems. ROS, such as superoxide, hydrogen peroxide, and hydroxyl radicals, are generated as byproducts of mitochondrial metabolism and by specific enzymes like NADPH oxidases (Ray et al., 2012, Cell Signal). While they are essential for cellular signaling and the immune oxidative burst, their excess leads to oxidative stress, causing damage to lipids, proteins, and nucleic acids. DNA radicals are formed when ROS or ionizing radiation interact with DNA, leading to base modifications and strand breaks that can result in mutations and genomic instability (Cadet & Wagner, 2013, Cold Spring Harb Perspect Biol). These processes are central to the development of various pathologies, including cancer, cardiovascular diseases, and neurodegeneration (Sies et al., 2017, Annu Rev Biochem). Pharmacological intervention typically involves antioxidant drugs like N-acetylcysteine or radioprotectors like Amifostine, which neutralize these radicals to prevent tissue damage (Pamujula et al., 2005, J Pharm Pharmacol). However, because ROS are necessary for normal physiological functions, non-specific scavenging can lead to adverse effects or reduced therapeutic efficacy.
Neutralization of reactive species through radical scavenging, electron donation, or catalytic conversion into less reactive forms.
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