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Biological macromolecules, including DNA, proteins, and lipids, are the primary substrates for damage by reactive oxygen species (ROS) and lipid peroxidation products (Source: NIH/NCBI, PMC4066722). ROS such as hydroxyl radicals cause direct oxidative modifications like 8-hydroxy-2'-deoxyguanosine (8-OHdG) in DNA and carbonyl groups in proteins, which can lead to mutations and loss of protein function (Source: StatPearls, Oxidative Stress). Lipid peroxidation involves the degradation of membrane lipids, producing reactive electrophiles like malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE) that form covalent adducts with proteins and DNA (Source: PubMed, PMID: 24903357). Although these macromolecules are not classical therapeutic targets like receptors or enzymes, they are the critical sites of injury in neurodegenerative diseases, cardiovascular disorders, and cancer. Pharmacological strategies, such as the use of N-acetylcysteine or edaravone, focus on scavenging ROS or inhibiting lipid peroxidation to preserve the structural and functional integrity of these essential cellular components.
Antioxidants and radical scavengers neutralize reactive oxygen species or terminate lipid peroxidation chain reactions to prevent the covalent modification and degradation of DNA, proteins, and lipids.
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