Cellular macromolecules

Cellular macromolecules, encompassing deoxyribonucleic acid (DNA), proteins, and phospholipids, serve as the collective pharmacological targets for agents that exert their effects through the induction of oxidative stress (Sies et al., 2017). Rather than interacting with a specific receptor or enzyme binding site, drugs associated with this target generate highly reactive oxygen species (ROS)—such as hydroxyl radicals, superoxide anions, and singlet oxygen—that non-specifically attack and degrade biological polymers (Hole et al., 2011). This process, often described as ROS-mediated damage, results in irreversible oxidative modifications: lipid peroxidation disrupts membrane integrity, protein carbonylation impairs enzymatic and structural functions, and DNA strand breaks lead to genomic instability and cell death (Ray et al., 2012). This broad-spectrum mechanism is primarily exploited in the use of topical antiseptics like hydrogen peroxide and benzoyl peroxide to destroy microbial pathogens, as well as in certain oncology interventions such as photodynamic therapy and specific redox-cycling chemotherapeutics (DrugBank). However, because this damage is inherently non-discriminatory, the primary therapeutic challenge lies in managing the lack of specificity, which can lead to collateral damage in healthy tissues, localized necrosis, and potential secondary malignancies due to the mutagenic nature of ROS-induced DNA damage (StatPearls).

Other names

Biological macromoleculesDNA, proteins, and lipidsOxidative stress targetsROS targets

Induction of oxidative stress through the generation of reactive oxygen species (ROS) which cause non-specific covalent modification and degradation of DNA, proteins, and lipids.