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The chlorine radical (Cl•) is a highly reactive, short-lived chemical species belonging to the family of reactive halogen species (RHS) [4, 14]. In biological systems, it is primarily generated through the enzymatic activity of myeloperoxidase (MPO) in neutrophils or via the reaction of hypochlorous acid (HOCl) with superoxide, playing a role in the innate immune response by contributing to the oxidative destruction of pathogens [4, 13]. However, its extreme reactivity leads to non-specific damage of host tissues, where it induces lipid peroxidation, DNA strand breaks, and the formation of chlorinated protein adducts [15, 17]. These processes are associated with the pathogenesis of chronic inflammatory conditions, such as cardiovascular disease and asthma, as well as acute respiratory injuries resulting from chlorine gas exposure [8, 15]. While not a traditional therapeutic target like a receptor or enzyme, the chlorine radical is a focus of research as a pathological effector that can be neutralized by antioxidant scavengers such as N-acetylcysteine or vitamin C [9, 13, 17]. Its presence in tissues is often monitored using biomarkers like 3-chlorotyrosine and chloro-fatty acids to assess the extent of MPO-mediated oxidative stress [15, 16]. More recently, experimental cancer therapies have explored the controlled generation of chlorine radicals using near-infrared light and specific nano-generators as a localized 'oxidative stress' tool to induce tumor cell death, particularly in hypoxic environments where traditional oxygen-dependent reactive species production is limited [1].
Neutralization of reactive species through free radical scavenging to prevent non-specific oxidative damage to cellular biomolecules.
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