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The chlorine oxide radical (ClO•), also known as the chlorine monoxide radical, is a highly reactive and short-lived chemical species belonging to the reactive chlorine species (RCS) family [1, 14, 21]. While extensively characterized in atmospheric chemistry and advanced oxidation processes for water treatment, its biological significance arises from its role as a mediator of oxidative stress and immune-mediated host defense [4, 12, 23]. In the human body, ClO• is primarily generated as a downstream byproduct of the enzyme myeloperoxidase (MPO), which produces hypochlorous acid (HOCl) that can subsequently react with other radicals or undergo photolysis to yield ClO• [12, 14]. As a powerful one-electron oxidant, the radical assists in the inactivation of pathogens by damaging their cell walls and genetic material; however, its persistent or excessive production leads to the non-selective oxidation of host proteins, lipids, and DNA [4, 15, 23]. This collateral oxidative damage is a key factor in the pathogenesis of chronic inflammatory conditions, such as atherosclerosis and neurodegenerative disorders [4, 23]. From a pharmacological perspective, ClO• is not considered a traditional therapeutic target (e.g., a receptor or enzyme), but it is a target for scavenging by antioxidants like N-acetylcysteine and for prevention through the therapeutic inhibition of MPO [14, 21].
Neutralization via radical scavenging and one-electron reduction; inhibition of enzymatic production through myeloperoxidase (MPO) antagonism.
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