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Reactive oxygen species (ROS) and oxidized lipids are highly reactive chemical entities that play dual roles in human physiology, acting as essential signaling molecules at low concentrations and as potent toxins at high levels [1]. ROS, including superoxide radicals and hydrogen peroxide, are primarily generated as byproducts of mitochondrial respiration or by specialized enzymes like NADPH oxidase during immune responses [2]. Oxidized lipids, such as lipid hydroperoxides and malondialdehyde, result from the free-radical-mediated degradation of polyunsaturated fatty acids in cellular membranes, a process known as lipid peroxidation [3]. When the production of these species exceeds the capacity of endogenous antioxidant systems, oxidative stress occurs, leading to non-specific damage to DNA, proteins, and lipids [1]. This oxidative damage is a central driver in the pathogenesis of various conditions, including neurodegenerative diseases like Amyotrophic Lateral Sclerosis (ALS), atherosclerosis, and chronic inflammation [4]. Therapeutic strategies targeting these species involve non-specific chemical scavenging, where antioxidant drugs directly react with and neutralize radicals to terminate damaging chain reactions [5]. Examples of such interventions include edaravone, which is used to slow the progression of ALS by scavenging free radicals, and various vitamins that act as chain-breaking antioxidants [5, 6].
Direct chemical scavenging and neutralization of reactive oxygen species and lipid radicals to terminate oxidative chain reactions and prevent macromolecular damage.
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