Reactive oxygen species and lipid peroxidation processes (ROS/LPO)

Reactive oxygen species (ROS) and lipid peroxidation processes encompass the generation of highly reactive oxygen-derived molecules and the subsequent oxidative degradation of lipids, particularly polyunsaturated fatty acids in cell membranes (Ayala et al., 2014). ROS, including superoxide radicals and hydrogen peroxide, are produced during mitochondrial respiration and by enzymes like NADPH oxidase, playing dual roles as essential signaling molecules and agents of cellular damage (Sies et al., 2017). When ROS levels exceed the capacity of antioxidant defense systems, they initiate lipid peroxidation, a self-propagating chain reaction that compromises membrane integrity and produces reactive aldehydes such as malondialdehyde (Pizzino et al., 2017). These processes are implicated in the etiology of diverse pathologies, including Alzheimer's disease, atherosclerosis, and various cancers, where oxidative damage drives cell death and inflammation. Pharmacological intervention typically involves the use of scavengers, such as edaravone or N-acetylcysteine, or inhibitors of ferroptosis to prevent the catastrophic accumulation of lipid peroxides. However, the therapeutic application is complicated by the necessity of maintaining basal ROS levels for normal physiological functions like immune defense and intracellular signaling.

Other names

Oxidative stressLipid peroxidationReactive oxygen speciesOxidative lipid damageROS generation

Antioxidants and radical scavengers neutralize reactive oxygen species or terminate lipid peroxidation chain reactions by donating electrons or hydrogen atoms to reactive intermediates, thereby preventing oxidative damage to cellular components (Ayala et al., 2014; Pizzino et al., 2017).