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

Reactive oxygen species (ROS) generation and lipid peroxidation are interconnected biochemical processes involving the production of highly reactive oxygen-derived molecules and the subsequent oxidative degradation of cellular lipids (Ayala et al., 2014, PMC3924987). ROS, such as superoxide and hydroxyl radicals, are natural byproducts of mitochondrial metabolism and enzymatic activities, playing dual roles as signaling molecules and agents of cellular damage (Halliwell & Gutteridge, 2015). When ROS levels exceed the capacity of antioxidant defense systems, they initiate lipid peroxidation, a chain reaction that damages polyunsaturated fatty acids in cell membranes (Gaschler & Stockwell, 2017, Nature Chemical Biology). This process leads to the formation of toxic aldehydes like malondialdehyde and 4-hydroxynonenal, which can further damage proteins and DNA (StatPearls, Lipid Peroxidation). This cascade is a primary driver of ferroptosis, a regulated form of cell death, and contributes significantly to the pathogenesis of neurodegenerative diseases, cardiovascular disorders, and cancer. Therapeutic strategies focus on neutralizing ROS through scavengers or inhibiting the enzymatic sources of ROS to preserve membrane integrity and cellular function.

Other names

Oxidative stressLipid peroxidationROS productionPeroxidation of polyunsaturated fatty acidsFerroptosis-related lipid peroxidation

Drugs targeting these processes typically act as radical scavengers, antioxidants, or inhibitors of pro-oxidant enzymes to prevent the chain reaction of lipid degradation and neutralize reactive oxygen species.