Reactive oxygen species and lipid membranes

The interaction between reactive oxygen species (ROS) and lipid membranes is a fundamental biochemical process that, when uncontrolled, leads to lipid peroxidation and cellular damage. ROS, such as the hydroxyl radical and superoxide, can initiate a chain reaction by abstracting hydrogen atoms from polyunsaturated fatty acids (PUFAs) within the phospholipid bilayer, resulting in the formation of lipid hydroperoxides and reactive aldehydes like malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE) (Ayala et al., 2014; Yin et al., 2011). This process compromises membrane integrity and fluidity, eventually leading to various forms of cell death, most notably ferroptosis (Stockwell et al., 2017). Pathologically, this interaction is a key driver in neurodegenerative diseases, cardiovascular disorders, and ischemia-reperfusion injury (Gaschler & Stockwell, 2017). Therapeutic strategies targeting this process include the use of radical-trapping antioxidants (RTAs) like Ferrostatin-1 and Liproxstatin-1, which terminate the peroxidation chain, as well as iron chelators that prevent the generation of initiating radicals. Maintaining the balance between ROS production and antioxidant defense is crucial, as ROS also serve as important signaling molecules in normal physiology.

Other names

Lipid peroxidationOxidative lipid damageMembrane lipid peroxidationROS-induced lipid peroxidation

Radical scavenging and inhibition of the lipid peroxidation chain reaction through hydrogen atom transfer or transition metal chelation.