Reactive oxygen species and oxidized sebum lipids (ROS and oxidized sebum lipids)

Reactive oxygen species (ROS) and oxidized sebum lipids are key mediators of oxidative stress and inflammation in the skin. ROS, including superoxide anions and hydroxyl radicals, are generated by both endogenous metabolic processes and exogenous factors such as ultraviolet (UV) radiation and environmental pollutants (Bowe and Logan, 2010, Clinical, Cosmetic and Investigational Dermatology). These highly reactive species initiate the peroxidation of sebum lipids, particularly squalene, leading to the formation of squalene monohydroperoxide (SQOOH) (Ottaviani et al., 2010, Journal of Investigative Dermatology). The accumulation of these oxidized lipids is a primary driver in the pathogenesis of acne vulgaris, as they promote follicular hyperkeratosis and trigger the release of pro-inflammatory cytokines like IL-1α and IL-6 via the activation of the NF-κB pathway (Saint-Leger et al., 1986, British Journal of Dermatology; Pappas, 2009, Dermato-endocrinology). Additionally, ROS and lipid peroxides contribute to skin aging and photoaging by damaging DNA, proteins, and the extracellular matrix (Briganti and Picardo, 2003, Journal of the European Academy of Dermatology and Venereology). Pharmacological intervention typically involves the use of antioxidants to scavenge ROS or inhibit lipid peroxidation, as well as retinoids like isotretinoin that reduce the production of the sebum substrate (Bowe and Logan, 2010; Briganti and Picardo, 2003).

Other names

ROSLipid peroxidesSqualene peroxidesSqualene monohydroperoxideSQOOHOxidative stress mediators

Neutralization of free radicals through electron donation, inhibition of lipid peroxidation chain reactions, and reduction of sebum substrate availability.