Oxidative stress and lipoprotein oxidation

Oxidative stress is a pathological state characterized by an imbalance between the generation of reactive oxygen species (ROS) and the body's antioxidant defense systems, leading to oxidative damage of proteins, lipids, and DNA (Pizzino et al., 2017). In the context of plasma and lipoproteins, the oxidative modification of low-density lipoprotein (LDL) is a pivotal step in the initiation and progression of atherosclerosis (Steinberg, 1997). Oxidized LDL (oxLDL) triggers inflammatory responses in the vascular wall, promotes the formation of macrophage-derived foam cells, and contributes to plaque instability. Although oxidative stress is a broad biological process rather than a single molecular target, it has been the focus of numerous therapeutic strategies, including the use of antioxidants like Vitamin E and specialized drugs like Probucol (Yamashita et al., 2015). These agents aim to prevent the formation of lipid peroxides and the subsequent activation of pro-inflammatory pathways. However, the clinical translation of broad-spectrum antioxidants has been largely unsuccessful in cardiovascular trials, leading to a shift toward targeting specific ROS-generating enzymes such as NADPH oxidase or myeloperoxidase. Monitoring this process often involves measuring biomarkers like malondialdehyde or 8-isoprostane to assess systemic oxidative burden.

Other names

Lipid peroxidationLipoprotein oxidationOxidative modification of LDLSystemic oxidative stress

Pharmacological intervention involves the neutralization of reactive oxygen species (ROS), inhibition of lipid peroxidation chain reactions, or the modulation of enzymatic sources of oxidative stress such as NADPH oxidase and myeloperoxidase.