Hidayet, SihoAskin, Lutfu2026-04-042026-04-0420240010-86501803-7712https://doi.org/10.33678/cor.2024.082https://hdl.handle.net/11616/108714Due to where paraoxonase-1 (PON-1)'s hydrophobic lipid domain is located, high-density lipoprotein (HDL) protects low-density lipoprotein (LDL) and the cell membranes on the outside from oxidation. It doesn't stop the formation of conjugated dienes, but it changes the products of lipid peroxidation into harmless carboxylic acids instead of aldehydes that could link to apolipoprotein B. Serum PON-1 inversely affects new events in diabetes and atherosclerotic cardiovascular disease (ASCVD). Diabetes, dyslipidemia, and inflammation decrease PON-1 activity. Human PON-1 gene ablation or overexpression in animals enhances or reduces atherosclerosis susceptibility. Unlike AII, serum amyloid A, and myeloperoxidase, apolipoprotein AI and lecithin : cholesterol acyl transferase boost PON-1 antioxidant activity. Diet and pre-existing lipid-modifying drugs may impact PON-1 activity, but specific PON-1-raising therapy is required.eninfo:eu-repo/semantics/openAccessAtherosclerotic cardiovasculardiseaseHigh-density lipoproteinParaoxonase-1Review66660861410.33678/cor.2024.0822-s2.0-85214027023Q4WOS:001384326200011Q40000-0001-7768-2562