Lipoprotein oxidation is involved in the genesis of atherosclerosis. In chr
onic renal failure (CRF), oxidative stress is enhanced because of an imbala
nce between pro-oxidant and antioxidant systems. Oxidative modifications of
low-density lipoproteins (LDLs) occur not only at the level of lipid moiet
y, but also of protein moiety. We have shown that oxidation of LDL by hypoc
hlorous acid (HOCl) in vitro, reflecting increased myelo-peroxidase activit
y in vivo, leads to modifications of apoliproteins such that the latter in
turn are capable of triggering macrophage nicotinamide adenine dinucleotide
phosphate-oxidase activation. These oxidative changes of LDL protein moiet
y, if shown to occur to a significant extent in uremic patients in vivo, ma
y represent an important alternative pathway in the pathogenesis of atherom
atous lesions.