The study investigates the oxidative modification of low-density lipoprotein (LDL) in vivo, a key component in the development of atherosclerosis. The authors present three lines of evidence supporting the presence of oxidized LDL in atherosclerotic lesions: 1. **Immunoreactivity in Atherosclerotic Lesions**: Antibodies against oxidized LDL, malondialdehyde-lysine, or 4-hydroxynonenal-lysine recognize materials in the atherosclerotic lesions of LDL receptor-deficient rabbits. 2. **Isolation of Oxidized LDL**: LDL extracted from these lesions is recognized by an antiserum against malondialdehyde-conjugated LDL. 3. **Autoantibodies in Sera**: Autoantibodies against malondialdehyde-LDL are detected in rabbit and human sera, with titers ranging from 512 to >4096. The study also demonstrates that oxidized LDL contains MDA-lysine and 4-HNE-lysine epitopes, which are present in apolipoprotein B fragments derived from aortic lesions. These findings suggest that oxidized LDL accumulates in aortic lesions and may be a source of autoantibody production, contributing to the pathogenesis of atherosclerosis.The study investigates the oxidative modification of low-density lipoprotein (LDL) in vivo, a key component in the development of atherosclerosis. The authors present three lines of evidence supporting the presence of oxidized LDL in atherosclerotic lesions: 1. **Immunoreactivity in Atherosclerotic Lesions**: Antibodies against oxidized LDL, malondialdehyde-lysine, or 4-hydroxynonenal-lysine recognize materials in the atherosclerotic lesions of LDL receptor-deficient rabbits. 2. **Isolation of Oxidized LDL**: LDL extracted from these lesions is recognized by an antiserum against malondialdehyde-conjugated LDL. 3. **Autoantibodies in Sera**: Autoantibodies against malondialdehyde-LDL are detected in rabbit and human sera, with titers ranging from 512 to >4096. The study also demonstrates that oxidized LDL contains MDA-lysine and 4-HNE-lysine epitopes, which are present in apolipoprotein B fragments derived from aortic lesions. These findings suggest that oxidized LDL accumulates in aortic lesions and may be a source of autoantibody production, contributing to the pathogenesis of atherosclerosis.