ox-LDL/MDA Adduct ELISA

Lipid peroxidation is a natural process essential for cell growth. However, when the
oxidative stress overwhelms the antioxidative cell defense, the balance is disturbed
and enhanced formation of lipid peroxidation products occurs. At present, lipid peroxidation
is considered to be one of the basic mechanisms involved in the initiation
and progression of many diseases. Various studies have provided evidence that oxidative
stress resulting in lipid peroxidation and protein modification is involved in
the pathogenesis of atherosclerosis and coronary heart disease.
Lipid peroxidation products are formed during normal cell metabolism via producing
an excess of free radicals that can react with unsaturated fatty acids, in particular
low-density lipoprotein (LDL), the major carrier of plasma cholesterol. LDL is eliminated
by macrophages. Normally, receptor-mediated uptake of LDL is suppressed
through down-regulation of LDL receptor expression in response to increasing
cholesterol levels. Once LDL is oxidised, it is still internalised by macrophages but
through scavenger receptors whose expression is not controlled by cholesterol
loading. The binding of oxidised LDL (ox-LDL) is the step by which cholesterol accumulation
in macrophages is induced transforming them into lipid-loaded foam
cells. This process is accompanied by extensive cell proliferation and elaboration of
extra cellular matrix components and contributes to the genesis and progression of
atherosclerosis by promoting endothelial damage and amplifying the inflammatory
response within the vessel wall. Cholesterol-loaded macrophage foam cells are present
in the earliest detectable atherosclerotic lesions, the precursor of more complex
atherosclerosis that cause stenosis and limited blood flow. These advanced lesions
ultimately represent the sites of thrombosis leading to myocardial infarction.