Low-density lipoprotein (LDL) belongs to the lipoprotein particle family. Its size is approx. 22 nm and its mass is about 3 million daltons; but, since LDL particles contain a changing number of fatty acids, they actually have a mass and size distribution. Each native Low density lipoprotein (LDL) particle contains a single apolipoprotein B-100 molecule (Apo B-100, a protein with 4536 amino acid residues) that circles the fatty acids, keeping them soluble in the aqueous environment. In addition, LDL has a highly-hydrophobic core consisting of polyunsaturated fatty acid known as linoleate and about 1500 esterified cholesterol molecules. This core is surrounded by a shell of phospholipids and unesterified cholesterol as well as a single copy of B-100 large protein (514 kD).

Low density lipoprotein (LDL) transports cholesterol and triglycerides from the liver to peripheral tissues. LDL also regulate cholesterol synthesis at these sites. Low density lipoproteins (LDLs) transport cholesterol to the arteries and can be retained there by arterial proteoglycans starting the formation of plaques, increased levels are associated with atherosclerosis, and thus heart attack, stroke, and peripheral vascular disease. For this reason, cholesterol inside LDL lipoproteins is often called "bad" cholesterol. This is a misnomer. The cholesterol transported on Low density lipoprotein (LDL) is the same as cholesterol transported on other lipoprotein particles. The cholesterol itself is not "bad"; rather, it is how and where the cholesterol is being transported, and in what amounts over time, that causes adverse effects.

Low density lipoprotein (LDL) poses a risk for cardiovascular disease when it invades the endothelium and becomes oxidized, since the oxidized form is more easily retained by the proteoglycans. A complex set of biochemical reactions regulates the oxidation of Low density lipoprotein (LDL), chiefly stimulated by presence of free-radicals in the endothelium. Nitric oxide down-regulates this oxidation process catalyzed by L-arginine. In a corresponding manner, when there are high levels of asymmetric dimethylarginine in the endothelium, production of nitric oxide is inhibited and more Low density lipoprotein (LDL) oxidation occurs. 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 particularly low density lipoprotein (LDL), the major carrier of plasma cholesterol. Low density lipoprotein (LDL) is eliminated by macrophages. Normally, receptor-mediated uptake of Low density lipoprotein (LDL) is suppressed through down-regulation of LDL receptor expression in response to increasing cholesterol levels. Once Low density lipoprotein (LDL) is oxidized, it is still internalized by macrophages but through scavenger receptors whose expression is not controlled by cholesterol loading. The binding of oxidized LDL (oxLDL) 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 extracellular 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.

Low density lipoprotein (LDL) appears to be harmless until oxidized by free-radicals, it is postulated that ingesting antioxidants and minimizing free-radical exposure may reduce Low density lipoproteins (LDL's) contribution to atherosclerosis, though results are not conclusive.

Chemical measures of lipid concentration have long been the most-used clinical measurement, not because they have the best correlation with individual outcome, but because these lab methods are less expensive and more widely available. However, there is increasing evidence and recognition of the value of more sophisticated measurements. To be specific, Low density lipoprotein (LDL) particle number (concentration), and to a lesser extent size, have shown much tighter correlation with atherosclerotic progression and cardiovascular events than is obtained using chemical measures of total LDL concentration contained within the particles. LDL cholesterol concentration can be low, yet LDL particle number high and cardiovascular events rates are high. Also, Low density lipoprotein (LDL) cholesterol concentration can be relatively high, yet LDL particle number low and cardiovascular events are also low. If Low density lipoprotein (LDL) particle concentration is tracked against event rates, many other statistical correlates of cardiovascular events, such as diabetes mellitus, obesity, and smoking, lose much of their additive predictive power.

When a cell requires cholesterol, it synthesizes the necessary LDL receptors, and inserts them into the plasma membrane. The LDL receptors diffuse freely until they associate with clathrin-coated pits. LDL particles in the blood stream bind to these extracellular LDL receptors. The clathrin-coated pits then form vesicles that are endocytosed into the cell. After the clathrin coat is shed, the vesicles deliver the LDL and their receptors to early endosomes, onto late endosomes to lysosomes. Here the cholesterol esters in the LDL are hydrolysed. The LDL receptors are recycled back to the plasma membrane.

oxLDL ELISA Kit is intended for the quantitative determination of oxLDL in EDTA-plasma and serum.