OxLDL ELISA

LDL (low density lipoproteins) are implicated in the development of the much dreaded atherosclerosis. But there is a more perilous condition that prevails prior to the development of atherosclerosis and which favours the formation of even smaller LDL. This is a condition called prolonged lipaemia.

Normal lipaemia follows ingestion of food. The lymph is milky and stays that way for about 4 hours before it clears up. The most important enzyme that clears a milky plasma after food ingestion (postprandial lipaemia) is lipoprotein lipase (LPL). LPL is an enzyme that appears stuck to fibrilar structures called heparan sulphate (like the heads of matchsticks).

What happens in prolonged lipaemia? In certain conditions, lipaemia remains for very long and is thus referred to as prolonged lipaemia. The plasma doesn't seem to clear up for a long long time. This is a clear sign of a danger that will be quite difficult to solve and resolve. Prolonged lipaemia is a clear sign of the inability of LPL to clear up plasma and make it clear again. Why LPL cannot clear up plasma as fast is another realm of research.

When prolonged lipaemia prevails, it gives LDL an opportunity to be made even smaller, so much smaller that they become highly penetrative, ie they easily penetrate the arterial intima and cause damage. What damage can small LDL possibly do in the underlying tissues? A lot of irreversible damages.

Small LDL are "dense" and are referred to as small dense LDL. Due to their small size (a continuum of sizes), they have a large surface area and are highly prone to oxidation. What is oxidised? What are the surface components of LDL which can be possibly oxidised? There is apolipoprotein B-100 (apoB-100) and some of the surface lipids (can be mono- or polyunsaturated fatty acids of the phospholipids). Cholesterol in the surface layer should not be changed (cholesterol itself is stable). So most probably apoB-100 and some of the unsaturated fatty acid components of the surface lipids can be oxidised. ApoB-100 itself is a huge protein that occupies practically the entire surface of small dense LDL. So it is most likely that in small dense LDL, apoB-100 are oxidised to such an extent that it renders the LDL "good enough" to be consumed by macrophages. So macrophages consume all the oxidised LDL and in turn die from over-consumption of oxidised LDL. This is referred to as the scavenger-receptor pathway, an unregulated pathway where macrophages eat up as much oxidised LDL as they possibly can till they die, becoming foam cells. Foam cells are a key cell found in atherosclerosis.

We can detect oxidised LDL (oxLDL) in the clinical research laboratory using enzyme-linked immunoassay (oxLDL ELISA). A high level of oxLDL indicates a high level of oxLDL in the plasma sample and in the real life situation. High oxLDL possibly equates to high macrophage activity in the underlying tissues of the common carotid artery (CCA), and possible changes/damages to the arterial intima, and intima media thickness (IMT).


OxLDL ELISA:
http://www.cellbiolabs.com/human-oxidized-ldl-elisa-kit
http://www.cellbiolabs.com/human-oxidized-ldl-elisa-kit
http://www.cellbiolabs.com/sites/default/files/STA-369-human-oxldl-elisa-kit.pdf

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