Serum Oxidized Low Density Lipoprotein (oxLDL) levels are increased in hyperlipidemic subjects but not associated with LDL size

Hamed Al-Riyami, Mohsin Al-Saleh and Jumana Saleh

Biochemistry department, Faculty of Medicine, Sultan Qaboos University, Muscat, Oman

It is well established that hyperlipidemia is associated with formation of smaller, denser LDL particles (sdLDL) in plasma. Many studies suggested that sdLDL particles have increased atherogenicity compared to larger buoyant subtypes. Several reasons were suggested in this regard: I) sdLDL particles have decreased receptor-mediated uptake by peripheral tissues due to their altered structure. II) sdLDL particles are easily trapped in the sub-endothelial space predisposed by injury to the arterial wall. In vitro studies suggest that small LDL particles are more prone to oxidation in the sub-endothelial space than the normal large buoyant LDL particles. Oxidation of LDL (oxLDL) is believed to be a key factor in atherosclerosis progression. Macrophages recognize OxLDL forming “foam cells” that develop into fatty streaks predisposing plaque formation initiating atherosclerosis.

AIM: To examine if increased sdLDL in hyperlipidemia is associated with increased serum oxLDL levels by measuring oxLDL in hypertriglyceridemic and control subjects, and to determine the association serum oxLDL with different lipid profile measures.

This study showed that mean LDL size was smaller, and ox-LDL levels were significantly higher in the hypertriglycemic group compared with the normotriglycemic control group. However, there was no significant correlation of LDL size or lipid parameters with oxLDL levels in plasma. Interestingly, apoB showed the strongest association with oxLDL excluding the rest of the metabolic factors, as predictors of oxLDL.

These results suggest that the higher “number” of LDL particles, as reflected by apoB levels (one apoB molecule per LDL particle), exceed size, or cholesterol content in determining increased oxLDL levels in serum probably as a result of increased “number’ of small LDL particles entering the sub-endothelial space and their ability to escape in their oxidized form into the serum. Although size may be a determinant of oxidation vulnerability, it does not appear as a predicting factor in this study. It may be also that apoB protein is more prone to malonaldeyde induced oxidation compared to apoA1 and other lipoprotein constituents.

These results support the notion that the number of particles, rather than cholesterol content , contribute to increased atherosclerosis risk probably due to increased availability of apoB molecules for oxidation.

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