Serum paraoxonase 1 (PON1) is now known to be related to cardiovascular diseases (CVD). The aim of this study was to determine the relationship between PON1 concentration and high-density lipoprotein (HDL) subclasses in patients with proven CVD, cardiovascular risk factors but no CVD (CRF), and in healthy controls (control group).

Cardiovascular diseases (CVD) are disorders of the heart and blood vessels and include coronary heart disease, cerebrovascular disease, rheumatic heart disease, and other conditions. It is estimated that 17.3 million people die from CVD each year (80% of deaths occur in low- and middle-income countries), which makes it the leading cause of death in the world. Individuals at risk of CVD may experience elevated blood pressure, glucose, and lipids as well as overweight and obesity.

It is well known that atherosclerosis is the underlying cause of coronary heart disease, which is a progressive disease characterized by the accumulation of lipids and fibrous elements in the large arteries. Epidemiological studies over the past 50 years have revealed numerous risk factors for atherosclerosis. The relative abundance of the different plasma lipoproteins appears to be of primary importance, because raised levels of atherogenic lipoproteins are a prerequisite for most forms of the disease. It is well documented that high-density lipoprotein (HDL) exerts a protective effect on the cardiovascular system, and serum HDL levels have been negatively associated with the risk of coronary artery disease (CAD).

The HDL comprises a heterogeneous group of lipoproteins that are continually being remodeled and interconverted by plasma factors. In clinical practice, HDL concentration is determined as the simple concentration of cholesterol in circulating HDL particles (HDL-C); however, cholesterol is just one of more than 200 distinct molecular species of lipids in HDL and therefore does not represent a metric of atheroprotective HDL function. Indeed, HDL-C is rather a nonfunctional surrogate marker for estimating HDL particle number and size, and does not reflect the heterogeneous composition and functionality of HDL.

The HDL comprises a heterogeneous group of lipoproteins that are continually being remodeled and interconverted by plasma factors. HDL particles may be classified by decreasing size as HDL2a, HDL2b, HDL3a, HDL3b and HDL3c. These HDL subclasses have a different capacity to promote cholesterol efflux from peripheral tissues, as well as different antioxidative properties. Several proteins physically associated with HDL are involved in preventing lipid oxidation or the metabolism of lipid-hydroperoxides, including apoprotein A-1 (apoA1), lecithin, cholesterol acyltransferase (LCAT), platelet-activating factor acetylhydrolase (PAF-AH), and, in particular, paraoxonase 1 (PON1).

Human serum PON1 is a Ca²⁺-dependent HDL-associated ester hydrolase enzyme that protects low-density lipoprotein (LDL) and cell membranes from oxidation through hydrolysis of the biologically active lipid peroxides. Therefore, the antiatherogenic property of HDL is to a great extent conferred by PON1 and its capacity for preventing the formation of oxidized LDL. The PON family comprises 3 members: PON1, PON2, and PON3. They are widely expressed in mammalian tissues. PON2 is an exclusively intracellular antioxidant. PON1 and PON3 are located in the plasma associated with HDL. Both prevent LDL peroxidation in the circulation, conferring antagonistic effects against atherosclerosis development.

The antioxidant and anti-inflammatory capacity of HDL is a feature of its beneficial impact on vascular health. Reductions in its capacity could contribute to dysfunctional HDL and increased vascular risk. Defining functions of HDL subpopulations and their dysfunctions are of particular interest for refining our understanding of the role of lipoproteins in CVD. Furthermore, studies have shown that dyslipidemia may cause a decrease in HDL size as a result of depletion of large HDL and an increase in small HDL.

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