Paraoxonase 1 and HDL subfractions in hypercholesterolemic children and adolescents

Free Radic Biol Med. 2014 Oct:75 Suppl 1:S29. doi: 10.1016/j.freeradbiomed.2014.10.756. Epub 2014 Dec 10.

Abstract

Background: Assessment of the cardiovascular disease (CVD) risk factors in children can predict clinical manifestations of atherosclerosis in adulthood. The arylesterase (PON1-A) and lactonase (PON1-L) activities of paraoxonase 1 (PON1) and lipid parameters (Total cholesterol (TCH), VLDL-cholesterol (VLDL), triacylglycerols (TAG), HDL-cholesterol (HDL), LDL-cholesterol (LDL) and LDL- and HDL-subfractions and their mutual associations in 27 hypercholesterolemic children and adolescents were investigated.

Methods: Serum levels of TCH and TAG were determined using a Hitachi 911 analyser (Roche Diagnostics, Switzerland). LDL- and HDL-subfractions were determined by Lipoprint® system (Quantimetrix, Corp., USA). PON1-A and PON1-L activities were determined according to Gan et al. (1991) and Aviram and Rosenblat (2008).

Results: PON1-A activity was higher compared to healthy children (134.1±26.2 vs. 118.16±7.05 U/ml) and PON1-L was not different from healthy controls. Increased levels of atherogenic risk factors TCH, VLDL, IDL1 subfraction and decreased levels of the antiatherogenic IDL3 and LDL1 subfractions were observed in the hypercholesterolemic children compared to reference values. Increased levels of large HDL subfractions, comparable levels of intermediate HDL and lower levels of small HDL subfractions were observed in hypercholesterolemic children compared to healthy adults (in absence of data available for healthy children). No significant correlation between PON1-A and HDL subfractions was found. PON1-L activity positively correlated with antiatherogenic large HDL1 subfraction and negatively correlated with intermediate HDL4, 5 and 6 subfractions.

Conclusions: The findings suggest that the PON1-L activity rather than PON1-A activity play a protective role in atherosclerosis. We confirmed atheroprotective effect of large and atherogenic properties of small HDL subfractions. The intermediate HDL subfractions probably play no atheroprotective role.