کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
1968506 | 1059723 | 2016 | 5 صفحه PDF | دانلود رایگان |
• PON1 and lipid peroxides associated with abnormal lipid profile
• PON1 negatively correlated with HDL and ApoA-I
ObjectivesDecreased activity of HDL-associated paraoxonase 1 (PON1) and elevated levels of lipid peroxides together with abnormal lipid profile may prognosticate the progression of atherosclerosis. The aim of this study was to assess associations between selected oxidative stress markers (PON1, lipid peroxides) and lipid risk factors for cardiovascular disease in middle-aged subjects.Design and methodsArylesterase activity of PON1; lipid peroxides; total-, HDL-, LDL-, non-HDL-cholesterol; triglycerides; apolipoproteins A-I (ApoA-I) and B (ApoB), and lipid risk indexes were determined in serum of 75 volunteers (mean age 41.7 ± 8.2 years). Forty six volunteers were divided into normolipidemic (NL) and hyperlipidemic (HL) group.ResultsElevated levels of atherogenic cholesterol (LDL, non-HDL), lipid risk indexes (p < 0.0001), lipid peroxides (p < 0.001), and decreased activity of PON1 (p < 0.05) were found in HL group. Strong correlations between PON1 activity and HDL (r = 0.635, p = 0.0005), apolipoprotein A-I (r = 0.703, p < 0.0001), ApoA-I/ApoB ratio (r = 0.536, p = 0.004), and non-HDL/HDL ratio (r = − 0.445, p = 0.013) were observed in NL group. There was no significant association between PON1 activity and these parameters in HL group.ConclusionsSignificant abnormalities of lipid parameters, oxidative stress markers and associations between PON1, HDL and apolipoprotein A-I may influence the antioxidant and anti-atherogenic functions of HDL and result in the higher susceptibility of lipoproteins to oxidative modification. Monitoring of lipid profile together with oxidative stress markers in an asymptomatic population could be beneficial for early identification of atherosclerosis-related diseases.
Journal: Clinical Biochemistry - Volume 49, Issue 12, August 2016, Pages 868–872