Comparison of LDL TRAP assay to other tests of antioxidant capacity; Effect of vitamin E and lovastatin treatment

Oxidized low density lipoprotein (LDL) has a major impact in the developmen t of atherosclerosis. Risk for oxidative modification of LDL is usually det ermined indirectly by measuring the capability of LDL to resist radical ins ult. We compared three different methods quantifying the antioxidative capa city of LDL ex vivo in dyslipidemic patients with coronary heart disease. P lasma samples were obtained from two double-blinded cross-over trials. The duration of all inter ventions (placebo, lovastatin 60 mg/day, RRR-alpha -t ocopherol 300 mg/day and lovastatin + RRR-alpha -tocopherol combined) was 6 weeks. The total radical capturing capacity of LDL (TRAP) in plasma was de termined using 2,2-azobis(2,4-dimethyl-valeronitrile) (AMVN) -induced oxida tion, and measuring the extinction time of chemiluminescence. TRAP was comp ared to the variables characterizing formation of conjugated dienes in copp er-induced oxidation. Also the initial concentrations and consumption times of reduced alpha -tocopherol (alpha -TOH) and ubiquinol in AMVN-induced ox idation were determined. Repeatability of TRAP was comparable to that of the lag time in conjugated diene formation. Coefficient of variation within TRAP assay was 4.4% and be tween TRAP assays 5.9%. Tocopherol supplementation produced statistically s ignificant changes in all antioxidant variables except those related to LDL ubiquinol. TRAP increased by 57%, the lag time in conjugated diene formati on by 34% and consumption time of alpha -TOH by 88%. When data of all inter ventions were included in the analyses, TRAP correlated with the lag time ( r = 0.75, p < 10(-6)), with LDL <alpha> -TOH (r = 0.50, p < 0.001) and with the consumption time of <alpha>-TOH (r = 0.58, p < 0.0001). In the baselin e data, the associations between different antioxidant variables were weake r. TRAP correlated with the lag time (r = 0.55, p < 0.001) and alpha -TOH c onsumption time (r = 0.48, p < 0.05), and inversely with apolipoprotein Al (r = -0.51, p < 0.05). Lag time at the baseline did not correlate with ubiq uinol or tocopherol parameters, or with any plasma lipid or lipoprotein lev els analyzed. Lovastatin treatment did not significantly affect the antioxi dant capacity of LDL. In conclusion, TRAP reflects slightly different prope rties of LDL compared to the lag time. Thus, LDL TRAP assay may complement the other methods used to quantify the antioxidant capacity of LDL. However , TRAP and the lag time react similarly to vitamin E supplementation.