Copper-induced plasma
lipoprotein oxidation resistance has usually been determined in separated
low density lipoprotein (
LDL) fractions, that do not contain water-soluble
antioxidants present in blood plasma. The aim of this study was to find the main determinants of the measurements of
copper-induced
lipid oxidation resistance (lag time) in whole serum and plasma total
peroxyl radical trapping capacity (TRAP) in a population sample of smoking (n = 25) or non-smoking (n = 26) middle aged men at high risk of
cardiovascular diseases. Smokers had significantly lower plasma
ascorbic acid values, but only slightly lower
alpha-tocopherol,
beta-carotene and serum
urate values than non-smokers. Plasma
ascorbic acid concentration explained 23.5% of the lag time variation (standardized regression coefficient beta = 0.48; P = 0.004) in smokers and 5.6% in non-smokers. Serum
urate concentration was the strongest determinant of lag time in non-smokers (beta = 0.64, P < 0.001). In addition,
serum albumin,
lipid standardized
alpha-tocopherol and serum
high density lipoprotein (
HDL) cholesterol entered the multivariate regression mode for lag time. For plasma TRAP, only
urate and
ascorbic acid entered the multivariate regression model. Lag times in serum and in isolated
very low density lipoprotein (VLDL) and
LDL fraction did not correlate, but the maximal rate of these reactions correlated significantly. These results confirm that lipid peroxidation resistance in serum or plasma are associated with
ascorbic acid,
urate,
alpha-tocopherol,
albumin and HDL concentrations. The measurement of
lipid oxidation resistance in whole serum might be more physiological than in isolated
lipoprotein fraction, as the effects of water-soluble
antioxidants are not artificially removed.