Abstract
Whether the incidence of coronary heart disease (CHD) is related to a decrease in total antioxidant capacity (TAC) has not yet been completely clarified. We assessed TAC of blood serum in a group of 163 men with CHD aged 34.8–77.0 years and in 163 age-matched peers without CHD. Two spectrophotometric methods were applied to assess TAC: ferric reducing ability of serum (TAC-FRAS) and 2.2-diphenyl-1-picryl-hydrazyl (TAC-DPPH) tests. In the CHD group, multivariate analysis revealed that uric acid (UA), triglycerides, and systolic blood pressure contributed independently to the TAC-FRAS variance. TAC-DPPH was favorably predicted by UA concentration, but negatively so by current smoking and glucose levels. In men without CHD, UA was the only independent determinant of both TAC-FRAS and TAC-DPPH. Presence of CHD was not an independent predictor of TAC—observed between-group differences (higher TAC in CHD patients) disappeared after adjustment for other confounders. We conclude that UA is the main determinant of TAC of blood serum in men. TAC is not directly influenced by age or CHD but is related to several indices of overweight/obesity and laboratory measures of metabolic syndrome, especially in patients with CHD.
Highlights
An increasing number of studies focus on the role of reactive oxygen species (ROS) in the pathogenesis of premature ageing as well as of numerous civilization diseases, such as cardiovascular diseases [1,2,3]
Among the males with Coronary heart disease (CHD) 130 had a history of myocardial infarction (MI) (13 patients-twice), 137 underwent coronary catheterization, 107 underwent percutaneous transluminal coronary angioplasty (PTCA), 23 underwent coronary artery bypass surgery (CABG), 107 men demonstrated arterial hypertension (HA), and 25 displayed diabetes mellitus (DM)
In CHD patients, SBP and DBP were positively correlated with total antioxidant capacity (TAC)-Ferric reducing ability of serum (FRAS) (Figure 2) while DBP was positively correlated with uric acid (UA)
Summary
An increasing number of studies focus on the role of reactive oxygen species (ROS) in the pathogenesis of premature ageing as well as of numerous civilization diseases, such as cardiovascular diseases [1,2,3]. It has been suggested that higher antioxidant potential can protect the organism against undesirable ROS activity and prevent disease incidence [1]. The present state of knowledge on such dependence is still not complete [4]. Coronary heart disease (CHD) is the most important cause of mortality in developed countries. Numerous discrepancies have been observed in the study results and no unequivocal answer has been reached whether the incidence of CHD is related to a decrease in antioxidant potential. Relationship of CHD to antioxidant defenses may be modified by many demographic, anthropometric, physiological, and biochemical confounders and by different exogenic substances such as applied medications or cigarette smoking [5, 6]
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