We hypothesized that redox analysis could provide sensitive markers of the oxidative pathway associated to the presence of an increasing number of cardiovascular risk factors (RFs), independently of type. We classified 304 subjects without cardiovascular disease into 4 groups according to the total number of RFs (smoking, hypertension, hypercholesterolaemia, hyperhomocysteinaemia, diabetes, obesity, and their combination). Oxidative stress was evaluated by measuring plasma total and reduced homocysteine, cysteine (Cys), glutathione, cysteinylglycine, blood reduced glutathione, and malondialdehyde. Twenty-seven percent of subjects were in group 0 RF, 26% in 1 RF, 31% in 2 RF, and 16% in ≥3 RF. By multivariable ordinal regression analysis, plasma total Cys was associated to a higher number of RF (OR = 1.068; 95% CI = 1.027–1.110, P = 0.002). Total RF burden is associated with increased total Cys levels. These findings support a prooxidant effect of Cys in conjunction with RF burden, and shed light on the pathophysiologic role of redox state unbalance in preclinical atherosclerosis.
To investigate whether GGT (gamma-glutamyltransferase) is associated to specific redox patterns. GGT, total and reduced aminothiols and malondialdehyde, were measured in 150 subjects (83 males, 48 (39-56) years), with none, one or more risk factors. By univariable analysis GGT was positively associated with age (p =0.001), male gender (p <0.001), risk factor number (p <0.001), ACE-inhibitors (p =0.008), anti-platelet agents (p =0.029), atherothrombotic events (p =0.001), glucose (p =0.013), malondialdehyde (p =0.029), plasma total cysteine (p =0.046) and inversely associated with plasma total glutathione (p =0.001). By multivariable analysis only male gender (p <0.001), risk factor number (p <0.001) and glutathione (p <0.001) were independently associated with GGT activity. These findings suggest that an ongoing redox imbalance, in terms of decreased plasma glutathione, is associated with raised GGT activity in subjects with a greater risk factor burden.
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