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Both paraoxonase activity and -SH levels are independently associated with the presence and extent of CAD. Reduced paraoxonase activity and -SH levels may play a role in the severity of coronary atherosclerosis.

A b s t r a c tBackground: The balance of oxidant and antioxidant status plays a key role in the coronary artery diseases (CAD). Thiol is one of the most important antioxidant barriers in humans, and thiol/disulphide homeostasis is a novel oxidative stress marker. Aim:We aimed to investigate the relation of serum thiol levels and thiol/disulphide homeostasis with the presence and severity of CAD. Methods:A total of 161 patients who underwent coronary angiography owing to stable angina pectoris were consecutively enrolled. They were divided into three groups. Group I -47 age-and gender-matched subjects with normal coronary angiography (control); group II -71 newly diagnosed CAD patients with noncritical stenosis; and group III -43 newly diagnosed CAD patients with critical stenosis. Serum native thiol, total thiol, and disulphide levels were measured, and disulphide/thiol ratios were calculated. Gensini scores were calculated in CAD patients.Results: While the highest thiol levels were found in group I, the lowest one was observed in group III (p < 0.001). Total and native thiol levels were significantly lower in group II than in group I (p < 0.001 for each), but they increased considerably in group II compared with group III (p = 0.031 and p = 0.028, respectively). Disulphide levels decreased in group II and III compared with group I (p < 0.001 for each). No statistically significant changes were observed in disulphide/thiol ratios (p > 0.05). Gensini scores were negatively correlated with total and native thiols, and positively with age and dyslipidaemia.Stepwise linear regression analyses showed that native thiol was an independent predictor in the final model for Gensini score. Receiver operating characteristic curve analysis demonstrated that thiol values of 310.7 or below could predict CAD with 89% sensitivity and 85% specificity (AUC = 0.918; 95% CI 0.870-0.965). Conclusions:While the disulphide/thiol ratio did not change significantly, decreased native thiol levels were associated with the presence and severity of CAD. This result indicates that the reduction of thiols may be an important factor in the development of CAD.

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Findings of this study have shown that serum prolidase activity is significantly associated with the presence and severity of CAD, and elevated serum prolidase activity might be an independent predictor of coronary atherosclerosis.

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The purpose of this study was to assess DNA damage levels in subjects with metabolic syndrome (MetS). Sixty-five subjects with MetS and 65 controls were enrolled in this study. Levels of DNA damage, total antioxidant capacity (TAC), total peroxide and oxidative stress index (OSI) were measured. We found that DNA damage levels were significantly increased [155.5 (60-264) vs. 93.2 (0-208) arbitrary units; p < 0.001] and TAC levels were significantly decreased in MetS than in control (1.34 +/- 0.27 vs. 55 +/- 0.33 mmol Trolox equivalent/l; p < 0.001). A significant falling trend in TAC levels and a significant rising trend in DNA damage values with the increase in the number of metabolic disturbances (anova p < 0.001 for both) were observed. Total peroxide (30.9 +/- 4.9 vs. 21.3 +/- 2.5 micromol H2O2/l; p < 0.001) and OSI levels [2.4 (1.3-3.8) vs. 1.4 (0.7-2.3) arbitrary units; p < 0.001] were significantly higher in the subjects with MetS than in controls. We found significant negative correlation between DNA damage and TAC levels in MetS (r = -0.656, p < 0.001) and in control (r = -0.546, p < 0.001). In multiple linear regression analysis, age, body mass index, presence of MetS and number of the components of MetS were independent predictors of log-transformed DNA damage (p < 0.05, for all). DNA damage is increased in patients with MetS. The increase in DNA damage might be occur because of the increase in the imbalance between the production of oxidants and antioxidant defences in subjects with MetS.