Arzu Seven

Lipid, protein, DNA oxidation and antioxidant status in rheumatoid arthritis.

OBJECTIVES To investigate lipid, protein, DNA oxidation and antioxidant status in blood and synovial fluid of rheumatoid arthritis (RA) patients and to determine the importance of oxidative stress parameters in reflecting disease activity. DESIGN AND METHODS 20 RA patients and 15 healthy controls were included. Lipid peroxidation (thiobarbituric acid reactive substances (TBARS), lipid hydroperoxide, and conjugated diene), protein oxidation (carbonyl and thiol), DNA oxidation (8-OHdG) and antioxidant status markers (glutathione (GSH), glutathione peroxidase (GSH Px), superoxide dismutase (CuZn SOD), and catalase) were determined in blood and synovial fluid. RESULTS TBARS (p<0.001), lipid hydroperoxide (p<0.001), conjugated diene (p<0.001), carbonyl (p<0.001) and 8-OHdG (p<0.01) levels were significantly higher; thiol (p<0.01) and GSH levels (p<0.01) and GSH Px (p<0.001) and CuZn SOD (p<0.01) activities were significantly lower in blood of RA patients. TBARS (p<0.001), lipid hydroperoxide (p<0.001), conjugated diene (p<0.01), carbonyl (p<0.001) and 8-OHdG (p<0.05) levels were significantly higher, catalase activity (p<0.001) significantly lower in synovial fluid of RA patients. CONCLUSIONS Increased lipid, protein and DNA oxidation markers and impaired antioxidant status confirm the role of oxidative stress in the pathogenesis of RA. Lipid peroxidation markers can serve as surrogate markers for disease activity.

Evaluation of oxidative stress parameters in blood of patients with laryngeal carcinoma.

OBJECTIVES In this study, plasma lipid peroxidation as assessed by thiobarbituric acid reactive substances and erythrocyte antioxidant status markers namely CuZn superoxide dismutase, glutathione peroxidase, glutathione and plasma levels of vitamin C and E were investigated in 20 patients with larygneal carcinoma and 15 healthy controls. DESIGN AND METHODS Lipid peroxidation was observed to be significantly higher (0.01 > p > 0.001) in the larynx carcinoma group in comparison to the healthy controls. Both stage I + 11 and stage III carcinoma patients were observed to have significantly higher thiobarbituric acid reactive substances than the control group. A significant difference was found in plasma vitamin E level between the control group and stage I + 11 and stage III carcinoma patients (p < 0.01, 0.05 > p > 0.02, respectively). RESULTS Our findings reveal the presence of increased lipooxidative damage in laryngeal carcinoma patients, but no change with respect to the endogenous antioxidant components-GSH, GSH Px, and CuZn SOD.

Lipid peroxidation and antioxidant status in experimental animals: Effects of aging and hypercholesterolemic diet

Effects of aging and hypercholesterolemic diet on lipid peroxidation and antioxidant status were investigated in rats. The rats were divided into four groups of ten: Group I; young rats receiving standard lab chow; Group II; young rats on hypercholesterolemic diet (0.4 g/rat/day); Group III; aged rates receiving standard lab chow; Group IV; aged rats on hypercholesterolemic diet (0.4 g/rat/day). Plasma lipid peroxidation end product level was determined as thiobarbutiric acid reactive substances (TBARS). Plasma cholesterol concentration was analyzed by a kinetic enzymatic method. Erythrocyte superoxide dismutase (CuZn SOD), glutathione peroxidase (GSH Px) and glutathione (GSH) levels were determined spectrophotometrically. Cholesterol values were found to be significantly high (p < 0.001), TBARS (0.05 > p > 0.02) and GSH (p < 0.001) levels significantly low in aged rats in comparison with young rats. Hypercholesterolemic diet induced significant increases in GSH (p < 0.001) and CuZn SOD (p < 0.001) levels, whereas a significant decrease in GSH Px activity (0.05 > p > 0.02) was observed in aged rats. In young rats hypercholesterolemic diet caused a significant increase in both GSH and CuZnSOD levels. Our results indicate an imbalance between radical production and destruction in favour of prooxidant conditions in the young rats and the induction by hypercholesterolemic diet of the antioxidative response in erythrocytes.

Antioxidant status in experimental hyperthyrodism: effect of vitamin E supplementation

Free radical-mediated oxidative stress has been implicated in the genesis and exacerbation of degenerative diseases. In view of the role of oxidative processes in hyperthyroidism, in this study, we investigated the antioxidant status of erythrocytes in experimental hyperthyroidism and the effect of vitamin E supplementation on defense systems. Our findings of significantly increased T4 and T3 and undetectable TSH values in thyroxine administered rats confirmed the establishment of hyperthyroidism. Superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and glutathione (GSH) values were found to be significantly increased in hyperthyroid rats in comparison to the control group. Vitamin E supplementation to hyperthyroid rats induced a significant decrease in GSH-Px activity and a significant increase in GSH level. These findings show that hyperthyroidism increases the components of the antioxidant system in the erythrocytes. Furthermore, vitamin E supplementation reduces the burden of oxidative stress in hyperthyroidism.

Lipid Peroxidation and Antioxidant State after Laparoscopic and Open Cholecystectomy

OBJECTIVE To measure the amount of lipid peroxidation and erythrocyte antioxidation in patients undergoing laparoscopic and open cholecystectomy and healthy controls. DESIGN Non-randomised study. SETTING University hospital, Istanbul. SUBJECTS 31 patients, of whom 14 underwent open and 17 laparoscopic cholecystectomy, and 15 healthy controls. INTERVENTIONS Heparinised blood samples were taken from the patients immediately after operation and from the healthy controls. MAIN OUTCOME MEASURES Lipid peroxidation index as expressed by thiobarbituric-acid-reactive substances (TBARS) and components of the erythrocyte antioxidant defence system, namely reduced glutathione, reduced glutathione peroxidase (glutathione-Px) and CuZn superoxide dismutase (CuZn SOD) in patients undergoing open or laparoscopic cholecystectomy and healthy controls. RESULTS All 4 variables were significantly higher in the cholecystectomy groups than in controls (p < 0.001), and laparoscopic cholecystectomy caused significantly less oxidative stress than the open operation (p < 0.001). CONCLUSION Both types of cholecystectomy cause oxidative stress and lead to an adaptive antioxidant response in the body. However; both oxidative stress and the antioxidant response are more pronounced after traditional open cholecystectomy.

INFLUENCE OF PROPYLTHIOURACIL TREATMENT ON OXIDATIVE STRESS AND NITRIC OXIDE IN BASEDOW DISEASE PATIENTS

Oxidative stress parameters and nitric oxide (NO) values were determined in 27 newly diagnosed Basedow patients before and after 1 mo of propylthiouracil (PTU) therapy and in 15 healthy controls. Basedow patients exhibited increased triiodothyronine (T3) and thyroxine (T4

Biochemical Evaluation of Oxidative Stress in Propylthiouracil Treated Hyperthyroid Patients. Effects of Vitamin C Supplementation

Abstract In this study the impact of vitamin C supplementation on oxidative damage as assessed by thiobarbituric acid reactive substances and markers of antioxidant status: namely Cu/Zn superoxide dismutase, glutathione peroxidase, glutathione reductase and glutathione were investigated in 24 hyperthyroid patients under propylthiouracil therapy (3×100 mg/day) for five days and in 15 healthy controls. Ascorbic acid (1000 mg/day) was given as a supplement for 1 month to both the patients and controls during the study period. Heparinised blood samples were taken at the beginning and the end of one month ascorbic acid supplementation. Comparison of the hyperthyroid patients with the controls revealed higher lipid peroxidation (p<0.001), higher Cu/Zn superoxide dismutase activity (p<0.001), higher glutathione level (p<0.001) and lower glutathione reductase activity (p<0.001). Vitamin C supplementation to hyperthyroid patients caused significant increases in glutathione concentration (p<0.001) and glutathione peroxidase activity (p<0.001), whereas there were significant decreases in glutathione reductase (p<0.001) and Cu/Zn superoxide dismutase activities (p<0.01). Thiobarbituric acid reactive substances and thiobarbituric acid reactive substances/glutathione ratio were significantly decreased (p<0.01). Vitamin C supplementation to euthyroid controls caused significant increases in glutathione concentration (p<0.001) and glutathione peroxidase and Cu/Zn superoxide dismutase activities (p<0.001), whereas there was a significant decrease in glutathione reductase (p<0.001). The thiobarbituric acid reactive substances/glutathione ratio was significantly decreased (p<0.05). Our findings reveal the potentiation of antioxidant status and a relief in oxidative stress in both propylthiouracil treated hyperthyroid patients and controls in response to vitamin C supplementation.

Oxidative stress in heart tissue of hyperthyroid and iron supplemented rats.

This study was designed to investigate the effect of hyperthyroidism and/or iron supplementation on cardiac oxidative stress parameters--the lipid peroxidation end product glutathione (GSH), glutathione peroxidase (GSH-Px), and superoxide dismutase (CuZnSOD)--in rats. In plasma, ferritin as an indicator of iron status and glutamate oxaloacetate transaminase (GOT) as an indicator of damage to the heart tissue were analyzed. Our findings show that hyperthyroidism increased lipooxidative damage as reflected by higher lipid peroxidation end product levels and elevated antioxidant defense parameters--GSH and GSH-Px. Iron supplementation per se does not affect oxidative stress parameters studied in the euthyroid state. Although iron increased lipid peroxidation in the hyperthyroid state, this effect was less than that seen in euthyroidism. Iron supplementation to hyperthyroid rats significantly lowered plasma ferritin levels, suggesting increased iron elimination with consequently reduced oxidative stress.

Osteoprotegerin, leptin and IL-6: Association with silent myocardial ischemia in type 2 diabetes mellitus

Background: Diabetic patients often exhibit severe, asymptomatic coronary artery disease (CAD). The relationship between osteoprotegerin (OPG), inflammatory markers and silent myocardial ischemia remains to be elucidated. Methods: We recruited 45 type 2 diabetic patients and 33 healthy controls and assessed them for silent myocardial ischemia (SMI) by myocardial perfusion imaging. Patient blood was tested for OPG, IL-6 and leptin concentrations. Results: OPG, leptin and IL-6 levels were found significantly elevated in diabetic patients (p < 0.001, p < 0.01, p < 0.05). Based on our classification of presence/absence of SMI in our diabetic group, we found that there was a significant association between SMI and the biomarkers IL-6 (p < 0.001), leptin (p < 0.001) and OPG (p < 0.05). In multivariate regression analyses, OPG was found to be significantly related to diabetes mellitus and to SMI. Age, sex and smoking increased the association between OPG and SMI. Conclusion: High OPG, leptin and IL-6 levels are associated with the presence and severity of SMI in type 2 diabetic patients.

Oxidized LDL and anti‐oxLDL antibody levels in peripheral atherosclerotic disease

Objective. Oxidative modification of LDL (oxLDL) is important in atherogenesis and is proposed as a useful marker for identifying patients with coronary artery disease. Antibody to oxLDL (oxLDL Ab) is detected in human sera, although its biological significance is not well established. We aimed to measure oxLDL and oxLDL Ab in peripheral atherosclerotic disease (PAD) patients, and to examine the relation between them in an attempt to understand the role of oxLDL Ab. Total risk of atherosclerosis was estimated using the global risk assessment score (GRAS) calculated on the basis of age, total cholesterol, HDL cholesterol (HDL‐Chol), diabetes, hypertension and smoking. Material and methods. Twenty‐one patients aged 63.05±9.13 years, diagnosed by peripheric angiography as PAD, and 21 healthy controls aged 47.67±13.61 years took part in the study. Total LDL and HDL cholesterol levels were determined by enzymatic methods. Levels of circulating oxLDL were measured by monoclonal antibody 4E6‐based competition ELISA. IgG class oxLDL Ab titre was measured by ELISA. Results. Compared to healthy controls, PAD patients had higher levels of oxLDL (p<0.05), oxLDL Ab (p<0.05), LDL cholesterol (LDL‐Chol) (p<0.05), total cholesterol (p<0.05) and lower HDL‐Chol (p<0.05). OxLDL was found to be positively correlated with total cholesterol (r = 0.471, p<0.05) and LDL‐Chol (r = 0.614, p<0.01) and GRAS (r = 0.435, p<0.05) and negatively with HDL‐Chol (r = −0.459, p<0.05), but not with oxLDL Ab in PAD patients. Conclusions. These findings might indicate that high LDL‐Chol levels influence the oxidation of LDL and that oxLDL is a possible marker of PAD. However, the role of oxLDL Ab in atherosclerosis remains controversial.