Gülden Burçak

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.

Involvement of neutrophils in ischemia-reperfusion injury of inguinal island skin flaps in rats

&NA; Increased production of oxygen free radicals and infiltration of neutrophils into tissue subjected to ischemia‐reperfusion have emphasized that neutrophils play a direct role in the development of injury. The present study was designed to elucidate the effect of FK506, a new immunosuppressive drug, on 11 hours of complete ischemia and reperfusion of the inguinal island skin flaps in rats. Group 1 (n = 10) control animals underwent ischemia and reperfusion and no treatment. Group 2 (n = 10) animals received FK506 0.3 mg/kg/day, and group 3 (n = 9) animals received 0.5 mg/kg/day intramuscularly for 3 days before the ischemia. The effect of the drug was evaluated by measuring flap survival and tissue malondialdehyde content and myeloperoxidase activity and also by histopathologic examination of the skin specimens taken at the 1st and 24th hour after reperfusion. The survival of flaps controlled for 7 days was found to be significantly improved in group 2 (65.0 ± 10.93 percent) and group 3 (93 ± 6.25 percent) when compared with the control group (14 ± 10.12 percent) (p < 0.04 and p < 0.0001). The tissue contents of malondialdehyde and activities of myeloperoxidase were significantly lower in groups 2 and 3 than in the control group. Three days of pretreatment with FK506 significantly reduced neutrophil infiltration in groups treated with either of the doses. These results showed that neutrophils play an important role in island flap survival associated with ischemia‐reperfusion injury. Increased neutrophil infiltration was found related with increased levels of malondialdehyde and myeloperoxidase. Flap necrosis and the increase in malondialdehyde, myeloperoxidase, and neutrophil infiltration were improved by FK506 pretreatment, a neutrophil modulating agent. (Plast. Reconstr. Surg. 102: 153, 1998.)

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.

Involvement of Neutrophils in Ischemic Injury. I. Biochemical and Histopathological Investigation of the Effect of FK506 on Dorsal Skin Flaps in Rats

The purpose of this study was to investigate the role of neutrophils in ischemic tissue injury and the possible inhibition by pretreatment with FK506, a neutrophilic modulating agent. A dorsal caudally based skin flap (3x9 cm) was used as an ischemic injury model in experimental groups. Prior to flap elevation, FK506 at doses of 0.3 mg per kilogram (group 2), 0.5 mg per kilogram (group 3), and 1.0 mg per kilogram (group 4) was given for 3 days intramuscularly. The relationship among neutrophil accumulation (histopathologically), myeloperoxidase (MPO) activity, malondialdehyde (MDA) content (biochemically) of the flap tissue, and flap survival were studied. Skin flaps showed reduced necrosis in the FK506-treated groups (p < 0.08, p < 0.0001, and p < 0.0001 respectively). The increase in accumulation of neutrophils, and MDA and MPO levels (which were induced by ischemia) observed 1 and 24 hours after flap elevation was diminished by FK506 pretreatment. The increased neutrophilic infiltration, and raised tissue MDA content and MPO activity revealed involvement of both free radical production and neutrophils in ischemia. This injury was decreased by FK506, probably by inhibition of neutrophilic chemotaxis, infiltration, and releasing factors.

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.

Oxidative damage to nuclear DNA in hyperthyroid rat liver: inability of vitamin C to prevent the damage.

The effects of hyperthyroidism on oxidative DNA damage in liver tissue and modification by vitamin C supplementation were investigated in rats. Animals were rendered hyperthyroid by administration of l-thyroxine (0.4 mg/100 g food) for 25 d. In the plasma samples, T3, T4, and thyroid-stimulating hormone (TSH) were measured by radioimmunoassay and ascorbate spectrophotometrically. Oxidative damage to hepatic nuclear DNA was determined by measuring deoxy-guanosine (dG) and 8-oxodG by high-performance liquid chromatography with diode array detector electrochemical detection (HPLC-DAD-ECD). In hyperthyroidism, 8-oxodG/ (105 dG) levels were significantly higher and plasma vitamin C levels lower than in control rats. The results of this experimental study show that oxidative damage to hepatic nuclear DNA increases in the hyperthyroid state and that vitamin C was not effective in preventing this damage.

OXIDATIVE DAMAGE TO NUCLEAR DNA IN STREPTOZOTOCIN-DIABETIC RAT LIVER

1. Accumulating evidence suggests that oxidative and glycative stress is enhanced in diabetes. Oxidative stress induces DNA damage. In the present study, we assessed the 8‐oxo‐2′‐deoxyguanosine (8‐oxodG) content of DNA, an indicator of oxidative DNA damage, in streptozotocin (STZ)‐induced diabetic (n = 21) and control rats (n = 18).