Oxidant and antioxidant levels and DNA damage in tuberous sclerosis.

OBJECTIVE: The pathogenesis of inherited diseases is thought to involve oxidative stress and the associated DNA damage, which are also implicated in many other conditions including cancer. Tuberous sclerosis is a genetic disease with autosomal dominant inheritance pattern that is characterized by the development of hamartomas in multiple organ systems. Oxidative stress and the related DNA damage are also likely to play a significant role in the pathogenesis of this condition. Thus, our study aimed to assess total oxidant-antioxidant level, oxidative stress index and DNA damage in patients diagnosed with tuberous sclerosis. METHODS: The study included 30 patients with tuberous sclerosis between the ages of 0 and 16 years. The control group consisted of 29 age-matched healthy children. Blood samples obtained from each subject were centrifuged to separate the sera. The Total Antioxidant Status (TAS) and Total Oxidant Status (TOS) were measured in serum samples with a Thermo Scientific Multiscan plate reader (FC, 2011-06, USA) at wavelengths of 240 nm and 520 nm, respectively. The measured TAS and TOS values were used to calculate the Oxidative Stress Index (OSI). In addition, the Comet Assay Method was used to determine DNA damage in the samples. Data were analyzed using SPSS software. RESULTS: Patients with tuberous sclerosis complex (TSC) and controls were compared with respect to TAS, TOS, and OSI. TAS was significantly lower (p < 0.01), while TOS and OSI were significantly higher (p < 0.01, for both) in patients as compared to controls. In addition, patients had significantly higher DNA damage as shown by the Comet Assay (p < 0.01). CONCLUSIONS: Increased oxidative stress and DNA damage may contribute to the pathogenesis of tuberous sclerosis.

Oxidative Stress Status in Childhood Obesity: A Potential Risk Predictor.

BACKGROUND Childhood obesity characterized by excessive fat in the body is one of the most serious health problems worldwide due to the social, medical, and physiological complications. Obesity and associated diseases are triggering factors for oxidative stress and inflammation. The aim of this study was to explore the possible association between childhood obesity and inflammatory and oxidative status. MATERIAL AND METHODS Thirty-seven obese children and 37 healthy controls selected from among children admitted to BLIND University Paediatrics Department were included in the study. Anthropometric measurements were performed using standard methods. Glucose, lipid parameters, CRP, insulin, total oxidant status (TOS), total anti-oxidant status (TAS) levels, and total thiol levels (TTL) were measured in serum. HOMA index (HOMA-IR) were calculated. The differences between the groups were evaluated statistically using the Mann-Whitney U test. RESULTS Body mass index was significantly higher in the obese group (median: 28.31(p<0.001). Glucose metabolism, insulin, and HOMA-IR levels were significantly higher in the obese group (both p<0.001). Total cholesterol, HDL cholesterol, LDL cholesterol, and triglyceride levels were significantly higher in the obese group (p<0.001). TAS (med: 2.5 µmol Trolox eq/L (1.7-3.3)) and TOS (med: 49.1 µmol H2O2 eq/L (34.5-78.8)) levels and TTL (med: 0.22 mmol/L (0.16-0.26)) were significantly higher in the obese group (p=0.001). CRP levels showed positive correlation with TOS and negative correlation with TTL levels (p=0.005, r=0.473; p=0.01, r=-0.417; respectively). TTL levels exhibited negative correlation with TOS levels (p=0.03, r=-0.347). CONCLUSIONS In conclusion, obese children were exposed to more oxidative burden than children with normal weight. Increased systemic oxidative stress induced by childhood obesity can cause development of obesity-related complications and diseases. Widely focussed studies are required on the use of oxidative parameters as early prognostic parameters in detection of obesity-related complications.

The predictive value of M30 and oxidative stress for left ventricular remodeling in patients with anterior ST-segment elevation myocardial infarction treated with primary percutaneous coronary intervention.

BACKGROUND: Left ventricular (LV) remodeling is an important pathophysiological event that develops following acute myocardial infarction and causes LV systolic dysfunction. Mechanisms such as apoptosis, necrosis, and oxidative stress play an important role in LV remodeling. OBJECTIVES: This study aimed to determine the relationship between the development of LV remodeling and the apoptosis marker M30 in patients with anterior ST-segment elevation myocardial infarction (STEMI) who were treated with primary percutaneous coronary intervention (PCI). MATERIALS AND METHODS: This retrospective study included 255 consecutive patients (210 men, 45 women, mean age 54.9±11.8 years) with anterior STEMI who were treated with primary PCI. Blood samples were obtained from each patient at admission and 24 h after admission for measurements of M30, M65, oxidative parameters, and biochemical parameters. Transthoracic echocardiography was performed in each patient within 24 h of infarction and 6 months after infarction. LV remodeling was defined as greater than or equal to 20% increase in end-diastolic volume 6 months after primary PCI. The patients were divided into two groups on the basis of 6 months of post-primary PCI follow-up findings: LV remodeling group and non-LV remodeling group. RESULTS: In all, 60 patients received LV remodeling and 195 did not receive LV remodeling at 6 months after primary PCI. Total oxidative stress, M30 and M65 levels, and the oxidative stress index were significantly higher and the total antioxidant capacity and M65/M30 ratio were lower in the LV remodeling group (P<0.05, for all). Brain natriuretic peptide, M30, and oxidative stress index were independent predictors of LV remodeling (P<0.05 for all). Receiver operating characteristic curve analysis showed that the M30 cut-off value for predicting LV remodeling was 144.9 U/l (80% sensitivity and 77% specificity, P<0.001). CONCLUSION: In patients with anterior STEMI treated with primary PCI, the apoptosis marker M30 might be useful for predicting LV remodeling and subsequent LV systolic dysfunction.

Oxidative Stress and Spontaneous Reperfusion of Infarct-Related Artery in Patients With ST-Segment Elevation Myocardial Infarction.

In the pathogenesis of atherosclerosis, oxidative stress plays a major role in plaque instability, rupture, and erosion, which subsequently leads to thrombus formation and causes total infarct-related artery (IRA) occlusion. We investigated the relationship between spontaneous reperfusion (SR) of IRA and oxidative stress in patients with anterior ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention. A total of 341 consecutive patients with anterior STEMI were prospectively included in the present study. Patients were divided into 2 groups according to their thrombolysis in myocardial infarction (TIMI) flow grade: SR group (66 patients, TIMI flow 3) and non-SR group (275 patients, TIMI flow 0-2). On multivariate logistic regression analysis, oxidative stress index (ß = 0.868, 95% confidence interval [CI] = 0.806-0.934, P < .001), neutrophil to lymphocyte ratio, uric acid, mean platelet volume, Killip 2 to 4 class, and initial SYNTAX score were independently associated with SR. Oxidative stress as well as inflammation may play a pivotal role in the pathogenesis of SR in patients with STEMI.

The effect of upper gastrointestinal system endoscopy process on serum oxidative stress levels.

Some authors have investigated the effects of oxidative stress in some process such as undergoing laparoscopic. However, the effect of upper gastrointestinal system endoscopy process on oxidative stress is unclear. We evaluated the short-term effect of upper gastrointestinal system endoscopy process on oxidative stress. Thirty patients who underwent endoscopy process and 20 healthy controls were enrolled in the prospective study. Serum total antioxidant capacity and total oxidant status measurements were measured before and after endoscopy process. The ratio percentage of total oxidant status to total antioxidant capacity was regarded as oxidative stress index. Before endoscopy process, serum total antioxidant capacity levels were higher, while serum total oxidant status levels and oxidative stress index values were lower in patients than controls, but this difference was not statistically significant (all, p > 0.05). After endoscopy process, serum total antioxidant capacity and total oxidant status levels were significantly higher in patients than before endoscopy process (both, p < 0.05). However, oxidative stress index values were slight higher in patients but this difference was not statistically significant (p > 0.05). We observed that serum TAC and TOS levels were increased in patients who underwent endoscopy process after endoscopy process. However, short-time upper gastrointestinal system endoscopy process did not cause an important change in the oxidative stress index. Further studies enrolling a larger number of patients are required to clarify the results obtained here.

Serum paraoxonase activity, total thiols levels, and oxidative status in patients with acute brucellosis.

It is well known that paraoxonase-1 (PON1) activity may decrease during the course of infection and inflammation. The aim of this study was to investigate serum PON1 activity, oxidative status, and thiols levels in patients with acute brucellosis. In addition, we investigated the PON1 phenotype in patients with acute brucellosis. Thirty patients with acute brucellosis and 35 healthy controls were enrolled. Serum paraoxonase and arylesterase activities, thiols levels, lipid hydroperoxide levels, total antioxidant capacity (TAC), total oxidant status (TOS) and oxidative stress index (OSI) were determined. Serum basal and salt-stimulated paraoxonase-arylesterase activities, TAC levels and thiols levels were significantly lower in patients with acute brucellosis than controls (for all, p < 0.05), while LOOH levels, TOS levels, and OSI values were significantly higher (for all, p < 0.05). We concluded that oxidative stress is increased, while serum PON1 activity is decreased in patients with acute brucellosis. These results indicate that lower PON1 activity is associated with oxidant-antioxidant imbalance.

Gamma glutamyl transferase activity is independently associated with oxidative stress rather than SYNTAX score.

BACKGROUND: Gamma glutamyl transferase (GGT) is involved in the pathophysiologic process of coronary atherosclerosis. GGT activity plays a role in the catabolism of glutathione which is known as one of the major antioxidants. However, there is a lack of research on direct examination of relevance between serum GGT activity with systemic oxidative stress. OBJECTIVES: We aimed to investigate the relationship between GGT activity with systemic oxidative stress markers and the extent and complexity of coronary artery disease (CAD) assessed with SYNTAX score in stable CAD. METHODS: Measurements were obtained from 359 patients with stable CAD (Mean age = 57.7 ± 10.1 years). The patients were divided into two groups according to the median GGT level (GGT < median group < 22 and GGT > median group ≥ 22). Angiography was performed and SYNTAX score was calculated in all patients. Oxidative stress markers (total oxidant status [TOS], total antioxidant capacity [TAC] and oxidative stress index [OSI]) were measured in all patients. RESULTS: While SYNTAX score and oxidative stress markers such as TOS and OSI have been increased, TAC was decreased in GGT > median group compared with GGT < median group (p < 0.05, for all). GGT activity was independently associated with diabetes (ß = 0.106, p = 0.015) and OSI (ß = 0.556, p < 0.001) in multiple linear regression analysis. However, the independent association between GGT activity and SYNTAX score was not found in present study (ß = 0.063, p = 0.238). CONCLUSION: In stable CAD, increased GGT activity within the normal range is associated with increased oxidative stress rather than increased extent and complexity of CAD.

Oxidative stress and paraoxonase 1 activity predict contrast-induced nephropathy in patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention.

Reactive oxygen species have been implicated in the pathogenesis of contrast-induced nephropathy (CIN). We investigated the relationship between CIN with paraoxonase 1 (PON-1) activity and oxidative stress markers (total antioxidant status [TAS], total oxidant status [TOS], and oxidative stress index [OSI]) in patients with anterior ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention; 289 consecutive patients with STEMI were prospectively included. The patients were divided into 2 groups: CIN (n = 69) and non-CIN (n = 220). Activity of PON-1 and TAS levels were significantly lower and OSI and TOS levels were significantly higher in patients with CIN compared to the non-CIN group (P < .05, for all). On multivariate logistic regression analysis, PON-1 activity and OSI as well as the amount of contrast medium and diabetes were independent predictors for CIN in patients with anterior STEMI. Activity of PON-1 and oxidative stress may play a role in the pathogenesis of CIN.

Gamma Glutamyl Transferase Activity is Associated With Both Paraoxonase Activity and Aortic Stiffness in Hypertensive Patients.

BACKGROUND: We aimed to investigate relationship between gamma glutamyl transferase (GGT) activity with paraoxonase 1 (PON1) activity and aortic stiffness (AS) parameters such as pulse wave velocity (PWV) and augmentation index (AIx). METHODS: Measurements were obtained from 324 patients with newly diagnosed essential hypertension (mean age: 55.0 ± 8.2 years). The patients were divided into two groups according to their median GGT values. PWV and AIx were calculated using the single-point method via the Mobil-O-Graph® ARCsolver algorithm. RESULTS: PWV, Aix, and high-sensitive C-reactive protein (hs-CRP) values were higher and PON1 activity values were lower in GGThigh group compared with GGTlow group (P < 0.05, for all). Multiple linear regression analysis showed that GGT activity was independently associated with PWV (ß = 0.496, P < 0.001) and PON1 activity (ß = -0.343, P < 0.001) as well as hs-CRP (ß = 0.334, P < 0.001). CONCLUSION: These results may support that increased GGT activity would be associated with both impaired antioxidant system and increased AS in hypertensive patients.

Paraoxonase-1 activity and oxidative stress in patients with anterior ST elevation myocardial infarction undergoing primary percutaneous coronary intervention with and without no-reflow.

BACKGROUND: Reperfusion and ischemic injuries are pathogenetic mechanisms of no-reflow. Oxidative stress plays a critical role during ischemia as well as during the reperfusion phase following ST elevation myocardial infarction (STEMI). We sought to investigate the relationship between no-reflow with paraoxonase-1 (PON-1) activity and oxidative stress markers (total antioxidant capacity (TAC), total oxidant status (TOS), oxidative stress index (OSI), lipid hydro-peroxide (LOOH)) in patients with anterior STEMI undergoing primary percutaneous coronary intervention (PCI). METHODS: In this study, 319 consecutive anterior STEMI patients undergoing primary PCI were prospectively included (mean age 56.5 ± 12.5 years). The patients were divided into two groups as normal flow (n = 231) and no-reflow (n = 88) groups. Serum PON-1 activity was measured spectrophotometrically. TAC and TOS levels were determined by using an automated measurement method. LOOH levels were measured by ferrous oxidation with xylenol orange assay. RESULTS: PON-1 activity and TAC levels were significantly lower and TOS, OSI and LOOH levels were significantly higher in patients with no-reflow compared to normal flow group (p < 0.05, for all). On multivariate logistic regression analysis, PON-1 activity (ß = 0.976, 95% CI = 0.962-0.990, p = 0.001) and OSI (ß = 1.094, 95% CI = 1.042-1.148, p < 0.001) as well as diabetes, infarction time, thrombus score and initial SYNTAX score were independently associated with no-reflow. CONCLUSION: In patients with no-reflow compared with normal flow, oxidants are increased, while serum PON-1 activity and antioxidants are decreased. This result shows that increased oxidative stress has a role in the pathogenesis of no-reflow.

Paraoxonase (PON1) activity in patients with subclinical thoracic aortic atherosclerosis.

High density lipoprotein (HDL), a powerful antioxidant, protects low density lipoprotein (LDL) particles against oxidative stress. By limiting LDL oxidation, HDL plays an important role in preventing atherosclerosis (AS). The antioxidant effect of HDL is mostly associated with the paraoxonase (PON1) activity. It has been known that increased aortic intima-media thickness (IMT) is an earlier marker AS than carotid IMT. We aimed to investigate the association between thoracic aortic IMT and serum PON1 activity. We studied 133 patients (mean age: 46.3 ± 8 years) who underwent transesophageal echocardiography (TEE) for various indications. The measurements of thoracic aortic IMT by TEE are classified into four grades (1, 2, 3 and 4). Serum PON1 activity was measured spectrophotometrically. Oxidative and anti-oxidative status was evaluated by measuring serum lipid hydroperoxide (LOOH), total anti-oxidant status (TAS). Serum PON1 activity was progressively decreasing from grade 1 IMT to grade 4 IMT (p < 0.001). However, serum LOOH was significantly lower and TAS was significantly higher in patients with grade 1 when compared with other grades. In multiple linear regression analysis, IMT was independently correlated with PON1 activity (ß = -0.495, p < 0.001), TAS level (ß = -196, p < 0.009), age (ß = 0.145, p = 0.029) and LDL cholesterol level (ß = 0.169, p = 0.009). Decreased PON1 activity was independently associated with the extent of thoracic AS. PON1 activity may play a role in pathogenesis of thoracic AS besides age, TAS and LDL cholesterol levels.

Ferrous sulfate (Fe2+) had a faster effect than did ferric polymaltose (Fe3+) on increased oxidant status in children with iron-deficiency anemia.

OBJECTIVE: The purpose of this study was to compare the total oxidant and antioxidant effect of different oral iron preparations in children with iron-deficiency anemia (IDA). METHODS: A total of 65 children with IDA were randomized to receive 5 mg Fe/kg/d iron (II) sulfate (Fe(2+) group, n=33) or iron (III)-hydroxide polymaltose complex (Fe(3+) group, n=32); healthy controls (n=28) were also included in the study. Serum total thiol (-SH), total antioxidant capacity (TAC), total oxidant status (TOS), oxidative stress index (OSI), and hematological profile were evaluated at the baseline and on day 8 and day 30 of the therapy. RESULTS: Serum TOS and OSI levels were significantly higher and total -SH and total antioxidant capacity levels were significantly lower in the study groups at the beginning of therapy than in the controls (P>0.001). In multivariate analysis, after controlling for multiple confounding factors, on days 8 and 30, serum TOS and OSI levels were not different in the Fe(3+) group, whereas they were significantly reduced in the Fe(2+) group (P≤0.033). CONCLUSIONS: Serum total oxidant status was significantly increased in children with IDA, and Fe(2+) was highly effective in correcting elevated oxidative status.

Paraoxonase-1 activity and oxidative status in patients with knee osteoarthritis and their relationship with radiological and clinical parameters.

BACKGROUND: The aim of this study was to investigate serum paraoxonase-1 (PON1) activity and oxidative/anti-oxidative status in knee osteoarthritis (OA), and evaluate their relationship using radiological and clinical parameters. MATERIALS AND METHODS: The study population comprised 127 patients with knee OA and 107 healthy volunteers. Patients with knee OA were divided into four subgroups according to the Kellgren-Lawrence (K&L) grading scale. In addition, each patient was clinically evaluated by the Western Ontario and McMaster University Osteoarthritis Index (WOMAC). Serum PON1 activity was measured spectrophotometrically. Oxidative status was assessed by measuring serum lipid hydroperoxide (LOOH) and total oxidant status (TOS). Anti-oxidative status was assessed by measuring serum free sulfydryl groups (-SH = total thiol) and total antioxidant capacity (TAC). Oxidative stress index (OSI) was calculated. Lipid parameters were determined by routine laboratory methods. RESULTS: Serum PON1 activity was significantly lower in the knee OA group compared to the control group (p < 0.001), whereas serum LOOH, TOS, and OSI levels of the knee OA group were significantly higher than those of the controls (p < 0.001 for all). However, TAC and -SH levels did not differ between the two groups (p > 0.05). The lowest and highest mean serum PON1 activities were detected in patients with grades 4 and 1, respectively (ANOVA p < 0.001). In multiple regression analysis, WOMAC score was independently associated with serum PON1 activity (ß = -0.248, p = 0.027). CONCLUSIONS: Decreased serum PON1 activity and elevated LOOH, TOS, and OSI levels may be associated with knee OA, and serum PON1 activity may be a useful adjunctive indicator of the severity of knee OA for follow-up.

The effects of dexmedetomidine on mesenteric arterial occlusion-associated gut ischemia and reperfusion-induced gut and kidney injury in rabbits.

OBJECTIVE: We assessed the antioxidant activity of dexmedetomidine (Dex) administered during the ischemic period in a rabbit model of mesenteric ischemia/reperfusion (I/R) injury using biochemical and histopathological methods. METHODS: A total of 24 male New Zealand white rabbits weighing between 2.5 and 3.0 kg were randomly divided into three groups: the sham group (Group S, n = 8), the I/R group (Group I/R, n = 8), and the I/R plus Dex treatment group (Group Dex, n = 8). In the I/R group, ischemia was achieved with 60 min of mesenteric occlusion. The sham group provided normal basal values. The rabbits in Group I/R were operated to achieve I/R. Group Dex received intravenous Dex 30 min after the commencement of reperfusion (10 µg/kg Dex was infused within 10 min, and then a maintenance dose of 10 µg/kg/h Dex was infused intravenously). For the measurement of tissue malondialdehyde, total antioxidant status, total oxidant status, lipid hydroperoxide levels, superoxide dismutase, catalase, and myeloperoxidase activity levels in the renal tissue samples of animals, the rabbits in each group were sacrificed 3 h after reperfusion. The histopathological examination scores were determined using the intestinal and renal tissues. RESULTS: The mean malondialdehyde, total oxidant status, myeloperoxidase, and lipid hydroperoxide levels were significantly higher in Group I/R than in Groups S and Dex (P < 0.05). There also were significant decreases in the mean total antioxidant status, catalase, and superoxide dismutase activities in Group I/R compared with Groups S and Dex (P < 0.05). The histopathological examination scores of the intestinal and renal tissues were significantly higher in Group I/R compared with Groups S and Dex (P < 0.05). CONCLUSION: Dex treatment may have biochemical and histopathological benefits by preventing I/R-related cellular damage of intestinal and renal tissues as shown in an experimental mesenteric ischemia model. The preference to use Dex for anesthesia during the mesenteric ischemia procedure may attenuate I/R injury in intestinal and renal tissues.

Peripheral DNA damage in active pulmonary tuberculosis.

In pulmonary tuberculosis patients, little is known about peripheral DNA damage, although increased oxidative stress is a well documented entity. Therefore, we aimed to investigate DNA damage along with oxidative status parameters in pulmonary tuberculosis patients. Twenty-seven pulmonary tuberculosis patients and 26 controls were included. DNA damage was assessed by comet assay. Total oxidant and antioxidant status, and oxidative stress index were determined. DNA damage, total oxidant status and oxidative stress index were higher in pulmonary tuberculosis patients than controls (all P < 0.05), while total antioxidant status was lower (P < 0.05). DNA damage was correlated with total oxidant and antioxidant status, and oxidative stress index (r = 0.69, P < 0.05; r = 0.48, P < 0.05, r = -0.47, P < 0.05; respectively) in pulmonary tuberculosis patients. Oxidative stress and DNA damage are increased in pulmonary tuberculosis patients. Increased oxidative stress associated DNA damage may be one of the pathogenetic mechanisms involved in the disorders suggested to be associated with pulmonary tuberculosis.

Serum paraoxonase activity and oxidative stress in patients with adult nephrotic syndrome.

OBJECTIVE: It has been shown that low paraoxonase-1 (PON1) activity is associated with a risk of an early development of atherosclerosis. In the present study, we investigated serum paraoxonase, and arylesterase activities and oxidative stress in patients with adult nephrotic syndrome (NS). In addition, we examined the relationship between these measurements and atherosclerosis. METHODS: Twenty-one patients with NS and 21 healthy controls were enrolled in the study. Serum basal and salt-stimulated paraoxonase activities, arylesterase activity, lipid hydroperoxide (LOOH) and total thiol (SH) levels were measured. RESULTS: Serum basal and salt-stimulated paraoxonase activities, arylesterase activity and total SH levels were significantly lower in patients with NS than in controls (p<0.05, p<0.05, p<0.01 and p<0.05, respectively), whereas LOOH levels were significantly higher (p<0.05). Serum LOOH levels were significantly correlated with total-SH levels in patients with NS (r=-0.467; p<0.01). Moreover, proteinuria levels were significantly correlated with serum LOOH levels (r=0.397; p<0.01), whereas no correlation was found among serum paraoxonase activity, arylesterase activity and total-SH levels in NS patients (p>0.05). CONCLUSIONS: We concluded that oxidative stress is increased, while serum PON1 activity is decreased in patients with adult NS. In addition, these results indicate that lower PON1 activity is associated with an oxidant-antioxidant imbalance that may contribute to atherosclerosis in adult patients with NS.

Serum paraoxonase enzyme activity and oxidative stress in obese subjects.

INTRODUCTION: Obesity is an important risk factor for atherosclerotic cardiovascular disease. Paraoxonase-1 (PON1) may play a significant role in the prevention of obesity-related accelerated atherosclerosis by hydrolyzing lipid peroxides in oxidized low-density lipoproteins. OBJECTIVES: The aim of this study was to evaluate PON1 and arylesterase enzyme activities and lipid hydroperoxide (LOOH) levels, and to investigate whether there is increased susceptibility to atherogenesis in obese subjects, which might be reflected by increased oxidative stress and decreased PON1 activity. We also aimed to investigate the association between PON1 activity and body mass index (BMI) in this patient group. PATIENTS AND METHODS: The study involved 25 obese subjects and 23 controls. Serum PON1 and arylesterase activity was measured spectrophotometrically. LOOH levels were measured by the FOX-2 assay. RESULTS: Serum basal/salt-stimulated PON1 and arylesterase activities were significantly lower in obese subjects than in controls (P <0.001 for both enzymes), while LOOH levels were significantly higher (P <0.001). BMI was significantly correlated with PON1, arylesterase and LOOH levels (P <0.001, r = -0.720; P <0.001, r = -0.634; P <0.001, r = 0.491; respectively). Serum high-density lipoprotein (HDL) levels were positively correlated with PON1 activity (r = 0.347, P <0.05). CONCLUSIONS: Our results indicate that obese subjects have increased oxidative stress and decreased PON1 activity, which might contribute to accelerated atherosclerosis. A decrease in PON1 activity seems positively correlated with BMI and inversely correlated with HDL levels.

Evaluation of oxidative status in patients with hyperthyroidism.

Data on the antioxidant levels enzyme in patients with hyperthyroidism are limited and conflicting. Therefore, the objective of this study was to evaluate the oxidative status using an automated method in patients with hyperthyroidism. Thirty-six subjects with hyperthyroidism and 30 healthy controls were enrolled in this study. Serum oxidative status was determined via measurement of total antioxidant capacity (TAC) and total oxidant status (TOS) and calculation of oxidative stress index (OSI). Serum TAC levels were significantly lower in patients with hyperthyroidism than controls (P=0.002), while serum TOS levels and OSI values were significantly higher (P=0.008, 0.004; respectively). Serum TAC levels were correlated with TSH levels (rho=0.223, P=0.032), FT3 levels (rho=-0.434, P=0.002) and FT4 levels (rho=-0.363, P=0.003) in patients. Further, TOS levels and OSI values were correlated with TSH levels (rho=-0.245, P=0.037; rho=-0.312, P=0.011, respectively), FT3 levels (rho=0.293, P=0.017, rho=0.505, P=0.002, respectively), and FT4 levels (rho=0.302, P=0.006, rho=0.321, P=0.008, respectively) in patients. Duration of disease was significantly correlated with OSI values in patients (rho=0.420, P=0.011), while no correlation with serum TAC levels and TOS levels (P>0.05). Oxidants are increased and antioxidants are decreased in patients with hyperthyroidism; as a result, the oxidative-antioxidative balance is shifted to the oxidative side. Increased oxidative stress may play a role in the pathogenesis of hyperthyroidism. It is believed that supplementation of antioxidant vitamins such as vitamins C and E may be helpful for these patients.

Mononuclear leukocyte DNA damage and oxidative stress: the association with smoking of hand-rolled and filter-cigarettes.

Cigarette smoking is a major cause of human cancer at various sites, although its carcinogenic mechanisms still remain unestablished. Based on the use of a filter, cigarette smoke can be divided into a gas phase and a tar phase. Both contain different concentrations of oxidants, free radicals and tobacco-specific carcinogens. To explore the effects of both filtered and non-filtered cigarette smoke on DNA damage and oxidative status, we measured the level of mononuclear leukocyte DNA damage by use of the single-cell gel electrophoresis (Comet) assay. We also determined malondialdehyde (MDA), protein carbonyl content (PC) and total antioxidative capacity (TAC) levels in blood plasma of smokers of manufactured filter-cigarettes and of hand-rolled cigarettes. Cotinine levels were also measured in plasma to estimate the degree of smoking. Mononuclear leukocyte DNA damage, plasma MDA, plasma PC and plasma cotinine levels were found significantly higher, while plasma TAC levels were found significantly lower in smokers of filter-cigarettes and smokers of hand-rolled cigarettes, compared with control subjects. TAC levels in hand-rolled and manufactured filter-cigarette smokers were not significantly different from each other. However, the levels of DNA damage, plasma MDA, plasma cotinine, and plasma protein oxidation were significantly higher in hand-rolled cigarette smokers than in filter-cigarette smokers. There was a significant positive correlation between MDA and DNA damage in both hand-rolled cigarette smokers and manufactured filter-cigarette smokers. This study indicates that smoking of hand-rolled cigarettes has stronger genotoxic and oxidative effects on the metabolism than smoking of manufactured filter-cigarettes. We propose that these harmful effects could be attributed to the higher level of oxidants.

Prolidase activity dysregulation and its correlation with oxidative-antioxidative status in chronic obstructive pulmonary disease.

BACKGROUND: Chronic obstructive pulmonary disease (COPD) is a consequence of an underlying chronic inflammatory disorder of the airways that is usually progressive and causes dysregulation in the metabolism of collagen. Prolidase has an important role in the recycling of proline for collagen synthesis and cell growth. OBJECTIVE: We measured and compared prolidase activity in healthy individuals with COPD patients to find out that whether its activity might reflect disturbances of collagen metabolism in the patients. We also investigated oxidative-antioxidative status and its relationship with prolidase activity in this disease. METHODS: Thirty voluntary patients with COPD and 30 healthy control subjects with similar age range and sex were included into the study. Plasma prolidase activities, total antioxidant capacity (TAC) and lipid peroxidation (LPO) levels were measured in the patient and control groups. RESULTS: Plasma prolidase activity and TAC levels were significantly lower, and LPO levels were significantly higher in the patients than those in the control subjects (P<0.05, P<0.001, and P<0.001, respectively). Significant correlations were detected between plasma prolidase activity and TAC and LPO levels in the patients group (r=0.679, P<0.001; r=-426, P<0.05, respectively). CONCLUSIONS: The results suggest that oxidative-antioxidative balance and collagen turnover are altered by the development of COPD in human lungs, and prolidase activity may reflect disturbances of collagen metabolism in this pulmonary disease. Monitoring of plasma prolidase activity and oxidative-antioxidative balance may be useful in evaluating fibrotic processes and oxidative damage in the chronic inflammatory lung disease in human.