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.

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.

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.

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.

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.

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.

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.

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.

The relationship between leptin level and oxidative status parameters in hemodialysis patients.

Both serum leptin level and oxidative stress are increased in hemodialysis (HD) patients. In the present study, we aimed to investigate whether there is association between oxidative status and leptin level in HD patients. Thirty-five HD patients and 25 healthy controls were enrolled in the present study. Serum leptin level, total peroxide (TP) level, total antioxidant capacity (TAC), and oxidative stress index (OSI) were determined. Serum leptin level, TP level, and OSI were significantly higher in HD patients than controls (all P < 0.001) while TAC was lower (P < 0.001). In HD patients, serum leptin level was significantly correlated with TP level and OSI (r = 0.372, P < 0.001 and r = 0.409, P < 0.001, respectively). The correlation of serum leptin level with TP level and OSI remained statistically significant after adjusting for age, gender, and body-fat percentage (r = 0.446, P < 0.001 and r = 0.463, P < 0.001, respectively). Hyperleptinemia seems to be associated with increased oxidative stress in HD patients, and this association may provide better understanding about the disorders related to either elevated serum leptin levels and/or increased oxidative stress in HD patients.

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.

PON1 activity and total oxidant status in patients with active pulmonary tuberculosis.

OBJECTIVES: The aim of this study was to the investigate effect of tuberculosis infection on paraoxonase-1 (PON1) activity and oxidative status in patients with pulmonary tuberculosis (PTB). DESIGN AND METHODS: Twenty-five active PTB subjects and 33 healthy controls were included in the study. Serum PON1 activity, total oxidant status (TOS), lipid hydroperoxide (LOOH) and total free sulfydryl (-SH) groups were determined. RESULTS: Serum basal/salt-stimulated paraoxonase activities, arylesterase activity and total -SH group levels were significantly lower in patients with PTB than controls (p<0.05, p<0.05, p<0.001 and p<0.01 respectively), while TOS and LOOH levels were significantly higher (p<0.01 and p<0.05, respectively). In PTB patients, TOS, LOOH and total -SH group levels were significantly correlated with paraoxonase (r=-0.371, p<0.05; r=-0.286, p<0.05; r=0.625 p<0.01; respectively) and arylesterase (r=-0.437, p<0.01; r=-0.352, p<0.05; r=0.653, p<0.01; respectively). CONCLUSIONS: Patients with active PTB are exposed to potent oxidative stress and they have decreased PON1 activity. These predisposal factors may, in part, play a role in the pathogenesis of atherosclerosis in PTB.

Protective effects of melatonin on oxidative-antioxidative balance and cataract formation in rats.

We investigated the effects of melatonin on cataract formation in rats exposed to selenite. We concluded that the imbalance between oxidants and antioxidants plays an important role in cataract formation and melatonin decreases cataract incidence in rats by increasing antioxidant activity.

Assessment of paraoxonase and arylesterase activities in patients with iron deficiency anemia.

Paraoxonase-1 (PON1) is a high-density lipoprotein (HDL) associated enzyme with three activities which are paraoxonase, arylesterase and dyazoxonase. We aimed to determine serum (a) paraoxonase and arylesterase activities and, lipid hydroperoxide (LOOH) levels in patients with iron deficiency anemia (IDA) (b) whether there is an association between the development of atherosclerosis and paraoxonase/arylesterase activities in patients with IDA. Twenty-five female with IDA and 22 healthy female as control were enrolled in the study. Serum basal/salt-stimulated paraoxonase and arylesterase activities were measured spectrophotometrically. LOOH levels were measured by ferrous oxidation with xylenol orange assay. Basal/salt-stimulated paraoxonase and arylesterase activities were significantly lower in patients with IDA than controls (p<0.001; for all), while LOOH levels were significantly higher (p<0.001). Our results show that paraoxonase and arylesterase activities, which have antiatherogenic capability, are decreased in patients with IDA. Reduced paraoxonase and arylesterase activities may play a role in pathogenesis of atherosclerosis through increased susceptibility to lipid peroxidation in patients with IDA.

Oxidative status and serum PON1 activity in beta-thalassemia minor.

OBJECTIVES: Paraoxonase-1 (PON1) deficiency is related to increased susceptibility to low density lipoprotein oxidation and development of atherosclerosis. The aim of this study was to investigate paraoxonase and arylesterase activities along with oxidative status parameters, and to find out if there is any increased susceptibility to atherogenesis, which might be reflected with increased oxidative stress and decreased serum PON1 activity in beta-thalassemia minor (BTM) subjects. DESIGN AND METHODS: Thirty-two subjects with BTM and 28 healthy subjects as control were enrolled in the study. Serum paraoxonase and arylesterase activities, lipid hydroperoxide (LOOH) levels, total antioxidant capacity (TAC), total oxidant status (TOS) and oxidative stress index (OSI) were determined. RESULTS: Serum TAC, paraoxonase and arylesterase activities were significantly lower in BTM subjects than controls (for all p<0.001), while TOS, LOOH levels and OSI were significantly higher (p<0.001, p<0.05 and p<0.001; respectively). In BTM subjects, OSI, TOS, LOOH levels and TAC were significantly correlated with serum paraoxonase (r=-0.245, p<0.05; r=-0.231, p<0.05; r=-0.264, p<0.05 and, r=0.342, p<0.05, respectively) and arylesterase activities (r=-0.332, p<0.05, r=-0.308, p<0.05; r=-0.320, p<0.05 and r=0.443, p<0.05). Additionally, hemoglobin level was also correlated with serum paraoxonase (r=0.501, p<0.001) and arylesterase activities (r=0.501, p<0.001), TAC (r=0.402, p<0.05), TOS (r=-0.274, p<0.05) and OSI (r=-0.352, p<0.05). CONCLUSIONS: Oxidative stress is increased, while serum PON1 activity is decreased in BTM subjects. Decrease in PON1 activity seems to be associated with both the degree of oxidative stress and anemia. BTM subjects may be more prone to development of atherogenesis due to low serum PON1 activity.

PON1 status in haemodialysis patients and the impact of hepatitis C infection.

OBJECTIVES: Paraoxonase-1 (PON1) activity has been reported to decrease in both haemodialysis patients and patients with HCV infection. We aimed to investigate paraoxonase and arylesterase activities, and lipid hydroperoxide levels (LOOH) in haemodialysis patients with or without hepatitis C infection, and to find out whether PON1 activity is affected further by the presence of HCV infection in HD patients. DESIGN AND METHODS: Twenty HCV (+) haemodialysis patients, 26 HCV (-) haemodialysis patients, and 26 controls were enrolled. Paraoxonase and arylesterase activities were measured spectrophotometrically. LOOH levels were measured by ferrous oxidation with xylenol orange assay. RESULTS: Haemodialysis patients with or without HCV infection had lower paraoxonase and arylesterase activities than controls (all p<0.001), while higher LOOH levels (both p<0.001). Paraoxonase and arylesterase activities, and LOOH levels were comparable between haemodialysis patients with or without HCV infection (p>0.05). Significant inverse correlation was observed between paraoxonase or arylesterase activities, and LOOH levels (p<0.05, beta=-0.319 and p<0.05, beta=-0.348, respectively). CONCLUSION: We concluded that PON1 activity significantly decreases in both haemodialysis patients with or without HCV infection. Nevertheless, PON1 activity is not affected further by the presence of HCV infection in haemodialysis patients.

Relationship between total oxidant status and severity of diabetic nephropathy in type 2 diabetic patients.

BACKGROUND AND AIM: Data on oxidative stress in type 2 diabetic patients with diabetic nephropathy is scant. The objective of this study was to investigate possible associations between total oxidant status (TOS) and the severity of diabetic nephropathy in type 2 diabetic patients by using a novel automated measurement method. METHODS AND RESULTS: Thirty-six patients with diabetic nephropathy (group 1), 25 diabetic patients without nephropathy (group 2) and 30 controls (group 3) were enrolled. Serum total antioxidant capacity (TAC), TOS levels and oxidative stress index (OSI) were determined. The severity of the disease was determined with microalbuminuria levels. TAC was lower, while TOS and OSI were higher in group 1 than in group 3 (P<0.01, P<0.001, P<0.001; respectively). There were no statistically significant differences between group 2 and group 3 with respect to TAC, TOS and OSI (all P>0.05). Group 1 had higher TOS and OSI than group 2 (both P<0.05), but there was no statistically significant difference with respect to TAC. Significant correlations were observed between microalbuminuria levels, and TAC, TOS and OSI levels (r=-0.616, P<0.001; r=0.488, P<0.01; r=0.567, P<0.001; respectively). CONCLUSION: Our results suggest that oxidative stress is increased in patients with diabetic nephropathy compared to diabetic patients without nephropathy and this increase seems to be related to the severity of microalbuminuria levels.

The association of circulating leptin level with peripheral DNA damage in hemodialysis subjects.

OBJECTIVES: Hemodialysis subjects have been shown to have both elevated serum leptin and peripheral DNA damage level, and leptin has been suggested to induce apoptotic features. Thus, in the present study, we aimed at finding out if there is any relationship between serum leptin level and peripheral DNA damage in hemodialysis subjects. DESIGN AND METHODS: Forty hemodialysis subjects and 21 controls were included in the present study. Serum leptin level and peripheral DNA damage were assayed in all subjects enrolled in the study. Comet assay was used in determining DNA damage in peripheral lymphocyte. RESULTS: Both serum leptin level and peripheral DNA damage were significantly higher in hemodialysis subjects than control (P<0.05 and P<0.001, respectively). Female subjects had significantly higher serum leptin level than male subjects in both hemodialysis and control group (both P<0.05). Significant correlation was observed between serum leptin level, and gender and body fat mass in both hemodialysis (P<0.05, beta=-0.637 and P<0.05, beta=0.386, respectively) and control group (P<0.05, beta=-0.569 and P<0.05, beta=-0.460, respectively). In hemodialysis subjects, peripheral DNA damage was significantly correlated with serum leptin level (P<0.05, beta=0.508). CONCLUSION: In end-stage renal disease subjects, elevated serum leptin level seems to be associated with peripheral DNA damage and thus, may, in part, have a role in the development of DNA damage associated disorders.

Oxidative stress in hepatitis C infected end-stage renal disease subjects.

BACKGROUND: Both uremia and hepatitis C infection is associated with increased oxidative stress. In the present study, we aimed to find out whether hepatitis C infection has any impact on oxidative stress in hemodialysis subjects. METHODS: Sixteen hepatitis C (+) hemodialysis subjects, 24 hepatitis C negative hemodialysis subjects and 24 healthy subjects were included. Total antioxidant capacity, total peroxide level and oxidative stress index were determined in all subjects. RESULTS: Total antioxidant capacity was significantly higher in controls than hemodialysis subjects with or without hepatitis C infection (all p < 0.05/3), while total peroxide level and oxidative stress index were significantly lower (all p < 0.05/3). Hepatitis C (-) hemodialysis subjects had higher total antioxidant capacity compared to hepatitis C (+) hemodialysis subjects (all p < 0.05/3). Total peroxide level and oxidative stress index was comparable between hemodialysis subjects with or without hepatitis C infection (p > 0.05/3). CONCLUSION: Oxidative stress is increased in both hepatitis C (+) and hepatitis C (-) hemodialysis subjects. However, hepatitis C infection seems to not cause any additional increase in oxidative stress in hemodialysis subjects and it may be partly due to protective effect of dialysis treatment on hepatitis C infection.

Increased DNA damage in patients with chronic obstructive pulmonary disease who had once smoked or been exposed to biomass.

OBJECTIVE: Chronic obstructive pulmonary disease (COPD) is a slowly progressive condition characterised by poorly reversible airflow limitation associated with an abnormal inflammatory response of the lung. The main causal factors of COPD are chronic oxidative stress as a result of long-term smoking, use of biomass fuels, and air pollution. In this study, basal levels of DNA strand breaks were investigated together with some additional oxidative markers implicating oxidative damage on the other biomolecules such as proteins and lipids in patients with COPD who were exposed to smoking and biomass. MATERIAL AND METHODS: We detected DNA strand breaks in peripheral blood mononuclear leukocytes by using a Single Cell Gel Electrophoresis (also called Comet Assay), plasma protein carbonyl (PC) content by using Reznick and Parker's spectrophotometric method, and lipid peroxidation by measurement of malondialdehyde (MDA) as indexes of oxidative stress in 47 patients with smoking-related COPD and 25 patients with biomass-related COPD and 36 age-and-sex matched control participants. RESULTS: The mean values of DNA strand breaks, MDA and protein carbonyl levels were significantly higher in smoking- and biomass-related COPD groups than in the control group (ANOVA P<0.001, <0.05 and <0.05, respectively). DNA damage levels were also higher in smoking-related COPD group than in biomass-related COPD group (P<0.05). There was a positive relationship between DNA damage and MDA levels in smoking-related COPD group (P<0.05). CONCLUSION: Oxidative stress markers and DNA damage were strongly increased in both patient groups with smoking- and biomass-related COPD. However, DNA is more affected in smoking-related COPD patients than in biomass-related COPD. These data indicate that cigarette smoking is a more significant DNA damaging risk factor than biomass smoke.