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Biomedical subjects

Sahbettin Selek

Publications and source records attributed to Sahbettin Selek.

11 recordsLinked to original sources

Insulin resistance in H pylori infection and its association with oxidative stress.

AIM: To determine the insulin resistance (IR) and oxidative status in H pylori infection and to find out if there is any relationship between these parameters and insulin resistance. METHODS: Fifty-five H pylori positive and 48 H pylori negative patients were enrolled. The homeostasis model assessment (HOMA) was used to assess insulin resistance. Serum total antioxidant capacity (TAC), total oxidant status (TOS) and oxidative stress index (OSI) were determined in all subjects. RESULTS: The total antioxidant capacity was significantly lower in H pylori positive group than in H pylori negative group (1.36 +/- 0.33 and 1.70 +/- 0.50, respectively; P < 0.001), while the total oxidant status and oxidative stress index were significantly higher in H pylori positive group than in H pylori negative group (6.79 +/- 3.40 and 5.08 +/- 0.95, and 5.42 +/- 3.40 and 3.10 +/- 0.92, respectively; P < 0.001). Insulin resistance was significantly higher in H pylori positive group than in H pylori negative group (6.92 +/- 3.86 and 3.61 +/- 1.67, respectively; P < 0.001). Insulin resistance was found to be significantly correlated with total antioxidant capacity (r = -0.251, P < 0.05), total oxidant status (r = 0.365, P < 0.05), and oxidative stress index (r = 0.267, P < 0.05). CONCLUSION: Insulin resistance seems to be associated with increased oxidative stress in H pylori infection. Further studies are needed to clarify the mechanisms underlying this association and elucidate the effect of adding antioxidant vitamins to H pylori eradication therapy on insulin resistance during H pylori infection.

Adult↗

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.

Adult↗

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.

Adult↗

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.

Adult↗

Breast milk provides better antioxidant power than does formula.

OBJECTIVE: We examined the effect of breast milk on plasma total antioxidant capacity (TAC), total peroxide (TP), and oxidative stress index (OSI), which are biomarkers of oxidative status. METHODS: Fifty-four healthy term infants 3 to 6 mo of age were fed breast milk or a cow's milk modified formula. Plasma TAC, vitamin C, albumin, bilirubin, and uric acid levels were measured as indexes of antioxidative markers. Plasma TP levels were measured as an oxidative stress marker. The OSI was calculated to assess oxidative status. RESULTS: No significant differences were observed between groups with respect to growth or anthropometric measurements. Plasma uric acid, total protein, and albumin concentrations were slightly higher in the breast-fed group than in the formula-fed group. There was a positive correlation between infant's age and serum albumin levels; between TAC and plasma uric acid, albumin, and total bilirubin; and between plasma iron and TP levels in both groups (r > 0.256, P < 0.05). In addition, there was a negative correlation between plasma iron and TAC (r = -0.267, P = 0.01). Plasma TAC and vitamin C levels were significantly higher in the breast-fed group than in the formula-fed group (P < 0.05). Plasma TP levels and the OSI were higher in the formula-fed group than those in the breast-fed group (P < 0.05). CONCLUSIONS: Our data suggest that breast milk provides better antioxidant power than does formula.

Antioxidants↗

Oxidative stress, inflammation and early cardiovascular damage in children with chronic renal failure.

The relationship between inflammation, oxidant stress and cardiovascular damage in children with chronic renal failure (CRF) has not previously been investigated. The aim of this study was to investigate markers of oxidative stress, inflammation and early cardiovascular abnormalities. Therefore, erythrocyte superoxide dismutase (SOD) and catalase (CAT) activities; blood glutathione (GSH) and serum malondialdehyde (MDA) levels; C-reactive protein (CRP) and proinflammatory cytokines (IL-6, TNF-alpha,); and left ventricular masses (LVM) and intima media thicknesses (IMT) were measured in children with CRF. A total of 29 children with CRF (19 nondialysis, 10 peritoneal dialysis) were included. The control group consisted of 25 healthy subjects. CRF children had significantly increased IL-6, TNF-alpha, CRP and MDA concentrations and decreased SOD, CAT and GSH levels compared with controls (P<0.05). Nondialysis and peritoneal dialysis subgroups had similar oxidative stress and inflammation biomarkers (P>0.05). Erythrocyte CAT was positively correlated with CRP, TNF-alpha, and IL2-R in the study group. Positive correlations were found between cytokine concentrations, CRP and urea/creatinine levels. Significantly increased LVM and IMT values were found in CRF children (P<0.05). In conclusion, increased oxidant stress and inflammation together with early cardiovascular damage were found in CRF children. Further studies with more patients are needed to verify these results.

Cardiovascular Diseases↗

Total antioxidant/oxidant status in meningism and meningitis.

The objective of this study was to investigate the antioxidant/oxidant status of serum and cerebrospinal fluid in children with meningismus and acute bacterial meningitis. Twenty-three children (age range, 0.75 to 9 years) with fever and meningeal signs that required analysis of the cerebrospinal fluid, but no cytologic or biochemical evidence of meningitis in their serum and cerebrospinal fluid, constituted the meningismus group. Thirty-one children (age range, 0.5 to 10 years) with acute bacterial meningitis constituted the meningitis group. Twenty-nine healthy children (age range, 0.5 to 11 years) were recruited as control subjects. Antioxidant status (ascorbic acid, albumin, thiol, uric acid, total bilirubin, total antioxidant capacity, catalase and ceruloplasmin concentrations) and oxidant status (lipid hydroperoxide and total oxidant status) were measured. The serum antioxidant status was lower, and oxidant status levels higher in both meningitis and meningismus subjects than in the control children (P < 0.001). Cerebrospinal fluid oxidant status was lower in the meningitis group than in the meningismus group (P < 0.05). These results indicate that serum antioxidant status was lower, and serum oxidant status was higher in children in the meningismus and meningitis groups, whereas cerebrospinal fluid oxidant status was higher in the meningismus group than in the meningitis group.

Acute Disease↗

Decrease of total antioxidant capacity during coronary artery bypass surgery.

OBJECTIVE: Cardiac surgery induces an oxidative stress, which may lead to impairment of cardiac function. In this study, we aimed to measure the changes of oxidative and antioxidative status of patients undergoing coronary artery bypass surgery (CABG). MATERIALS AND METHODS: We studied 79 patients who underwent CABG with and without cardiopulmonary bypass (CPB). Of the 79 patients, 39 had CPB and 40 did not. Blood samples were drawn before, during, and after the surgery. Antioxidant status was evaluated by measuring total antioxidant capacity (TAC), and oxidative status was evaluated by measuring total peroxide (TP) levels and oxidative stress index (OSI). RESULTS: TP and OSI levels increased, while TAC decreased progressively after the beginning of surgery, for all patients. There were negative correlations between TAC levels and aortic cross-clamping period and anastomosis time ( r = -0.553, p < 0.001 and r = -0.500, p < 0.001, respectively). In addition, there was a positive correlation between TAC and ejection fraction (r = 0.647, p < 0.001). CONCLUSIONS: During CABG, oxidant and OSI levels significantly increase and TAC significantly decreases. This situation is influenced by long CPB and anastomosis time, and also by low ventricular ejection fraction. We concluded that the patients who undergo CABG are exposed to potent oxidative stress that impairs their TAC. We speculate that supplementation with antioxidant vitamins such as vitamins C and E may be beneficial for patients undergoing CABG.

Antioxidants↗

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.

Aged↗

Increased DNA damage and oxidative stress in patients with cutaneous leishmaniasis.

Cutaneous leishmaniasis (CL) is a chronic infectious and granulomatous disease caused by the Leishmania parasite that invades the skin. Reactive oxygen and nitrogen species (ROS and RNS) produced during an inflammatory response are an important part of host-defense strategies of organisms to kill the parasite. However, it is not well known whether these intermediates cause DNA damage in CL patients. We investigated the effect of Leishmania infection on basal levels of DNA strand breaks and on the oxidative/anti-oxidative status of patients with CL, and compared the data with those of healthy subjects. Twenty-five CL patients and 19 age- and sex-matched control subjects were enrolled in the study. We used the single-cell gel electrophoresis (also called comet assay) to measure DNA strand breaks in peripheral blood mononuclear leukocytes. Plasma protein carbonyl (PC), malondialdehyde (MDA) and total peroxide (TP) concentrations were measured to determine oxidative status and total anti-oxidative response (TAR) in plasma was measured to determine anti-oxidative status. The mean values of DNA damage and MDA and TP concentrations were significantly higher in CL patients than in the control group (p<0.001, p<0.01 and p<0.001, respectively). PC levels were also higher in patients, but this was not statistically significant (p>0.05). There was a significantly positive correlation between plasma MDA and DNA damage (r=0.524, p<0.01), and a negative correlation between TAR and TP levels (r=-0.790, p<0.001) in the patient group. These findings support the notion that ROS and RNS produced by the organism as a defense strategy may amplify the leishmanicidal activity in patients with CL. However, these intermediates not only cause the killing of the parasite but also induce oxidative damage in non-infected cells. Therefore, these patients must be treated urgently to counteract the oxidative DNA damage.

Adolescent↗

Evaluation of oxidative-antioxidative status and the L-arginine-nitric oxide pathway in asthmatic patients.

BACKGROUND: Reactive nitrogen, oxygen species and oxidative stress are related to many pulmonary diseases. Nitric oxide (NO) may be involved in either the protection against or the induction of oxidative stress within various tissues. It is derived from the amino acid L-arginine by the action of NO synthase (NOS). L-arginine can also be metabolized by arginase with the production of ornithine and urea. Because of the competition between NOS and arginase for the same substrate, their activities are regulated reciprocally. Therefore, the rate of NO generation associated with oxidative stress is dependent on the relative activities of both NOS and arginase. The objective of this study is to investigate the L-arginine-NO pathway, evaluate oxidative-antioxidative status in the patients with asthma and demonstrate their reciprocal regulation. METHODS: 30 voluntary asthmatic patients and 30 healthy control subjects with similar age range and sex were included in the study. A total of 10 ml venous blood was drawn, plasma and packed erythrocytes were prepared for the biochemical analyses. Plasma arginase activities and NO levels, and erythrocyte malondialdehyde and reduced glutathione levels were detected. RESULTS: Plasma malondialdehyde levels were significantly higher and glutathione levels were lower in patients with asthma than those of the control subjects (P < 0.001 and P < 0.01, respectively). Arginase activities were significantly lower and NO levels were higher in the patients than those of the controls (P < 0.001 for both). The negative correlation between arginase and NO levels in the patients was significant (r = -0.47; P < 0.01). There was also a positive correlation between malondialdehyde and NO levels in the patients (r = 0.51; P < 0.01). CONCLUSIONS: The results suggest that the L-arginine-NO pathway is involved in the pathophysiology of asthma; the arginase activities decrease which causes an increase in the L-arginine levels thereby up-regulation of NO production may contribute to the increase of oxidative stress in asthma.

Adult↗