The levels of oxidant and antioxidant in patients with COPD

It is determinate that oxidant-antioxidant imbalance is responsible for pathogenesis of chronic obstructive pulmonary disease (COPD) and smoking is playing a part in the pathogenesis. It was aimed to investigate the oxidant-antioxidant imbalance in smokers and pathogenesis of COPD and their relations with lung functions. This study was done prospectively in Firat University Medical Faculty, Department of Chest Diseases. The levels of plasma malonyldialdehyde (MDA), erythrocyte reducted glutathione (GSH) and erythrocyte catalase were studied in 20 patients with COPD, in 20 smokers and in 20 nonsmokers. All of the cases were male. Pulmonary function tests were done to all cases and the predicted values of FEV1, FVC, and FEV1/FVC were measured. The levels of plasma MDA: 1.44 +/- 0.23 nmol/mL, 1.51 +/- 0.27 nmol/mL and 1.29 +/- 0.13 nmol/mL, the levels of erythrocyte GSH: 0.33 +/- 0.13 micromol/g.Hb, 0.34 +/- 0.17 micromol/g.Hb and 0.44 +/- 0.14 micromol/g.Hb and the levels of catalase were 22.82 +/- 17.47 k/g.Hb, 32.88 +/- 22.36 k/g.Hb and 55.73 +/- 26.56 k/g.Hb in patients with COPD, smokers and healthy nonsmokers respectively. There was no significance in each three parameters between smokers and patients with COPD. A significant difference was observed in each three parameters between nonsmokers and patients with COPD (MDA: p= 0.001, GSH: p= 0.028 and catalase: p< 0.001) and between smokers and nonsmokers (MDA: p= 0.035, GSH: p= 0.016 and catalase: p= 0.005). In all three groups, no significant correlation was found between FEV1 (predicted %), FEV1/FVC (predicted %) and the values of erythrocyte catalase, GSH and plasma MDA. In this study, there was an oxidant-antioxidant imbalance systemically in smokers and in patients with COPD. However, decreasing in the antioxidant capacity and/or increasing in the oxidant capacity either not correlate with spirometric measurements of airway obstruction in smokers or in patients with COPD were observed. We concluded that the use of cigarette increased oxidative stress by causing plasma lipid peroxidation and imbalance in erythrocyte antioxidant capacity.     

Exercise-induced quadriceps oxidative stress and peripheral muscle dysfunction in patients with chronic obstructive pulmonary disease

Exercise-induced muscle oxidative stress may be involved in the myopathy associated with chronic obstructive pulmonary disease (COPD). This study was designed to look at whether local exercise induces muscle oxidative stress and whether this oxidative stress may be associated with the reduced muscle endurance in patients with COPD. Quadriceps endurance was measured in 12 patients with COPD (FEV1 = 0.96 +/- 0.14 SEM) and 10 healthy sedentary subjects by repeated knee extensions of the dominant leg. Biopsies of the vastus lateralis muscle were obtained before and 48 hours after exercise. Muscle oxidative stress was measured by lipid peroxidation and oxidized proteins. Muscle antioxidant was evaluated by peroxidase glutathion activity. Quadriceps endurance was significantly reduced in patients with COPD when compared with the healthy control subjects (p < 0.01). Forty-eight hours postexercise, only patients with COPD had a significant increase in muscle lipid peroxidation (p < 0.05) and oxidized proteins (p < 0.05), whereas increased peroxidase glutathion activity was only observed in control subjects (p < 0.05). Both increases in muscle lipid peroxidation and oxidized proteins were significantly and inversely correlated with quadriceps endurance capacity in COPD (p < 0.05). In summary, local exercise induced muscle oxidative stress in patients with COPD, whereas it failed to raise antioxidant activity. In these individuals, muscle oxidative stress was associated with a reduced quadriceps endurance.     

Reduced muscle redox capacity after endurance training in patients with chronic obstructive pulmonary disease.

The present study was undertaken to test whether endurance training in patients with COPD, along with enhancement of muscle bioenergetics, decreases muscle redox capacity as a result of recurrent episodes of cell hypoxia induced by high intensity exercise sessions. Seventeen patients with COPD (FEV(1), 38 +/- 4% pred; PaO2), 69 +/- 2.7 mm Hg; PaCO2, 42 +/- 1.7 mm Hg) and five age-matched control subjects (C) were studied pretraining and post-training. Reduced (GSH) and oxidized (GSSG) glutathione, lipid peroxidation, and gamma-glutamyl cysteine synthase heavy subunit chain mRNA expression (gammaGCS-HS mRNA) were measured in the vastus lateralis. Pretraining redox status at rest and after moderate (40% Wpeak) constant-work rate exercise were similar between groups. After training (DeltaWpeak, 27 +/- 7% and 37 +/- 18%, COPD and C, respectively) (p < 0.05 each), GSSG levels increased only in patients with COPD (from 0.7 +/- 0.08 to 1.0 +/- 0.15 nmol/ mg protein, p < 0.05) with maintenance of GSH levels, whereas GSH markedly increased in C (from 4.6 +/- 1.03 to 8.7 +/- 0.41 nmol/ mg protein, p < 0.01). Post-training gammaGCS-HS mRNA levels increased after submaximal exercise in patients with COPD. No evidence of lipid peroxidation was observed. We conclude that although endurance training increased muscle redox potential in healthy subjects, patients with COPD showed a reduced ability to adapt to endurance training reflected in lower capacity to synthesize GSH.     

Oxidative stress and enzymatic antioxidant status in patients with hypothyroidism before and after treatment.

The present study was designed to investigate the relationship between the serum levels of oxidant-antioxidant system (malondialdehyde (MDA) level, Paraoxonase (PON1) activity, nitric oxide (NO) level and superoxide dismutase (SOD) activity) and thyroid hormone status in hypothyroidism pre and posttreatment. The study group comprised 33 patients with primary hypothyroidism. 18 of these patients were reevaluated after euthyroid state i.e. at least 6 months of thyroxine replacement. The patients were compared with 26 normal healthy controls. Serum MDA level, PON1 activity, NO level and SOD activity were measured according to an enzymatic spectrophotometric method. MDA levels were found higher in patients with hypothyroidism before the treatment than the controls. MDA levels were also found to be decreased after the treatment in patients with hypothyroidism. However MDA were found still higher than the controls after the treatment. PON1 activity was found to be lower in patients pretreatment when compared to posttreatment hypothyroidism and controls. Posttreatment of hypothyroidism mean PON1 activity significantly increased compared to pretreatment level but it was still significantly lower than control level. NO level was higher in pretreatment hypothyroidism when compared to controls. SOD activity was not found different in patients before treatment when compared to controls. SOD activity was significantly higher in after treatment when compared to both pretreatment and control levels. In conclusion, increased ROS levels in hypothyroidism may result in a pro-oxidation environment, which in turn could result in decreased antioxidant PON1 activity, increased MDA and NO levels. As a result, lipid peroxidation may have a role in the pathogenesis of the atherosclerosis in hypothyroidism.     

alpha-Tocopherol levels in plasma in new-onset, insulin-dependent diabetes mellitus

BACKGROUND: Diabetic complications have been related to increased oxidative stress. Plasma antioxidant levels may be affected by hyperglycemia-induced oxidative stress as well as by insulin therapy. We evaluated the immediate effect of insulin treatment and improved metabolic control on the important antioxidant alpha-tocopherol plasma (vitamin E) levels in new-onset, insulin-dependent diabetes mellitus. METHODS: The study was performed in 15 consecutive patients, aged 20-67 years, with new-onset diabetes mellitus requiring acute insulin treatment. Plasma alpha-tocopherol levels were measured before the start of intensive insulin treatment and monthly for 6 months thereafter. Simultaneously, we studied plasma malondialdehyde (MDA) as a reflection of lipid peroxidation. In addition, comparisons were made to a nondiabetic reference group. RESULTS: Baseline alpha-tocopherol levels did not differ from those in nondiabetic subjects. alpha-Tocopherol decreased significantly, from 33.5+/-12.1 mumol/l before treatment to 28.11+/-6.85 mumol/l (-16%) after 1 month of insulin therapy (p<0.04) to 26.6+/-7.03 mumol/l (-20%) after 3 months of insulin therapy (p<0.02). This trend did not change after adjusting for variations in cholesterol levels. After 6 months, alpha-tocopherol was no longer decreased compared to baseline levels (29.6+/-7.4 mumol/l). MDA concentrations at baseline were significantly higher in the diabetic patients (3.79+/-2.91 mumol/l) than in the nondiabetic subjects (1.57+/-0.21 mumol/l, p=0.006). MDA concentrations decreased significantly following the start of insulin treatment. CONCLUSIONS: Patients with new-onset, insulin-dependent diabetes mellitus have alpha-tocopherol levels that are similar to those in normal subjects. Insulin treatment and/or improved metabolic control cause a significant decrease in alpha-tocopherol levels during the first months.     

Short-term effects of an intensive lifestyle modification program on lipid peroxidation and antioxidant systems in patients with coronary artery disease

The purpose of this study was to compare the short-term effects of an intensive lifestyle modification (ILM) program on lipid peroxidation and antioxidant systems in patients with coronary artery disease (CAD). Twenty-two patients in the control group continued to receive their conventional treatment with lipid-lowering drugs, whereas 22 patients in the experimental group were assigned to intensive lifestyle modification (ILM) without taking any lipid-lowering agent. The ILM program comprised dietary advice on low-fat diets, high antioxidants and high fiber intakes, yoga exercise, stress management and smoking cessation. After 4 months of intervention, patients in the experimental group revealed a statistically significant increase in plasma total antioxidants, plasma vitamin E and erythrocyte glutathione (GSH) compared to patients in the control group. There was no significant change in plasma malondialdehyde (MDA), a circulating product of lipid peroxidation, in either group. We concluded that the ILM program increased circulating antioxidants and reduced oxidative stress in patients with CAD.     

Oxidative stress in chronic obstructive pulmonary disease patients submitted to a rehabilitation program

Pulmonary rehabilitation (PR) improves physical capacity and health quality in patients with chronic obstructive pulmonary disease (COPD). However, the effect of exercise on oxidative stress markers in COPD patients is only partially known. This study was designed to evaluate the oxidative stress response to long-term exercise in patients with COPD enrolled in a PR program. Fifteen COPD patients (FEV1 < 60%), age between 50 and 60 years, ex-smokers, were separated in two groups: exercise-trained (n=8) and sedentary group (n=7). Exercise consisted of an 8-week conditioning program using a cycle ergometer (three times a week, 1h session). An endurance test (60% of maximal load in an incremental cycle test) was performed before and after PR. Blood samples were obtained at baseline and immediately after each endurance test. We measured the index of lipid peroxidation, thiobarbituric acid reactive species (TBARS), total radical-trapping antioxidant parameter (TRAP) and xanthine oxidase (XO) activity. TRAP was significantly different between the exercise-trained group and sedentary group of COPD patients. Baseline TBARS values were increased after the exercise training program but decreased after the endurance test. XO decrease after effort in the trained and untrained groups. The results suggest that patients with COPD are characterized by increased systemic and pulmonary oxidative stress markers both at rest as well as induced by cardiopulmonary exercise test and that PR program was associated with decreased systemic exercise-induced oxidative damage.     

Oxidative stress and antioxidant status in type 1 diabetes mellitus

OBJECTIVES: To test the hypothesis that type 1 diabetes is associated with increased oxidative stress and/or antioxidant status by investigating concentrations of 8-iso-prostaglandin F2alpha (8-iso-PGF2alpha) in urine and plasma and malondialdehyde (MDA) in plasma as indicators of lipid peroxidation in vivo, and antioxidant status in diabetic subjects compared with healthy control subjects. DESIGN AND SUBJECTS: Thirty-eight subjects with type 1 diabetes mellitus and 41 healthy age- and sex-matched control subjects were included in the study. Blood and urine samples were obtained and analysed for 8-iso-PGF2alpha with a newly developed radioimmunoassay, as well as for MDA, total antioxidant capacity (TAOC) and serum tocopherol levels. RESULTS: None of the variables of lipid peroxidation showed any significant difference between the two groups. Similarly, there were no significant correlations between the levels of 8-iso-PGF2alpha or MDA, and degree of glycemic control (HbA1c). Total antioxidant capacity in plasma was 16% lower amongst the subjects with type 1 diabetes than in the control group (P < 0.0005). Lipid corrected levels of alpha-tocopherol in serum were significantly increased in type 1 diabetic subjects (P < 0.05), as were gamma-tocopherol levels (P < 0.005). CONCLUSIONS: In spite of lower total antioxidant defence, our results do not support the oxidative stress hypothesis for type 1 diabetes mellitus. The higher tocopherol levels suggest that no vitamin E supplementation is necessary for subjects with type 1 diabetes mellitus.     

The effect of glycemic control on salivary lipid peroxidation in type II diabetic patients

Background and objectiveHyperglycemia and some disturbance in antioxidant system lead to free radicals production and oxidative stress. Assessment of some products of oxidative stress could be effective in evaluation of diabetic control. This study aimed at evaluation of glycemic control on salivary lipid peroxidation in diabetic patients.MethodsThis case control study has been done on 44 diabetic (type II) and 44 healthy subjects. Un-stimulated saliva was collected and correlation between malondialdehid (MDA) as an end -product of lipid peroxidation and HbA1c was assessed.ResultsMDA and HbA1c of diabetic patients were significantly higher than control group. There was a indirect correlation between MDA and glycemic control level.ConclusionEvaluation of salivary MDA levels could be useful in prediction of glycemic control.     

Moderate exercise with a dietary vitamin C and e combination protects against streptozotocin-induced oxidative damage to the kidney and lens in pregnant rats.

Moderate exercise and vitamin C and E (VCE) supplementation can be beneficial to diabetes due to reducing free radical production in lens and kidney of diabetic pregnant rats. We investigated the effect of VCE supplementation and moderate exercise on lipid peroxidation (MDA) and scavenging enzyme activity in the kidneys and lens of STZ-induced diabetic pregnant rats. Fifty female Wistar rats were used and were randomly divided into five groups. First and second were used as the control and pregnant control group. Third group was the pregnant diabetic group. The fourth group was the diabetic-pregnant-exercise group. VCE-supplemented feed was given to pregnant-diabetic-exercise rats constituting the fifth group. Animals in the exercised groups were moderately exercised daily on a treadmill (16.1 m/min, 45 min/d) for three weeks (five days a week). Diabetes was induced on day zero of the study. Plasma, lens, and kidney samples were taken from all animals on day 20. Exercise and administration of VCE to pregnant diabetic rats resulted in significant decrease in the albumin and total protein values and the elevated MDA, plasma creatinine, and urea levels as an indicator of oxidative stress and renal functional parameters. Exercise and VCE supplementation also increased glutathione peroxidase (GSH-Px), reduced glutathione (GSH), vitamin E, and beta-carotene levels in the kidney, GSH-Px and GSH in the lens, the albumin and total protein values in plasma. In the diabetic pregnant animals, the decreased vitamins A and E concentration and GSH levels in kidney, creatinine, and urea values in plasma did not improve through exercise only although their concentrations were increased by VCE supplementation. Kidney weight did not also affect either by exercise or VCE supplementation. In conclusion, these results suggest that exercise plus VCE affects antioxidant metabolism and reduces lipid peroxidation, thereby improving the damage caused by oxidative stress involved in the pathogenesis of lens and kidney in diabetic pregnant rats. Moderate exercise with dietary VCE may play a role in preventing nephropathy and cataract formation in diabetic pregnant rat.     

Effect of melatonin on lipid peroxidation, glutathione and glutathione-dependent enzyme activities in experimental otitis media with effusion in guinea pigs

Melatonin plays a role in the prevention of oxidative damage. In the present study, we investigated whether the increased oxidative stress in experimental otitis media with effusion (OME) induced by histamine is reflected in erythrocytes and middle ear effusion fluid. Lipid peroxidation in effusion fluid was measured to determine the effects of melatonin on oxidative stress. Erythrocyte and middle ear effusion malondialdehyde (MDA) levels, erythrocyte glutathione (GSH) levels and glutathione peroxidase (GPx), glutathione reductase (GRd) and glutathione-S-transferase (GST) activities were measured in three groups of six guinea pigs each at 3 hr after the injection of 0.1 mL of histamine (or saline) into the middle ear. In erythrocyte and middle ear effusion samples, MDA levels showed a significant increase in guinea pigs with experimental OME group when compared with the control animals. Erythrocyte GPx, GST, GRd activities and GSH levels significantly reduced in experimental OME guinea pigs when compared with the control and melatonin-treated animals. Erythrocyte GPx activity also significantly increased after melatonin treatment when compared with the control group. These findings suggest that reactive oxygen species play a role in histamine-induced OME. Pretreatment with melatonin increases antioxidant enzyme activities and reduced formation of MDA, an indicator of lipid peroxidation, in histamine-induced OME.     

Increased lipid peroxidation in type 2 poorly controlled diabetic patients.

An increased lipid peroxidation, due to the altered intracellular ratio between free radicals and antioxidant systems, has been recently related to diabetes. To study the possible relationship between lipid peroxidation and metabolic control, we measured the plasma concentrations of malondialdehyde (MDA), end product of the oxidation of polyunsaturated fatty acids, in poorly and well controlled Type 2 diabetic patients. A significant increase in plasma malondialdehyde concentrations was found in poorly controlled diabetics when compared to well controlled patients (p < 0.001) and to healthy normoglycaemic subjects (p < 0.001), whereas no significant difference was observed between the two latter groups. Plasma MDA/Cholesterol and MDA/triglyceride ratios were both higher in poorly controlled diabetics than in well controlled (p < 0.005) and in normal subjects (p < 0.01 and p < 0.02 for MDA/CHOL and MDA/TG respectively). In diabetic patients a positive correlation was found between plasma MDA levels and mean daily blood glucose (p < 0.01), plasma fructosamines (p < 0.001), HbA1 (p < 0.05) and plasma triglycerides (p < 0.05), while no significant correlation was shown between plasma malondialdehyde and total cholesterol. Malondialdehyde levels were followed-up for 7 days running (T1-T7) in five poorly controlled diabetics, treated with conventional insulin therapy. This group showed normalized plasma lipid peroxide values (0.486 +/- 0.13 mumol/l, T5, M +/- SEM) 72 h after the restoration of glycaemic control (145 +/- 25 mg/dl, T2, M +/- SEM). These results confirm the increase of lipid peroxidation during Type 2 diabetes. The correlation with the degree of metabolic imbalance suggests a possible role for lipid peroxidation in the occurrence of glucose-induced macromolecular changes.     

Persistent Oxidative Stress in Patients with Chronic Active Hepatitis-C Infection After Antiviral Therapy Failure

Background/Aims:

Oxidative stress and hepatocellular pathological changes are common associations with chronic hepatitis C virus (CHC) disease. The aim of this study was to assess serum antioxidant-oxidant (Redox) balance in patients with CHC infection before and after intake of the traditional antiviral therapy (pegylated interferon α-2b and oral ribavirin).

Patients and Methods:

Blood samples from 50 biopsy-proven CHC patients, with no prior anti-viral treatment and persistently elevated serum transaminase levels for 6 months, as well as 15 age- and sex-matched healthy subjects were used for determination of the antioxidants: reduced glutathione (GSH), superoxide dismutase (SOD), α tocopherol and ascorbic acid as well as lipid peroxidation (LPO) index (malondialdehyde [MDA]). The measurements were repeated in the diseased group 25 weeks after pegylated interferon α-2b and ribavirin combination therapy.

Results:

Serum levels of bilirubin, aspartate aminotransferase (AST), and alanine aminotransferase (ALT) were significantly higher in CHC patients than in the control group (P < 0.05). Pretreatment serum MDA values were significantly higher in patients with CHC infection than the control group (P < 0.001), while serum antioxidant levels were significantly lower (P < 0.001). Responders (10 patients) had lower pretreatment serum levels of MDA than non-responders (35 patients) (P < 0.001). Both groups were comparable for the antioxidant serum levels. There was significant negative correlation between serum MDA and serum SOD, GSH, α tocopherol, and ascorbic acid concentrations in CHC patients. On the other hand, there was no correlation between the studied parameters and serum bilirubin, albumin, ALT, and AST.

Conclusions:

Redox imbalance was detected in patients with CHC. Responders had significantly lower levels of MDA than non-responders. Serum MDA may be used as a pretreatment predictor of response to antiviral treatment in patients with CHC.     

维生素 E 抗心肌再灌注损伤

<正> 防止心肌再灌注损伤,对促进心外科术后患者的心功能恢复,减少心律失常的发生有重要意义。本文从心外科临床心肌保护角度观察心肌脂质过氧化物的变化,研究活性氧自由基对心肌再灌注损防的影响及观察维生素 E 抗脂质过氧化,减轻再灌注损伤的作用。实验方法一、研究对象及分组:随机选取临床拟行心脏瓣膜手术的风湿性心脏病患者14名,其中男性2例,女性12例,对照组和治疗组各7例。两组病人均按常规行各项术前检查及治疗,不同的是,治疗组患者每日加服维生素 E 300mg(100mg/次,3次/日)至手术日,见表1。     

Rehabilitation decreases exercise-induced oxidative stress in chronic obstructive pulmonary disease

The effect of exercise at different intensities as well as the effect of intensive supervised pulmonary rehabilitation on oxidative stress were studied for chronic obstructive pulmonary disease (COPD). Eleven patients with COPD and 11 healthy age-matched control subjects performed a maximal and submaximal exercise cycle ergometry test at 60% of peak workload. Patients with COPD performed these tests before and after 8 wk of pulmonary rehabilitation. Measurements were done before, immediately after, and 4 h after both exercise tests. At rest, increased oxidative stress was observed in patients compared with control subjects, as measured by urinary malondialdehyde (MDA; p < 0.05) and hydrogen peroxide (H2O2) in breath condensate (p < 0.05). In healthy control subjects, a significant increase in urinary MDA was observed 4 h after both exercise tests (p = 0.05), whereas H2O2 significantly increased immediately after maximal exercise (p < 0.05). In patients with COPD, before rehabilitation, reactive oxygen species-induced DNA damage in peripheral blood mononuclear cells, urinary MDA, and plasma uric acid were significantly increased after both exercise tests (p < 0.05), whereas no significant increase was observed in plasma MDA. In contrast, exhaled H2O2 was only significantly increased after maximal exercise (p < 0.02). Although after rehabilitation peak workload was increased by 24%, a similar oxidative stress response was found. Remarkably, a decrease in reactive oxygen species-induced DNA damage was detected after exercise at submaximal intensity despite increased exercise duration of 73%. In summary, patients with COPD had increased pulmonary and systemic oxidative stress both at rest and induced by exercise. In addition, pulmonary rehabilitation increased exercise capacity and was associated with reduced exercise-induced oxidative stress.     

Melatonin inhibits lipid peroxidation and stimulates the antioxidant status of diabetic rats

Although melatonin has been established as a free radical scavenger and antioxidant, its effects in diabetes have not been thoroughly investigated. The purpose of this study, therefore, was to investigate the effects of melatonin administration on lipid peroxidation and antioxidant status in streptozotocin (STZ)-induced diabetes in rats. Concentrations of malondialdehyde (MDA) and reduced glutathione (GSH) in erythrocytes and activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were compared in 3 groups of 10 rats each [control non-diabetic rats (group I), untreated diabetic rats (group II) and diabetic rats treated with melatonin (group III)]. In the study groups, diabetes developed 3 days after intraperitoneal (i.p.) administration of a single 60-mg/kg dose of STZ. Thereafter, while the rats in group II received no treatment, the rats in group III began to receive a 10-mg/kg i.p. dose of melatonin per day. After 6 wk, the rats in groups II and III had significantly lower body weights and significantly higher blood glucose levels than the rats of group I (P<0.001 and P<0.001, respectively). There were no significant differences in body weight or blood glucose levels between groups II and III. MDA levels in untreated diabetic rats were higher than those in control group rats and in diabetic rats treated with melatonin (P<0.01 and P<0.05, respectively). However, MDA levels in diabetic rats treated with melatonin were not different from those of the control group. The GSH, GSH-Px and SOD levels of untreated diabetic rats were significantly lower than those of the control group (P<0.02, P<0.002 and P<0.05, respectively). In group III, however, melatonin prevented decreases in the thiol antioxidant and the associated enzymes, and so these levels were not significantly different from those in the control group. These results confirm the presence of oxidative stress in STZ-induced experimental diabetes and indicate the beneficial free radical-scavenging and antioxidant properties of melatonin.     

Oxidative stress in adult dengue patients

An association between viral diseases and increased oxidative stress has been suggested. The time course of serum levels of total antioxidant status (TAS), peroxidation potential (PP), glutathione (GSH), lipid peroxidation measured as hydroperoxides, and malondyaldehyde and 4-hydroxyalkenals (MDA + 4-HDA), as well as antioxidant enzymatic activity of superoxide dismutase (SOD) and glutathione peroxidase (GPx), were measured in 22 serologically confirmed dengue patients. Most of the patients had dengue fever and three of them had dengue hemorrhagic fever. The redox parameters were compared with those of age- and sex- matched controls. No significant difference was observed for levels of GSH and TAS between patients and controls. Levels of PP, MDA + 4-HDA, and SOD were significantly higher. Levels of GPx and total hydroperoxides were significantly lower in patients in comparison with controls. These findings suggest that the alteration in redox status could result of increased oxidative stress and it may play a role in the pathogenesis of the disease.     

Amelioration of altered antioxidant enzymes activity and glomerulosclerosis by coenzyme Q10 in alloxan-induced diabetic rats

Coenzyme Q10 is a natural antioxidant and scavenging free radicals. In the present study, we examined antioxidative activities of coenzyme Q10 and possible protective effect of coenzyme Q10 on in vivo and in vitro lipid peroxidation, antioxidant enzymes activity and glomerulosclerosis in alloxan-induced type 1 diabetic rats. Thirty Sprague–Dawley male rats were divided into three groups randomly: group 1 as control, group 2 as diabetic untreatment, and group 3 as treatments with coenzyme Q10 by 15 mg/kg i.p. daily, respectively. Diabetes was induced in the second and third groups by alloxan injection subcutaneously. After 8 weeks, animals were anaesthetized, liver and kidney were then removed immediately and used fresh or kept frozen until their lipid peroxidation analysis. Blood samples were also collected before killing to measure the lipid peroxidation and antioxidant enzymes activity. Kidney paraffin sections were prepared and stained by periodic acid-Schiff method. Glomerular volume and leukocyte infiltration were estimated by stereological rules and glomerular sclerosis was studied semi-quantitatively. Coenzyme Q10 significantly inhibited leukocyte infiltration, glomerulosclerosis and the levels of malondialdehyde (MDA) serum and kidney content in treated group compared with the diabetic untreated group. Coenzyme Q10 significantly inhibited LDL oxidation in vitro. Coenzyme Q10 significantly increased the serum levels of glutathione (GSH) and serum activity of catalase (CAT) and superoxide dismutase (SOD) in treated group compared with the diabetic untreated group. Coenzyme Q10 alleviates leukocyte infiltration and glomerulosclerosis and exerts beneficial effects on the lipid peroxidation and antioxidant enzymes activity in alloxan-induced type 1 diabetic rats.     

慢性阻塞性肺疾病患者氧化应激与肺功能的相关性

目的探讨COPD患者氧化应激状态以及对肺功能的影响。方法选择COPD患者88例,行肺功能测定,根据FEV1%及FEV1/FVC分为轻、中、重三组,并对所有入选者抽取静脉血,化学比色法检测血清还原型谷胱甘肽(GSH)、丙二醛(MDA)、超氧化物歧化酶(SOD)的水平。结果与轻度组比较,中、重度COPD患者SOD、GSH水平明显下降,MDA明显升高(P<0.05、P<0.01)。相关分析显示:MDA与肺功能(FEV1%、FEV1/FVC)呈负相关(P<0.01、P<0.05),SOD、GSH与肺功能呈正相关(P<0.01、P<0.05)。结论 COPD患者体内存在氧化应激失衡,随着氧化/抗氧化功能失衡加重,肺功能下降加剧。     

Oxidative stress in gastric mucosa in Helicobacter pylori infection.

BACKGROUND: Infection with Helicobacter pylori is believed to be associated with generation of reactive oxygen molecules which leads to oxidative stress in the gastric mucosa; but the relation between oxidative stress and gastrointestinal mucosal damage has not been documented. AIM: To look for evidence of oxidative stress and lipid peroxidation in the gastric mucosa in H. pylori-associated peptic ulcer. METHODS: 34 duodenal ulcer (DU) patients with H. pylori infection, 14 DU patients without H. pylori infection and 10 healthy subjects without H. pylori infection were studied. H. pylori infection was diagnosed by histology and rapid urease test on endoscopic biopsies from the gastric body and antrum. Reduced glutathione (GSH) and malondialdehyde (MDA) content were measured in biopsies taken from the gastric antrum. Statistical analysis was done using Student's t test. RESULTS: Tissue levels of GSH were significantly lower (91.7 [35.4] nmole/100 mg versus 147.3 [41.2] nmole/100 mg; p < 0.001) and MDA higher (163.0 [83.4] nmole/100 mg versus 109.2 [51.3] nmole/100 mg; p < 0.01) in patients with DU associated with H. pylori infection as compared to those without H. pylori infection. GSH levels were significantly lower and MDA levels higher in DU patients with or without H. pylori infection as compared to control subjects. Serum MDA levels in DU patients with H. pylori infection were also significantly higher than in patients without H. pylori infection. CONCLUSION: Depletion of gastric mucosal glutathione in H. pylori-infected DU patients may be due to failure of the antioxidant defense system. Failure of the glutathione-dependent defense system results in accumulation of free radicals which can initiate membrane damage by lipid peroxidation.