Effects of organophosphorus insecticide phosphomidon on antioxidant defence components of human erythrocyte and plasma.

Effect of organophosphorus insecticide, phosphomidon (250 and 500 ppm) on human erythrocyte and plasma were studied in vitro to get insight into the cellular antioxidant defence mechanism and malondialdehyde formation. The antioxidant defence system of erythrocyte was altered as evident by depression of glutathione reductase, glucose 6 phosphate dehydrogenase, whereas the level of reduced glutathione, glutathione peroxidase, glutathione-S-transferase, superoxidedismutase and catalase were stimulated. In the case of plasma fraction, glutathione reductase, glutathione peroxidase, glutathione-s-transferase, glucose-6-phosphate dehydrogenase, superoxide dismutase and levels of reduced glutathione were significantly depressed and the malondialdehyde formation and catalase activity were elevated indicating the less adaptive response of plasma to protect it from oxidative damage.     

Increased Oxidant Stress and Decreased Antioxidant Status in Erythrocytes of Rats Fed with Zinc-deficient Diet

The aim of this study was to evaluate the lipid peroxidation, nitric oxide (NO), and free radical scavenging enzyme activities in erythrocytes of zinc (Zn)-deficient rats and to investigate the relationship among these parameters in either group. Sixteen male rats with a weight of 40-50 g were used for the experiment. The rats were divided into control (n = 8) and Zn-deficient groups. At the end of the experiment, the animals were anesthetized with ketamine-HCl (Ketalar, 20 mg/kg(-1), i.p.), and the blood was collected by cardiac puncture after thoracotomy. Blood samples were collected in vacutainer tubes without and with K(3)-EDTA as anticoagulant. Erythrocyte catalase (CAT), glutathione peroxidase (GSH-Px), glutathione reductase (GRD), glutathione-S-transferase (GST), superoxide dismutase (SOD) activities, total (enzymatic plus nonenzymatic) superoxide scavenger activity (TSSA), nonenzymatic superoxide scavenger activity (NSSA), antioxidant potential (AOP), and serum zinc (Zn) values in the Zn-deficient group were significantly lower than those of the control group, whereas NO and malondialdehyde (MDA) levels were significantly higher than those of the control group. The results show that Zn deficiency causes a decrease in antioxidant defense system and an increase in oxidative stress in erythrocyte of rats.     

Does the platelet-activating factor affect the antioxidant defense system?

The platelet-activating factor (PAF) is an inflammatory mediator and it may exert some of its effects by reactive oxygen species (ROS). We investigated the effects of PAF and hyperbaric oxygenation (HBO) on copper (Cu) and zinc (Zn) levels in plasma and the intracellular antioxidant enzyme activities of rats. PAF administration caused a decrease in erythrocyte catalase (CAT) and glutathione peroxidase (GPx) activities and in the plasma zinc level. Following PAF administration, exposure to HBO also caused a decrease in erythrocyte GPx activity. These results support the hypothesis that PAF may produce free oxygen radicals and HBO enhances this effect. The enzyme activities of the antioxidant defense system were found to be affected by these oxidative processes. This is likely to be the result of excessive production of ROS or overutilization and/or inhibition of the antioxidant enzymes.     

Age-related peculiarities of antioxidant system functioning in the blood of ostriches

The intensity of lipid peroxidation, activity of some enzymes antioxidant system - superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glutathione-S-transferase, amount of recovered glutathione and ceruloplasmin in the blood serum of ostriches in a period from 6- to 60-month age were first investigated. The increase of concentration of lipid peroxidation products is accompanied by the decline of amount of general lipids in the ostriches blood. Every life cycle period of ostriches is characterized by the indexes of functioning of the antioxidant system and intensity of accumulation intermediate lipid peroxidation products inherent in it. The pubescence period and intensive oviposition are characterized by the increase of products lipid peroxidation concentration and decrease of antioxidant enzymes activity, which can testify to the exhaustion of protective possibilities of enzymatic link of antioxidant defence.     

Naringin Mitigates Erythrocytes Aging Induced by Paclitaxel: An In Vitro Study

In this study, the protective role of naringin (NAR) against paclitaxel (PTX)‐induced erythrocytes aging has been investigated using human erythrocyte as an in vitro model. Erythrocytes were incubated with PTX in the presence and absence of NAR. Incubation of erythrocytes with PTX resulted in increased protein carbonyl content and malondialdehyde and hemolysis percentage compared with control. Furthermore, a significant increase in the ratios of glutathione peroxidase/glutathione reductase, superoxide dismutase/glutathione peroxidase, and superoxide dismutase/catalase in PTX‐treated cells was observed, compared with control cells. In contrast, reduced glutathione/oxidized glutathione ratio and glucose‐6‐phosphate dehydrogenase activity were decreased upon PTX treatment. The simultaneous incubation of erythrocytes with PTX and NAR restored these variables to values similar to those of control erythrocytes. These results suggest that NAR inhibited PTX‐induced aging by lessening the PTX‐induced oxidative stress.     

Protective role of <Emphasis Type="SmallCaps">l</Emphasis>-ascorbic acid on antioxidant defense system in erythrocytes of albino rats exposed to nickel sulfate

In this experimental study, we investigated whether l-ascorbic acid has any influence on the blood antioxidant defense system, lipid peroxidation and hematological parameters of the albino rats exposed to nickel sulfate(NiSO₄).Twenty four adult rats were divided into four groups of six animals in each group. The control rats were untreated and comprised Group I. Group II rats were administered nickel sulfate (2.0 mg/100 g b.wt.; intraperitonially, i.p.). Group II rats were treated orally l-ascorbic acid (50 mg/100 g b.wt.) and Group IV rats were given both nickel sulfate and l-ascorbic acid simultaneously on alternate days until the tenth dose. The hematological parameters were assessed: red blood corpuscle counts, packed cell volume %, hemoglobin concentration, white blood corpuscle counts and platelets count decreased significantly and clotting time increased significantly in nickel treated rats. We also observed increase malondialdehyde (MDA) and decrease glutathione level (GSH) in erythrocytes of nickel treated rats. The activities of erythrocyte antioxidant enzymes like superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) were significantly increased in rats treated with nickel sulfate. Simultaneously treatment of l-ascorbic acid exhibited a possible protective role on the toxic effect of nickel sulfate on the hematological values, erythrocyte MDA and GSH concentrations as well as antioxidant enzymatic defense system.     

Effects of smoking and tumor process on the contents of key proteins of apoptosis and activity of antioxidant enzymes in blood

The effects of smoking on the contents of the apoptosis markers Bcl-2 and p53 proteins in blood plasma; the activity of the antioxidant (AO) enzymes Cu,Zn superoxide dismutase (SOD), glutathione peroxidase (GP), glutathione reductase (GR), glutathione S-transferase (GST), and catalase; and the content of malondialdehyde (MDA) in erythrocytes from healthy donors and cancer patients were studied. Two groups of donors were revealed among healthy smokers: one with high SOD and GP activities and high Bcl-2 protein levels and the other with lower Bcl-2 levels compared with those found in nonsmokers. In the group of cancer patients (both smokers and nonsmokers), significantly increased p53 protein levels and increased activity of GST were found. A negative correlation between MDA and GST in the group of smoking healthy donors and a positive correlation between MDA and p53 in cancer patients were found. The results suggest a relationship between the components of enzymatic defence and lipid peroxidation and the content of apoptosis regulator proteins in healthy smokers and cancer patients.     

Inactivation of red cell glutathione peroxidase by divicine and its relation to the hemolysis of favism

A significant inactivation of red blood cell glutathione peroxidase (25% less than the physiological value) was observed after exposure of intact erythrocytes to 2 mM divicine (an autoxidizable aminophenol from Vicia faba seeds) and 2 mM ascorbate for 3 h at 37 degrees C. Addition of catalase and conversion of Hb to the carbomonoxy derivative resulted in protection against enzyme inactivation. Oxidation of Hb was a concurrent phenomenon, and augmented the inactivating effect. In hemolysates, much stronger effects were observed at shorter times (2 h); divicine was effective also without ascorbate, and the presence of reductants (ascorbate or glutathione or NADPH) enhanced its inactivating power. Of the other antioxidant enzymes, superoxide dismutase was unaffected under the same experimental conditions. Catalase was found to be much less sensitive to the inactivation; it was almost unaffected in experiments with intact erythrocytes and specifically protected by NADPH in experiments with hemolysates. This specific damage of glutathione peroxidase, apparently involving interaction of H2O2 and HbO2, may be related to the pathogenesis of hemolysis in favism.     

Lipid peroxidation and antioxidant enzymes in vanadate-treated rats

Male Wistar rats received an aqueous solution of ammonium metavanadate (AMV) of 0.15 mg/V/ml concentration instead of water for 14 days. The erythrocyte count and haemoglobin level in blood were not changed; the haematocrit index was slightly increased. The spontaneous lipid peroxidation in kidney and liver homogenates was increased. The Fe(II)- or ascorbate-induced lipid peroxidation was more pronounced in the kidney than in the liver. No changes in lipid peroxidation were observed in erythrocytes after AMV treatment. The AMV treatment resulted in a decrease in the activity of the antioxidant enzymes, catalase and glutathione peroxidase in the kidney and liver; the cytosolic Cu,Zn-SOD and mitochondrial Mn-SOD were unchanged. The activity of the enzymes in blood was not changed. The results are discussed with a view to the participation of lipid peroxidation in vanadium toxicity.     

Antioxidant status and lipid peroxidation in type II diabetes mellitus

Diabetes Mellitus (DM), a state of chronic hyperglycaemia, is a common disease affecting over 124 million individuals worldwide. In this study, erythrocyte glutathione levels, lipid peroxidation, superoxide dismutase, catalase, and glutathione peroxidase and some extracellular antioxidant protein levels of patients with type II diabetes mellitus and healthy controls were investigated. Thirty-eight patients (21 males; with age of mean +/- SD, 53.1+/-9.7 years) and 18 clinically healthy subjects (10 males; with age of mean +/- SD, 49.3+/-15.2 years) were included in the study. Levels of erythrocyte lipid peroxidation, serum ceruloplasmin and glucose levels, HbA1C levels, and erythrocyte catalase activity were significantly increased, whereas serum albumin and transferrin levels, erythrocyte glutathione levels, and glutathione peroxidase activity were significantly decreased compared to those of controls. There was no significant difference in superoxide dismutase activity compared to controls. The results suggest that the antioxidant deficiency and excessive peroxide-mediated damage may appear in non-insulin dependent diabetes mellitus.     

Effect of vitamin E supplementation on diabetes induced oxidative stress in experimental diabetes in rats

Diabetes induced by streptozotocin (50 mg/kg body wt, i.p.) in the rats substantially increased the plasma glucose and malondialdehyde levels along with corresponding decrease in the antioxidants levels. Supplementation of vitamin E (200 mg/kg body wt., ip) for 5 weeks resulted in non-significant decrease in the blood glucose levels but plasma malondialdehyde levels were reduced to below normal levels. Plasma vitamin E, vitamin C, uric acid and red blood cell glutathione levels were also restored to near normal levels on vitamin E supplementation to diabetic rats as compared to control (diabetic) rats. The activities of antioxidant enzymes, catalase (EC 1.11.1.6), glutathione peroxidase (GSHPx EC 1.11.1.9), and glutathione reductase (GR EC 1.6.4.2) were also concomitantly restored to near normal levels by vitamin E supplementation to diabetic rats. The results clearly demonstrated that vitamin E supplementation augments the antioxidant defense mechanism in diabetes and provides evidence that vitamin E may have a therapeutic role in free radical mediated diseases.     

Evaluation of oxidative stress markers in neonates with intra-uterine growth retardation

Intra-uterine growth retardation (IUGR) is an abnormality of pregnancy. Neonates with IUGR weigh less than the 10th percentile for gestational age. The objective of the study was to identify the relationship between IUGR and the antioxidant status. Cord blood of 157 neonates with normal weight (control group) and 29 neonates with IUGR were included. The following parameters were determined and compared in the two groups: lipid peroxidation in the plasma, red blood cells and erythrocyte ghosts; protein and DNA damage; antioxidant enzyme activities (superoxide dismutase, catalase, glutathione peroxidase); the level of reduced glutathione; and the ferric reducing ability of the plasma. The level of lipid peroxidation was significantly higher in the IUGR group. The antioxidant enzyme activities and the levels of antioxidants were significantly lower in the IUGR group. Damage of proteins and DNA was slightly, but non-significantly, higher in the IUGR group. Neonates with IUGR seem to have significant deficiencies in antioxidant defence. IUGR is correlated with significant oxidative stress.     

Effects of halothane, enflurane, and isoflurane on plasma and erythrocyte antioxidant enzymes and trace elements

Alterations of the normal redox balance in mammals might be attributed to increases of plasma free-radical concentrations and/or a disruption of the protective mechanisms. These conditions lead to damage to cellular structure by the mechanism of lipoperoxidation, particularly in the liver, kidney, and central nervous system. In this study, the effect of general anesthesia on the oxidative metabolism of human plasma and erythrocytes was investigated. Forty-five patients undergoing anesthesia by using halothane, enflurane, or isoflurane were included in this study. Blood samples were taken preoperatively, the first hour, the first day, and the third day after the operation. Superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) enzyme activities and trace elements such as cofactor copper (Cu), zinc (Zn) and selenium (Se) levels were measured in plasma and red blood cells. Our results showed that halothane and enflurane administration increased the plasma GSH-Px activity and reduced zinc levels. In addition, they lowered SOD and GSH-Px activities and trace element levels on erythrocytes. Isoflurane had no effect on plasma antioxidant enzymes, but, similar to the other, isoflurane decreased the plasma zinc levels, erythrocyte SOD and GSH-Px activities and trace element levels. Gülhane Military Medical Academy     

Estimation of cell membrane properties and erythrocyte red-ox balance in patients with metabolic syndrome

Metabolic syndrome (MS) is associated with occurrence of the many cardiovascular risk factors such as atherogenic dyslipidemia, visceral fat distribution, arterial hypertension and pro-thrombotic and pro-inflammatory status. In our study the effect of disorders that appear in MS on red-ox balance and erythrocyte cell membrane properties were estimated. The study comprised 50 patients with diagnosed MS and in 25 healthy subjects. Content of thiobarbituric acid reactive substances (TBARS) and catalase, superoxide dismutase and glutathione peroxidase activity were estimated in red blood cells. Moreover, conformation status of membrane proteins, membrane fluidity and osmotic fragility were evaluated. MS was found to manifest: (1) the increase of the concentration of TBARS in erythrocytes with no statistically significant differences in antioxidant enzymes activity, (2) disorders in the structure of erythrocyte cytoskeleton proteins, (3) the increase in membrane lipids fluidity at the depth of 5th and 12th carbon atom of fatty acid hydrocarbon chain and significantly decreased fluidity at the depth of 16th carbon atom, (4) increased erythrocyte osmotic fragility.     

Protective influence of vitamin E on antioxidant defense system in the blood of rats treated with cadmium

The effects of acute exposure to cadmium (Cd) on the blood antioxidant defense system, lipid peroxide concentration and hematological parameters, as well as the possible protective role of vitamin E were studied. Male Wistar albino rats (3 months old) were treated with cadmium (0.4 mg Cd/kg b.m., i.p., 24 h before the experiment) or with vitamin E + Cd (20 IU Vit E/kg b.m., i.m., 48 h + 0.4 mg Cd/kg b.m., i.p., 24 h before the experiment). The hematological parameters were assessed: red blood cell counts, hematocrit value and hemoglobin concentration were significantly decreased in the blood of Cd-treated rats. Intoxication with cadmium was also followed by significantly increased lipid peroxide concentrations. We also observed increased activity of antioxidant defense enzymes: copper zinc containing superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glutathione-S-transferase as well as concentrations of non-enzymatic components of antioxidant defense system: reduced glutathione, vitamin C and vitamin E. Pretreatment with vitamin E exhibited a protective role on the toxic effects of cadmium on the hematological values, lipid peroxide concentration as well as on enzymatic and non-enzymatic components of antioxidant defense system.     

Oxidative damages in erythrocytes of patients with metabolic syndrome

The aim of the study was to estimate the changes caused by oxidative stress in structure and function of membrane of erythrocytes from patients with metabolic syndrome (MS). The study involved 85 patients with MS before pharmacological treatment and 75 healthy volunteers as a control group. Cholesterol level, lipid peroxidation, glutathione level (GSH), and antioxidant enzyme activities in erythrocytes were investigated. The damage to erythrocyte proteins was also indicated by means of activity of ATPase (total and Na⁺,K⁺ ATPase) and thiol group level. The membrane fluidity of erythrocytes was estimated by the fluorescent method. The cholesterol concentration and the level of lipid peroxidation were significantly higher, whereas the concentration of proteins thiol groups decreased in the patient group. ATPase and GSH peroxidase activities diminished compared to those in the control group. There were no differences in either catalase or superoxide dismutase activities. The membrane fluidity was lower in erythrocytes from patients with MS than in the ones from control group. These results show changes in red blood cells of patients with MS as a consequence of a higher concentration of cholesterol in the membrane and an increased oxidative stress.     

Effects of Lead on Hepatic Antioxidant Status and Transcription of Superoxide Dismutase Gene in Pigs

Ninety-six castrated boars (Duroc x Landrace x Yorkshire) were randomly divided into four groups, each of which was replicated three times with eight pigs. The groups received the same basal diet supplemented with 0, 5, 10, and 20 mg/kg lead, respectively. The malondialdehyde and glutathione levels, antioxidant enzymes activities, and zinc/copper superoxide dismutase (Zn/Cu SOD) mRNA content in the liver were determined to evaluate the lead hepatic intoxication caused by the lead. Results showed the increased lipid peroxides level and the reduced glutathione content, along with a concomitant decrease in the activities of superoxide dismutase, catalase, and glutathione peroxidase. Moreover, the level of hepatic Zn/Cu SOD mRNA was also significantly reduced. We suggest potential mechanism for lead intoxication in liver as follows: lead causes parallel decrease in Zn/Cu SOD mRNA and activities of antioxidant enzymes, leading to the declined ability of scavenging free radicals with excessive production of lipid peroxides, which seriously damages the hepatic structure and function.     

The state of the antioxidant system during therapy of patients with multiple sclerosis

Activity of erythrocyte glutathione peroxidase (GPx), glutathione reductase (GR), glutathione transferase (GT), glucose-6-phosphate dehydrogenase (G6PDH), catalase and superoxide dismutase (SOD), the level of erythrocyte malonic dialdehyde (MDA) and also total antioxidant activity of blood serum were studied in patients with different types of multiple sclerosis (MS). Investigation of peripherical blood was carried out on the first day of admission to the hospital and after the standard therapy with copaxone. During the whole period of observation all MS patients had a high level of MDA and activity of erythrocyte GP compared with a control group. Other erythrocyte antioxidant enzymes and total antioxidant activity of blood serum exhibited weak positive dynamics in patients with relapsing-remitting multiple sclerosis (RRMS). The pathological decrease of antioxidant system activity in patients with secondary progressive multiple sclerosis (SPMS) was more pronounced and remained unchanged after the treatment. This is consistent with a more severe clinical course of this disease.     

Inactivation of red cell glutathione peroxidase by divicine and its relation to the hemolysis of favism

A significant inactivation of red blood cell glutathione peroxidase (25% less than the physiological value) was observed after exposure of intact erythrocytes to 2 mM divicine (an autoxidizable aminophenol from Vicia faba seeds) and 2 mM ascorbate for 3 h at 37°C. Addition of catalase and conversion of Hb to the carbomonoxy derivative resulted in protection against enzyme inactivation. Oxidation of Hb was a concurrent phenomenon, and augmented the inactivating effect. In hemolysates, much stronger effects were observed at shorter times (2 h); divicine was effective also without ascorbate, and the presence of reductants (ascorbate or glutathione or NADPH) enhanced its inactivating power. Of the other antioxidant enzymes, superoxide dismutase was unaffected under the same experimental conditions. Catalase was found to be much less sensitive to the inactivation; it was almost unaffected in experiments with intact erythrocytes and specifically protected by NADPH in experiments with hemolysates. This specific damage of glutathione peroxidase, apparently involving interaction of H₂O₂ and HbO₂, may be related to the pathogenesis of hemolysis in favism.     

Study of the indices of antioxidant defense in mental maladaptation

Changes in the balance of the pro- and antioxidant systems were studied in patients with mental maladaptation induced by emotional stress. We found activation of lipid peroxidation associated with accumulation of malondialdehyde in erythrocytes and blood serum of the subjects. The activity of catalase and glutathione peroxidase in erythrocytes in patients with mental stress increased, whereas the activities of glutathione reductase, glutathione-S-transferase, and glucose-6-phosphate dehydrogenase significantly decreased as compared to the group of healthy individuals. Comparative chemiluminescent analysis of the blood serum revealed a decrease in general antioxidant properties of the blood in the groups studied after mental stress.