Erythrocyte Antioxidant System Research Articles

Erythrocyte antioxidant systems protect cultured endothelial cells against oxidant damage.

A study was undertaken to assess the ability of the erythrocyte to protect other tissues against oxidative damage. Radiolabelled (51Cr) human umbilical vein endothelial cells (HUVEC) were incubated with erythrocytes and neutrophils activated with phorbol myristate acetate (PMA). Damage to the endothelial cells was indicated by release of radioactivity into the suspending medium. We found that the co-incubation of HUVEC with an increasing range of erythrocyte concentrations resulted in a dose-dependent reduction in the release of radioactivity. When the ability of superoxide to cross the erythrocyte membrane or the glutathione systems was inhibited, the extent of endothelial cell damage increased. Inhibition of the catalase system did not affect results. It was concluded that the erythrocytes afforded some protection against oxidative damage to the endothelial cells by taking up and deactivating the superoxide ions. This protection depends upon intact erythrocyte antioxidant systems. These data support the hypothesis that erythrocytes can provide antioxidant protection to other tissues in vivo.

The role of erythrocytes in the inactivation of free radicals

We propose that, in addition to its function of gas exchange, the erythron provides a mechanism for the inactivation of reactive oxygen and oxide radicals in vivo. In carrying out this function, individual erythrocytes undergo changes in biochemical and structural properties, which are reflected by shape and functional alterations. The changes indicate damage to the labile components of the red cell and demonstrate the expendable nature of the individual red cell. We propose that a superoxide anion channel allows the transport of superoxide and other free radicals into the red cell, where they are deactivated by the erythrocyte antioxidant system which effectively prevents extensive oxidative damage to tissues.

Abnormal antioxidant system in erythrocytes of mercury-exposed workers

Abnormal antioxidant system in erythrocytes of mercury-exposed workers

The effect of selenium on antioxidant system in erythrocytes and liver of the carp (Cyprinus carpio L.)

The effect of selenium‐supplemented diet (sodium selenate and selenium yeast) on antioxidant in erthrocytes and liver of the carp (Cyprinus carpio L.) fingerlings was studied. With this goal, the activities of glutathione peroxidase (GSH‐Px), catalase (CAT), superoxide dismutase (SOD), glutathione reductase (GR) and glutathione‐S‐transferase (GST), as well as glutathione (GSH + GSSG) level, were determined. In the group supplemented with sodium selenate, no significant changes in the activity of the above enzymes were recorded in both the erythrocytes and in the liver, with the exception of GST activity that was significantly reduced in the plasma compared with the controls. Glutathione content was at the control level. In the group supplemented with selenium‐yeast, the activities of GSH‐Px, CAT, and SOD were significantly increased in erythrocytes, whereas GST activity and plasma content of GSH + GSSG were reduced compared with the controls. At the same time, the activities of hepatic SOD and GST were increased compared with the controls. These results demonstrate that organically bound selenium (selenium‐yeast) acts more efficiently on antioxidant system of the carp fingerlings than inorganic selenium salts.

Cadmium-Induced Lipid Peroxidation and the Antioxidant System in Rat Erythrocytes : the Role of Antioxidants

Cadmium (Cd)-induced oxidative damage in erythrocytes causes loss of membrane function by enhancing lipid peroxidation (LPO) and altering the erythrocyte antioxidant system. Vitamin E and/or selenium (Se) was administered to rats, prior to Cd intoxication, in order to prepare the animals to withstand oxidative assault. The treatment with Cd increased LPO in erythrocytes while animals pretreated with vitamin E and/or Se prior to Cd treatment showed decreased LPO as compared with animals given Cd alone. The erythrocyte SOD and CAT activities decreased significantly with Cd treatment. The pretreatment with vitamin E and/or Se prior to Cd administration partially reversed such changes. The erythrocytes showed a marked depletion in glutathione (GSH) content with Cd treatment. The antioxidant treatments before Cd administration helped to maintain the erythrocyte GSH content. The erythrocyte glutathione reductase (GSH-R) activity increased markedly when treatments with vitamin E and Se were applied. The GSH-R activity was not observed to decrease in animals treated with antioxidant prior to Cd intoxication, which may mean that the replenishment of erythrocyte GSH content is via GSH-R. The glutathione-S-transferase (GST) activity increased significantly with Cd intoxication; however, treatment with antioxidants prior to Cd treatment decreased erythrocyte GST activity. The results show that Cd-induced LPO decreased the antioxidant capability of the erythrocytes, causing erythrocyte membrane damage.

Erythrocyte selenium-glutathione peroxidase activity is lower in patients with coronary atherosclerosis.

To obtain further insight into the role of erythrocyte antioxidant systems in the development of atherosclerosis, intraerythrocyte enzyme activities and selenium levels in erythrocytes were determined in 37 patients with angiographically proved coronary artery stenosis and 15 subjects with normal coronary angiograms as controls. In a preliminary study, the enzymatic activities of glucose-6-phosphate dehydrogenase (G6PD), glutathione reductase (GR) and selenium-dependent glutathione peroxidase (Se-GPx) were measured in both venous and arterial blood samples obtained from patients before angiography. The data of the preliminary study, which showed that only the Se-GPx decreased in the patients, led us to concentrate on the Se-GPx and Se levels to determine the changes in these variables. Our results showed that there was a decrease in both the activity of Se-GPx and Se levels in erythrocytes parallel to the increase in the severity of coronary artery disease. It was concluded that these parameters might be used as determinants in the assessment of the severity of the disease.

Investigation of erythrocyte membrane lipid peroxidation and antioxidant defense systems of patients with coronary artery disease (CAD) documented by angiography

In the present study, erythrocyte membrane lipid peroxidation, erythrocyte superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and serum vitamin C levels of subjects with and without coronary artery disease (CAD) documented by coronary angiography have been determined. Patients consisted of 42 subjects (31 male, 11 female) aged between 41 and 77 years and controls consisted of 35 subjects (21 male, 14 female) aged between 40 and 69 years. Erythrocyte lipid peroxidation of the patients was significantly higher ( P < 0.005) whereas erythrocyte SOD, GSH-Px activities and serum vitamin C levels were lower than those of controls. Our results show significant alteration in erythrocyte membranes and antioxidant status of patients with CAD. However, whether such alterations are a primary cause or consequence of CAD and whether these alterations can be used in the diagnosis and management of the disease needs further investigation.

Antioxidant systems and erythrocyte life-span in mammals

1. 1. Erythrocyte antioxidant systems—superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH), glutathione peroxidase (GSH-Px), glutathione S-transferase (GST) and glutathione reductase (GR)—were discussed in relation to life-spans in some mammalian species. 2. 2. The erythrocyte life-span of different mammals was found to be correlated with the levels of SOD, GSH-Px and GSH. 3. 3. Data reviewed indicates that the erythrocyte life-span of each species is governed by both the oxygen radical formation and the efficiency of intrinsic antioxidant systems.

Erythrocyte antioxidant system and serum ceruloplasmin levels in welders.

The erythrocyte antioxidant system (superoxide dismutase, catalase, glutathione peroxidase, reduced glutathione) and serum ceruloplasmin were studied in workers chronically exposed to welding fumes and gases, which are thought to be oxidant pollutants. Fifty-four healthy men using two electric arc welding processes (manual metal arc on stainless steel and mild steel, and metal inert gas on mild steel) were studied. The possible effects of cigarette smoking were also considered. The erythrocyte antioxidant system was in the normal range for all welders. Serum ceruloplasmin was significantly enhanced only in smoking welders and higher in manual metal arc than in metal inert gas welders, suggesting that the increase is related to the severity of the oxidant threat, which is more stressful for the workers using the manual metal arc technique because of the presence of stainless steel particles in the fumes. Although cigarette smoking alone did not increase serum ceruloplasmin levels, it affected the response to oxidant stress in welders.

Erythrocyte Antioxidant Activity, Serum Ceruloplasmin, and Trace Element Levels in Subjects with Alcoholic Liver Disease

Erythrocyte antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase) and reduced glutathione, serum ceruloplasmin, and serum trace elements (copper, zinc, iron, and selenium) related to antioxidant enzymes were assayed in subjects with alcoholic liver disease of different degrees of severity. The erythrocytes of subjects with moderate and severe alcoholic liver cirrhosis had an unbalanced antioxidant system (normal superoxide dismutase, low catalase and glutathione peroxidase activities, and low glutathione content). Serum ceruloplasmin levels were in the normal range. Levels of the serum trace elements zinc and selenium were significantly low in subjects with moderate and severe cirrhosis, whose red cell half-life was also significantly short, as measured by radioactive chromium. These data suggest that the erythrocytes of subjects with moderate and severe alcoholic liver cirrhosis are less protected against oxidant stress. The particular erythrocyte antioxidant system and serum trace element pattern may play a role in the genesis of hemolytic disorders and of alcoholic hepatic damage.

Whole blood superoxide anion generation and efficiency of some erythrocyte antioxidant systems during recombinant human erythropoietin therapy of uremic anemia

Six chronic uremic patients on regular hemodialysis treatment were given recombinant human erythropoietin (r-huEPO) in a dose of 50 U/kg of body weight intravenously thrice weekly for 14 weeks. Following r-huEPO therapy, unstimulated whole blood superoxide anion ( ▪ 2) generation did not change significantly, while opsonized zymosan-stimulated whole blood ▪ 2 generation increased. At the same time, erythrocyte superoxide dismutase and, in particular, glutathione peroxidase activities were found to be reducing with concomitant lowering of erythrocyte malonydialdehyde (MDA) concentrations and increase in plasma MDA concentrations.

A method to evaluate the antioxidant system for radicals in erythrocyte membranes

The erythrocyte defense system against cellular oxidants is complex and efficient. Free radicals generated in cell membranes, however, are relatively sequestered from the cell's antioxidant mechanisms. When a oxidant challenge exceeds the capacity of the erythrocyte's antioxidant system, membrane damage may occur, causing red cell destruction and hemolytic anemia. In this study, we present a method for monitoring radical reduction in eryhrocyte membranes, using fatty acid spin labels with cells are used. The electron paramagnetic resonance signals of the 5-doxylstearic acid spin labels in the intact cells are obtained as a function of time, at 37°C over a period of 2 h. The pseudo first-order rate constant for reduction of the spin label in normal adult intact cells under our experimental conditions is 4.3. ± 1.8 × 10 −3/min. The reproducibility and variability of the measurements are discussed. Since the measurements we describe reflect the extent of radical reductions occuring in cell membranes, we suggest that this method can be used to measure the ability to defend oxidants in membranes of erythrocytes with defective antioxidant systems. This method is particularly useful for measuring the modification of the antioxidant system toward radicals in membranes by drugs, chemicals, or environmental toxins.

Effect of unithiol and acetylcysteine on lipid peroxidation and the erythrocyte antioxidant system of sensitized guinea pigs

The effect of unithiol and acetylcysteine on lipid peroxidation, thioldisulfide equilibrium, glucose-6-phosphate dehydrogenase, glutathione reductase and lactate dehydrogenase activity and on erythrocyte resistance was studied in guinea-pigs during sensitization with C. maltosa. Sensibilized animals receiving thiol antioxidants showed partial restoration of normal biochemical levels.

Antioxidant System in Sickle Red Cells

Erythrocytes containing abnormal haemoglobins with high affinity for red cell membrane are subjected to enhanced oxidant stress. Since HbS is known to have high affinity for red cell membrane and sickle cells are particularly susceptible to membrane lipid peroxidation, the behaviour of erythrocyte antioxidant system has been evaluated in 20 subjects, heterozygous for sickle cell anaemia. These subjects have shown normal levels of reduced glutathione, increased superoxide dismutase and glutathione peroxidase activities and low catalase activity. These data suggest that such an unbalanced antioxidant system can not prevent damage by the enhanced production of oxygen free radicals by membrane-bound HbS molecules.

The effect of ethanol ingestion on the erythrocyte antioxidant defence systems of rats

The effect of ingestion of water containing 1 or 10% ethanol for a period of four weeks on serum vitamin E, hepatic glutathione peroxidase, erythrocyte-glutathione peroxidase, glutathione transferase, Superoxide dismutase and selenium has been investigated in rats. The serum levels of total and free vitamin E were not significantly affected by ethanol ingestion at either level. The level of erythrocyte glutathione peroxidase was decreased to 43 or 28 per cent of the control level by intake of either 1 or 10% ethanol solution, respectively, whilst there was no alteration in glutathione transferase activity. Ethanol treatment did not alter erythrocyte selenium levels or Superoxide dismutase activity. Hepatic glutathione peroxidase activity was increased to approximately 166 per cent of the control value by either 1 or 10% ethanol ingestion. The results indicate that the activity of the enzyme principally involved in preventing lipohydroperoxide-induced haemolysis is significantly reduced by ethanol ingestion.