Antioxidant Defense System In Erythrocytes Research Articles

The effect of nettle extract on antioxidant defense system in piglets after weaning

Background. The effect of common nettle (Urtica dioica L.) extracts on the free radical processes and antioxidant system in piglets during the critical period of weaning from sows has been studied. Materials and Methods. Large white piglets were divided into 2 groups (control and experimental), 9 animals in each. Piglets of the experimental group from 14 days of age and before weaning received the standard diet and the nettle extract in the dose of 6 mg/kg of body weight for 22 days. The blood, as well as erythrocyte hemolysates and plasma of piglets obtained at 14, 36, and 42 days of age, were studied. Results. Our results have shown that weaning causes an oxidative stress in piglets. This state leads to an increase in the concentration of metabolites of free radical damage to protein molecules – carbonyl groups of proteins on the first day and primary products of lipid peroxidation on the seventh day after weaning. This activation of oxidative damage occurs in piglets against the background of a physiologically immature antioxidant system and is characterized by a decrease in the activity of the enzymatic chain – superoxide dismutase, glutathione peroxidase and catalase, as well as the concentration of its non-enzymatic antioxidant – reduced glutathione. Feeding piglets with nettle extract leads to activation of the antioxidant defense system in erythrocytes (higher activity of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and an increased reduced glutathione level compared to the control values) and a decrease in the concentration of oxidative damage products in the plasma (the content of lipid hydroperoxides, TBA-active products and carbonyl groups of proteins). Conclusion. The positive effect of nettle extract on the inhibition of free radical processes and activation of antioxidant systems indicates that this extract can be added to the standard diet of young animals to increase stress resistance and adaptability of their organism in critical periods of ontogenesis.

Impaired enzymatic antioxidant defense in erythrocytes of rats with ammonia-induced encephalopathy: role NMDA receptors

Hepatic encephalopathy (HE), a medical term that deals with a neuropsychiatric disorder seen in patients with severe hepatic dysfunction, has been known for more than a century, however, pathogenetic mechanisms underlying cerebral dysfunction during conditions of liver disease are still not entirely understood. There is a consensus that an accumulation of ammonia in brain as a result of impaired detoxification capacity of the liver or the appearance of a portosystemic shunt is a primary cause of HE. Current evidence suggests that ammonia toxicity is mediated by hyperactivation of glutamate receptors, mainly N-methyl-D-aspartate receptors (NMDA-R) and affects many processes of aerobic metabolism that provides energy for a myriad of specific functions and viability of nerve cells. Recent reports on the presence of functional NMDA receptors in erythrocytes and deviations from normal ranges in many blood test parameters that was indicative of impaired hemodynamics and reduced carrying capacity for oxygen in erythrocytes in most patients with HE implicate the relationship between “erythrocyte damage” and cerebral dysfunction. In order to understand how, during hyperammonemia, disturbances in energy metabolism in brain that needs a constant supply of a high level of oxygen in the blood lead to encephalopathy, it is necessary to reveal ammonia-induced disorders in energy metabolism and antioxidant defense system of erythrocytes and explore the potential role of ammonia in reduced brain oxygenation. To detect the said missing link, the activities of erythrocyte antioxidant enzymes and concentrations of GSH, GSSG and H2O2 were measured in animals with hyperammonemia by using MK-801, a powerful noncompetitive NMDA receptor antagonist. It was found that the accumulation of ammonia in the blood of animals with hyperammonemia occurs within rat erythrocytes in large amounts and makes these cells which do not contain enzymes for the removal of ammonia, more susceptible to a prooxidant environment of ammonia created during oxidative stress that was completely or partially inhibited with the help of MK-801. Data obtained provide a support to identification of extra risk factors in cognitive disorders and in the prediction of unfavorable outcome with hypoperfusion in patients with elevated concentrations of ammonia in the blood.

Impaired Enzymatic Antioxidant Defense in Erythrocytes of Rats with Ammonia-Induced Encephalopathy: Role of NMDA Receptors.

Hepatic encephalopathy (HE), a neuropsychiatric disorder developing in patients with severe hepatic dysfunction, has been known for more than a century. However, pathogenetic mechanisms of cerebral dysfunction associated with liver disease are still poorly understood. There is a consensus that the primary cause of HE is accumulation of ammonia in the brain as a result of impaired liver detoxification capacity or the portosystemic shunt. Current evidence suggests that ammonia toxicity is mediated by hyperactivation of glutamate receptors, mainly N-methyl-D-aspartate receptors (NMDARs), and affects brain aerobic metabolism, which provides energy for multiple specific functions and neuronal viability. Recent reports on the presence of functional NMDARs in erythrocytes and the data on the deviations of blood parameters from their normal ranges indicate impaired hemodynamics and reduced oxygen-carrying capacity of erythrocytes in most patients with HE, thus suggesting a relationship between erythrocyte damage and cerebral dysfunction. In order to understand how hyperammonemia (HA)-induced disturbances in the energy metabolism in the brain (which needs a constant supply of large amounts of oxygen in the blood) lead to encephalopathy, it is necessary to reveal ammonia-induced impairments in the energy metabolism and antioxidant defense system of erythrocytes and to explore a potential role of ammonia in reduced brain oxygenation. To identify the said missing link, the activities of antioxidant enzymes and concentrations of reduced glutathione (GSH), oxidized glutathione (GSSG), and H2O2 were measured in the erythrocytes of rats with HA that were injected with the noncompetitive NMDAR antagonist MK-801. We found that in rats with HA, ammonia was accumulated in erythrocytes (cells lacking ammonia removal enzymes), which made them more susceptible to the prooxidant environment created during oxidative stress. This effect was completely or partially inhibited by MK-801. The data obtained might help to identify the risk factors in cognitive disorders and facilitate prediction of unfavorable outcomes of hypoperfusion in patients with a blood elevated ammonia concentration.

Effect of Ficus carica extract on hematological parameters and antioxidant defense system in erythrocytes of albino rats exposed to nickel chloride

Heavy metals including nickel have adverse effects on hematological system and red blood cells antioxidant defense. The purpose of the study is to examine the possible corrective effect of fig (Ficus carica L.) extract (FCE) on hematological parameters and antioxidant enzyme activities in red blood cells of rats exposed to sub-lethal concentration of nickel. Male Wistar rats were exposed to nickel chloride (10 mg/kg) and then treated or no with FCE (350 mg/kg) for 4-weeks. The intoxication induces alteration of haematological parameters and enhances blood haemolysis, generates oxidative stress induced decrease in the antioxidant enzyme activities and depletion in reduced glutathione levels in intoxicated group compared to the control group. The oral administration of FCE increase significantly hemoglobin levels (Hb), red blood cells count (RBC), hematocrit (Ht) and decreases white blood cells counts (WBC), and platelets in F. carica treated groups, and also the extract increase the GSH-Px and SOD antioxidant activity, GSH reserves in red blood cells, and reduces lipids peroxidation. The present study concludes that fig fruits may exhibit potent antioxidant potential for erythrocytes and have a positive effect on hematological system.

The Effect of Fullerenol C60(OH)36 on the Antioxidant Defense System in Erythrocytes.

Background: Fullerenols (water-soluble derivatives of fullerenes), such as C60(OH)36, are biocompatible molecules with a high ability to scavenge reactive oxygen species (ROS), but the mechanism of their antioxidant action and cooperation with endogenous redox machinery remains unrecognized. Fullerenols rapidly distribute through blood cells; therefore, we investigated the effect of C60(OH)36 on the antioxidant defense system in erythrocytes during their prolonged incubation. Methods: Human erythrocytes were treated with fullerenol at concentrations of 50–150 µg/mL, incubated for 3 and 48 h at 37 °C, and then hemolyzed. The level of oxidative stress was determined by examining the level of thiol groups, the activity of antioxidant enzymes (catalase, glutathione peroxidase, glutathione reductase, and glutathione transferase), and by measuring erythrocyte microviscosity. Results: The level of thiol groups in stored erythrocytes decreased; however, in the presence of higher concentrations of C60(OH)36 (100 and 150 µg/mL), the level of -SH groups increased compared to the control. Extending the incubation to 48 h caused a decrease in antioxidant enzyme activity, but the addition of fullerenol, especially at higher concentrations (100–150 µg/mL), increased its activity. We observed that C60(OH)36 had no effect on the microviscosity of the interior of the erythrocytes. Conclusions: In conclusion, our results indicated that water-soluble C60(OH)36 has antioxidant potential and efficiently supports the enzymatic antioxidant system within the cell. These effects are probably related to the direct interaction of C60(OH)36 with the enzyme that causes its structural changes.

Protective Effect of Melatonin Against Malathion Induced Alterations in Antioxidant Defense System and Morphology of Erythrocytes in Wistar Rats

Malathion intoxication has been shown to produce oxidative stress due to the generation of free radicals and alter the antioxidant defense system in erythrocytes. Previous studies have shown the ameliorative role melatonin against oxidative stress induced by generation of free radicals. Present study was designed to investigate the protective effect of melatonin against malathion induced oxidative stress. For this purpose, male Wistar rats were randomly divided into four groups: Control; Melatonin (10mg/Kg body weight) group; Malathion (250mg/Kg body weight) treated group; Malathion + Melatonin treated group. Animals were administered an acute dose of malathion orally. The result of this study shows that in vivo administration of malathion caused inhibition in AChE activity in erythrocytes. Malathion intoxication also significantly increased the oxidative damage as evidenced by increased level of LPO and GSH content. The Inhibition of GSH level and increased lipid peroxidation in erythrocytes was relieved in malathion + melatonin group. Enhanced activities of SOD, CAT, GR and GPx were observed in erythrocytes of malathion treated rats as compared to control group. Moreover, melatonin supplementation in malathion treated rats maintain normal level of antioxidant enzymes as compared to malathion treated rats which indicates that melatonin provide protection against malathion-induced oxidative stress in erythrocytes. No significant change in the membrane bound enzymes such as Na+/K+-ATPase, Mg2+-ATPase and Ca2+-ATPase was observed in malathion intoxicated rats. Findings of scanning electron micrographs of erythrocytes revealed that both the malathion treated and malathion+melatonin treated groups exhibited morphological changes in erythrocytes. However, concomitant melatonin supplementation normalized the morphological alterations in erythrocytes induced by malathion toxicity. In conclusion, melatonin supplementation may ameliorate malathion-induced oxidative imbalance by enhancing the glutathione level, reducing lipid peroxidation and normalizing antioxidant enzyme activities in erythrocytes.

Indicators of the antioxidant system in the long-term period after acute mercury nitrate poisoning in the experiment

The article presents experimental data on the state of the antioxidant system in red blood cells of white outbred rats 1 and 3 months after acute mercury nitrate poisoning with a semilethal dose. It has been established that this form of intoxication is accompanied by pronounced changes in the state of the antioxidant defense system in erythrocytes of poisoned animals (a decrease in the concentration of reduced glutathione, a decrease in the activity of superoxide dismutase and glutathione peroxidase, and an increase in the concentration of lipid peroxidation products).It has been shown that the mercury content in the blood of experimental animals remains elevated during the entire study period.The results obtained indicate the importance of impaired functioning of the antioxidant system in the implementation of long-term consequences of acute mercury poisoning. The reasons for the occurrence of these biochemical shifts and their role in the development of the long-term cytotoxic effects of mercury nitrate are discussed.

Protective effects of extracts of lichen Dirinaria consimilis (Stirton) D.D. Awasthi in bifenthrin- and diazinon-induced oxidative stress in rat erythrocytes in vitro

The intoxication of insecticides such as bifenthrin and diazinon has been reported to generate free radicals, and thereby alter the antioxidant defense system in erythrocytes. The present study is aimed to investigate the protective effects of acetone (DA) and methanolic (DM) extracts of lichen Dirinaria consimilis against bifenthrin and diazinon toxicity in rats’ erythrocytes in vitro. Rats’ erythrocytes were exposed to bifenthrin and diazinon, individually and also in combination with DA or DM at 1 ppm for 3 h at 37 ˚C. By using spectrophotometric methods, all the samples were estimated for changes in hemoglobin (Hb) concentration, malondialdehyde (MDA) levels, and enzyme [Superoxide dismutase (SOD), catalase (CAT), and glutathione S-transferases (GST)] activities. The outcomes showed that both the insecticides were highly toxic to rats’ erythrocytes. Among all groups, both the insecticides and DA exposed groups showed very low levels of MDA content, and GST activity in rats’ erythrocytes, when compared to the control. Besides, DA groups pretreated with both insecticides showed significant improvement of total Hb concentration, SOD, and CAT activities, with respect to the control. Hence, the present results indicate that the extracts of D. consimilis act as an antioxidant agent that reduces oxidative stress burden in insecticides toxicity.

In vitro toxicity of dimethyl phthalate to human erythrocytes: From the aspects of antioxidant and immune functions

In the study, the effects of dimethyl phthalate (DMP) on the antioxidant defense capacity and immune functions of human erythrocytes were experimentally explored. DMP affected the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) and the contents of glutathione (GSH) and malondialdehyde (MDA) in erythrocytes, thus impairing the function of antioxidant defense system of erythrocytes. When DMP concentration increased from 0 to 28 μmol L−1, the SOD and GPX activities were increased firstly and then gradually decreased. When DMP concentration was below 20 μmol L−1, the relative activity of SOD was enhanced by DMP and the effect was known as hormesis. The relative activity of GPX was also increased when the concentration of DMP was below 12 μmol L−1. The CAT activity was more significantly inhibited by DMP than the activities of SOD and GPX, whereas the relative GSH content was increased by DMP. MDA levels were significantly changed after the exposure to DMP (0–24 μmol L−1). The experimental results of the activity of SOD and CAT, and the content of MDA also suggested that DMP could inhibit the immune functions of red blood cells (RBCs), which were further proved by the decrease of two indicators (RBC-C3b and RBC-IC) due to the destruction of C3b receptor with immune adherence function on erythrocyte membrane. The study provides a deep understanding of the toxicity of DMP on erythrocytes.

Vitamin C as a modulator of oxidative stress in erythrocytes of stored blood

AimTo determine the effects of Vitamin C (VC-ascorbic acid) as an additive on erythrocytes of stored blood. BackgroundOxidative stress (OS) plays a major role in the formation of storage lesion of erythrocytes. Antioxidants, such as VC could be beneficial in combating oxidative damage during storage. Materials and methodsBlood obtained from male Wistar rats was stored at 4°C in anticoagulant solution citrate-phosphate-dextrose-adenine solution. Blood samples were divided into 3 groups – (i) Controls, (ii) VC 10 (VC at a concentration of 10mM), (iii) VC 30 (VC at a concentration of 30mM). Markers of OS in erythrocytes such as – hemoglobin, superoxides, antioxidant enzymes (superoxide dismutase; SOD, catalase and glutathione peroxidase), hemolysis, lipid peroxidation products (conjugate dienes and malondialdehyde), protein oxidation products and ascorbic acid were determined on days 0, 10 and 15 of storage. ResultsAddition of ascorbic acid to the storage solution contributed to the protection of erythrocytes from oxidative damage. Ascorbic acid at a concentration of 30mM decreased SOD levels and increased protein sulfhydryls (P-SH) levels on day 15 showing that higher concentration supplemented the inherent antioxidant defense system of erythrocytes during blood storage. ConclusionVC proved to be effective in combating OS during blood storage. However, further exploration of antioxidants as additives and the erythrocyte storage lesion would result in better management of blood storage.

Condition of erythrocyte membranes in people with mental and behavioural disorders caused by alcohol consumption

We studied the morphological features of the restructuring and osmotic stability of erythrocytes of 30 people with mental disorders and disorders of behavioural reactions caused by 5-7 years consumption of alcohol, the objects of the research being in a state of abstinence during the period of the investigation,. The study of quantitative composition of red blood cells and hemoglobin, as well as their ratio in people with mental and behavioural disorders developed as a result of alcohol consumption showed a decrease in the number of red blood cells and hemoglobin of 42.2% and 25.1%, respectively, indicating the presence in those people of anemic hypoxia. This is closely correlated with a decrease of osmotic resistance of red blood cells to different concentrations of sodium chloride solutions, whereby the state of erythrocyte membranes deteriorates and their resistance to hemolysis decreases. Parallel to this, is a reduction in the size of red blood cells coupled with a variety of changes in their microrelief. Conformational changes of erythrocytes are closely correlated with changes in the activity of enzymes responsible for the biotransformation of xenobiotics, primarily products of lipid peroxidation. It is shown that activity of the erythrocyte antioxidant defense system is sharply reduced as a result of increase in partially oxidized products of metabolism. It was found that the state of red blood cells is a sensitive indicator of the normal course of physiological changes, biochemical and biophysical processes in the bodies of people with mental disorders and behaviour reactions developed due to consumption of alcohol.At the same time, the measurement of the osmotic resistance of red blood cells and changes in the shape of red blood cells connected with this phenomenon is an important research method for studying mechanisms of pathological processes and the action of certain drugs or biologically active substances, expands the possibilities of establishing the depth of destruction of body tissues, and also provides excellent opportunities for researchers to identify the effectiveness of treatment and prevention for people with mental disorders and behaviour reactions caused by consumption of alcohol. This article discusses prospects of studies of the level of glutathione peroxidase activity in the erythrocytes among people with mental and behavioural disorders as a marker of highly specific homeostasis in the human body in response to long-term alcohol consumption, and considers using this index as a criterion for selecting patients for different groups of physical rehabilitation and recreation according to the level of rehabilitation potential.

Effect of arsenic acid withdrawal on hepatotoxicity and disruption of erythrocyte antioxidant defense system.

We investigated the effects of withdrawal from Sodium arsenite (NaAsO2) on the hepatic and antioxidant defense system in male Wistar rats using a before and after toxicant design. Rats were orally gavaged daily with varying doses of NaAsO2 for a period of 4 weeks. One half of the population was sacrificed and the remaining half had the toxicant withdrawn for another further 4weeks. Biochemical and immunohistochemical techniques were used to assess the impact of withdrawal on the erythrocyte and hepatic systems. Exposure of Wistar rats to NaASO2 led to a significant (p<0.05) increase in hepatic and erythrocyte markers of oxidative stress (malondialdehyde, thiol contents and hydrogen peroxide generation). Concurrently, there was a significant (p<0.05) increase in hepatic and erythrocyte antioxidant enzymes (glutathione-S-transferase, glutathione peroxidase and superoxide dismutase) following exposure. Withdrawal from NaAsO2 exposure led to a decline in both erythrocyte and hepatic markers of oxidative stress and together with a significant improvement in antioxidant defense system. Histopathology and immunohistochemistry revealed varying degrees of recovery in hepatocyte ultrastructure alongside increased expression of the pro-survival protein Kinase B (Akt/PKB) after 4 weeks of NaAsO2 withdrawal. Conclusively, withdrawal from exposure led to a partial recovery from oxidative stress-mediated hepatotoxicity and derangements in erythrocyte antioxidant system through Akt/PKB pathway.

Effect of Resveratrol, Cinnamaldehyde and their Combinations on the Antioxidant Defense System and ATP Release of Rabbit Erythrocytes: In vitro Study

Effect of Resveratrol, Cinnamaldehyde and their Combinations on the Antioxidant Defense System and ATP Release of Rabbit Erythrocytes: In vitro Study

Динаміка вмісту загальних ліпідів у еритроцитах свиней різних типів вищої нервової діяльності за дії стресових факторів

Динаміка вмісту загальних ліпідів у еритроцитах свиней різних типів вищої нервової діяльності за дії стресових факторів

Yacon (Smallanthus sonchifolius (Poepp. &amp; Endl.) H. Robinson) Improved Erythrocyte Resistance to Oxidative Stress in Streptozotocin-induced Diabetic Rats

Yacon demonstrating prominent hypoglycemic action and having high content of biologically active compounds, is recognized for their ability to capture free radicals. This study is aimed to evaluate the influence of yacon leaves and root tubers water extracts and aqueous suspension of root tubers powder on rats' erythrocyte antioxidant defense system under the experimental diabetes mellitus type 1. Healthy animals and animals with diabetes mellitus were treated with water extracts of yacon leaves and root tubers at dose 70 or 500 mg / kg /day and with aqueous suspension of root tubers powder at dose 500 mg / kg /day or the same suspension which was stabilized by biocomplex PS. Thiobarbituric acid reactive substances (TBARS) and protein carbonyl content (PCC), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) activity in erythrocytes lysates were measured. Water extracts of yacon leaves and root tubers and aqueous suspension of root tubers powder possess significant antioxidant effect, which was indicated by the decrease of TBARS and PCC and increase in SOD, CAT and GPx activity. Root tubers of yacon water extract at a dose of 500 mg/kg/day and aqueous suspension of root tubers powder stabilized by biocomplex PS possess he most pronounced antioxidant effect.

Disruption of erythrocyte antioxidant defense system, hematological parameters, induction of pro-inflammatory cytokines and DNA damage in liver of co-exposed rats to aluminium and acrylamide

The individual toxic effects of aluminium and acrylamide are well known but there are no data on their combined effects. The present study was undertaken to determine (i) hematological parameters during individual and combined chronic exposure to aluminium and acrylamide (ii) correlation of oxidative stress in erythrocytes with pro-inflammatory cytokines expression, DNA damage and histopathological changes in the liver.Rats were exposed to aluminium (50mg/kg body weight) in drinking water and acrylamide (20mg/kg body weight) by gavage, either individually or in combination for 3weeks.Exposure rats to AlCl3 or/and ACR provoked an increase in MDA, AOPP, H2O2 and a decrease in GSH and NPSH levels in erythrocytes. Activities of catalase, glutathione peroxidase and superoxide dismutase were decreased in all treated rats. Our results showed that all treatments induced an increase in WBC, erythrocyte osmotic fragility and a decrease in RBC, Hb and Ht. While MCV, MCH, MCHC remained unchanged. Hepatic pro-inflammatory cytokines expression including tumor necrosis factor-α, interleukin-6, interleukin-1β was increased suggesting leucocytes infiltration in the liver. A random DNA degradation was observed on agarose gel only in the liver of co-exposed rats to AlCl3 and ACR treatment.Interestingly, co-exposure to these toxicants exhibited synergism based on physical and biochemical variables in erythrocytes, pro-inflammatory cytokines and DNA damage in liver.

Catalase activity in blood fractions of patients with sporadic ALS

BackgroundOxidative stress may be a key element in pathogenesis of sporadic amyotrophic lateral sclerosis (sALS). Several studies proved that markers of peroxidation of lipids, proteins or nucleic acids are increased in postmortem tissue of sALS patients. However, much less is known about enzymatic antioxidant defense mechanism in sALS. ObjectivesThe aim of the study was to assess catalase (CAT) activity that is implicated in the defense against oxidative stress, in three blood fractions, i.e. erythrocytes, plasma and serum of sALS patients and healthy controls. MethodsAltogether 46 sALS patients and 54 controls were enrolled in the study. CAT activity was estimated using a commercially available assay kit. ResultsCAT activity in erythrocytes of sALS patients was significantly decreased compared to neurologically healthy controls (p=0.04), whereas CAT activity in plasma and serum was similar in both studied groups. ConclusionsCAT activity in erythrocytes, in contrast to other blood fractions is reduced in sALS cases as compared to controls, which may indirectly indicate that antioxidant defense system in erythrocytes is involved in pathogenesis of sALS.

Effect of 3‐bromopyruvic acid on human erythrocyte antioxidant defense system

3-Bromopyruvate (3-BP) is a promising compound for anticancer therapy, its main mode of action being the inhibition of glycolytic enzymes, but this compound also induces oxidative stress. This study aimed at characterisation of the effect of 3-BP on the antioxidant defense system of erythrocytes. Suspensions of erythrocytes in PBS containing 5 mM glucose were treated with different concentration of 3-BP at 37°C for 1 h. Activities of antioxidant enzymes were estimated by standard colorimetric methods. The antioxidant capacity of erythrocytes was estimated using the 2,2'-azinobis(3-ethylbenzthiazoline-6-sulphonic acid) (ABTS(•+)) decolorisation assay and ferricyanide reduction. The content of reduced and oxidized glutathione was estimated fluorimetrically with o-phtalaldehyde. 3-BP did not affect the integrity of the erythrocyte membrane (lack of changes in the osmotic fragility). However, it induced oxidative stress in erythrocytes, as evidenced by the decrease in the content of acid-soluble thiols and reduced glutathione (GSH). Superoxide dismutase (SOD) and glutathione S-transferase (GST) activities were significantly decreased. 3-BP also decreased the transmembrane reduction of ferricyanide. Thus induction of oxidative stress in erythrocytes by 3-BP is due to depletion of glutathione and inhibition of antioxidant enzymes.

Protective role of vitamins C and E in diclorvos-induced oxidative stress in human erythrocytes in vitro

Organophosphate (OP) pesticides such as dichlorvos (DDVP) intoxication has been shown to produce oxidative stress due to the generation of free radicals, which alter the antioxidant defense system in erythrocytes. In this study, the effects of DDVP (1, 10, 100 µM) or DDVP + vitamin C (VC; 10 µM) or vitamin E (VE; 30 µM), on the levels of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) activities in human erythrocytes were examined in vitro. There were no statistical differences between all groups for 1 µM concentration of DDVP. Treatment with DDVP alone produced an increase in the level of MDA and decreased activities of antioxidant enzymes (P < 0.05). Groups treated with vitamins and DDVP showed protective effects of vitamins against DDVP-induced changes in antioxidant enzyme activity and lipid peroxidation (LPO) (10 µM). At 100 µM concentration of DDVP vitamins had no effect on DDVP-induced toxicity. The results show that administration of DDVP resulted in the induction of erythrocyte LPO and alterations in antioxidant enzyme activities, suggesting that reactive oxygen species (ROS) may be involved in the toxic effects of DDVP. Also the data show that the plasma level of VC and VE may ameliorate OP-induced oxidative stress by decreasing LPO in erythrocytes at certain doses of OP pesicides.

Oxidative Stress and Oxidative Damage in Male Rat Erythrocytes Associated with Prolonged Exposure to Smoke Pollution

Exposure of animals to different duration of smoke can result in a wide range of adverse clinical conditions. Toxicological consequences arising from prolonged exposure may not be totally enumerated. The present study was to evaluate the oxidative stress-inducing potential of a short and long-time exposure of male rat erythrocytes to environmentally relevant to public health. Male Wistar rats were exposed to open municipal land-fill smoke for 30 and/or 60 days. The oxidative stress in erythrocytes was evaluated by assessing the magnitude of malondialdehyde production and reduced glutathione (GSH) contents and the activities of superoxide dismutase (SOD), catalase (C) and glutathione reductase (GR) after 30 and/or 60 days of exposure. After 30 days there was no change in SOD, catalase and GR activities and no alterations in GSH and lipid peroxidation (LPO). After 60 days, the levels and activities of SOD (23.62%), catalase (5.24%), GR (14.87%) decreased. Overall, the study demonstrates that the chronic exposure of male rats to smoke results in induction of oxidative stress and simultaneous reduction in antioxidative defense system in erythrocytes at 60 days of exposure.