The effect of red wine on blood antioxidant potential

We investigated the effects of red wine on blood antioxidant potential in an attempt to elucidate molecular mechanisms concerning the possible protective role of red wine in atherosclerosis. Volunteer subjects in the study group consumed a standard meal and drank red wine (5 mg/kg) while controls consumed the same meal and drank water. Over 4 1/2 hours, blood samples were taken, and malondialdehyde (MDA) and antioxidant potential (AOP, obtained from MDA levels before and after superoxide radical attack) values were measured in the plasma and erythrocytes. We found that AOP values of plasma and erythrocyte samples from the study group were at their highest after 1 1/2 hours and then declined to basal values at 4 1/2 hours. There were no statistically significant differences between the basal AOP values of the study group and the control group. With regard to MDA levels, gradual increases were seen in the plasma of the control group during the 3 hours after food, but no changes were seen in the plasma of the study group in this period. Although there were increases in erythrocyte MDA levels of both groups over 3 hours, the MDA production rate was significantly higher in the control group. Our results suggest that red wine causes significant increases in AOP values of plasma and erythrocytes, which may prevent cellular peroxidation reactions and lessen atherosclerotic complications through inhibition of LDL.     

In vivo changes in antioxidant systems and protective role of melatonin and a combination of vitamin C and vitamin E on oxidative damage in erythrocytes induced by chlorpyrifos-ethyl in rats

Reactive oxygen species (ROS) may be involved in the toxicity of chlorpyrifos-ethyl (CE) [O,O-diethyl-O-(3,5,6-trichloro-2-pyridyl)phosphorothioate]. We have, therefore, examined the in vivo effects of CE on the rat erythrocyte antioxidant system and evaluated the ameliorating effects of melatonin and a combination of vitamin E and vitamin C on the oxidative damage induced by CE. The experimental groups were: (1) control group, (2) CE-treated group (CE), (3) vitamin E plus vitamin C treatment group (Vit), (4) melatonin-treated group (Mel), (5) vitamin E plus vitamin C plus CE treatment group (Vit + CE), and (6) melatonin plus CE treatment group (Mel + CE). Vitamin E and vitamin C were administered intramuscularly once a day for 6 consecutive days at 150 and 200 mg/kg, respectively, in the Vit and Vit + CE groups. Melatonin was administered intramuscularly at 10 mg/kg per day for 6 consecutive days in the Mel and Mel + CE groups. At the end of the fifth day, the rats of CE, Vit + CE and Mel + CE groups were treated orally with the first of two equal doses of 41 mg/kg CE, the second oral dose being given 21 h later. Blood samples were taken 24 h after the first CE administration. Levels of thiobarbituric acid reactive substance (TBARS), antioxidant defence potential (AOP), and the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) were determined in erythrocytes. In comparison with the control group, oral administration of CE significantly (P < 0.05) stimulated TBARS activity while significantly (P < 0.05) inhibiting AOP and the activities of SOD and CAT. However, GSH-Px activity remained unchanged by CE treatment. Treatment with melatonin and vitamins E plus C significantly (P < 0.05) reduced the CE-induced increase of TBARS, and overcame the inhibitory effect of CE on SOD and CAT, but not on AOP. Melatonin treatment significantly (P < 0.05) increased only GSH-Px activity, irrespective of the effect of CE. These results suggest that CE treatment increases in vivo lipid peroxidation and decreases antioxidant defence by increasing oxidative stress in erythrocytes of rats, and melatonin and a combination of vitamin E and vitamin C can reduce this lipoperoxidative effect.     

Effects of oxidative stress on the erythrocyte Na+,K+ ATPase activity in female hyperthyroid patients.

This study was planned to determine the effects of free-radical-induced damage on the Na+,K+-ATPase activity of erythrocytes during hyperthyroidism and 4 wk after propylthiouracil (PTU) therapy (400 mg/d). The levels of plasma thiobarbituric acid-reactive substances (TBARS) as a marker of lipid peroxidation, erythrocyte glutathione (GSH) concentration as an antioxidant, blood ATP concentration, and erythrocyte membrane Na+,K+-ATPase activity were determined in female hyperthyroid patients (n = 22, mean age 40.5 +/- 6.5 yr). Before the PTU therapy, plasma TBARS concentration was significantly higher and the levels of blood ATP and erythrocyte GSH and the activity of membrane Na+,K-+-ATPase were significantly lower in the hyperthyroid patients (n = 15 women, mean age 40.8 +/- 7.3 yr). Four weeks after PTU therapy, plasma TBARS concentration was decreased, and levels of erythrocyte GSH and blood ATP and of Na+,K+-ATPase activity of erythrocytes were elevated in the treated patients. There was a significant positive correlation between blood ATP concentration and Na+,K+-ATPase activity, and a negative correlation between plasma TBARS concentration and Na+,K+-ATPase activity before PTU. Our results might help to clarify the effects of the oxidative mechanisms on the erythrocyte membrane Na+,K+-ATPase activity in hyperthyroid patients.     

In vivo effects of meloxicam,celecoxib, and ibuprofen on free radical metabolism in human erythrocytes

One of the major groups of chemical mediators involved in the inflammatory response is the prostaglandins, which are synthesized from arachidonic acid by the enzyme cyclooxygenase. The aim of this study is to compare the in vivo effects of celecoxib, meloxicam, and ibuprofen on the activities of catalase (CAT), glutathione peroxidase (GSHPx), superoxide dismutase (SOD) as well as malondialdehyde (MDA), and antioxidant potential levels (AOP) in human erythrocytes. Patients diagnosed as osteoarthritis were included in the study. Patients were treated with Celecoxib (200 mg/d) (n = 12), Meloxicam (15 mg/d) (n = 12), and Ibuprufen (1200 mg/d) (n = 9) for 21 days. SOD, CAT, GSHPx activities, MDA, and AOP levels were investigated in human erythrocyte haemolysates. SOD activity and AOP levels were significantly decreased in all NSAID groups when we compared the values before and after 21 days of celecoxib, meloxicam, ibuprofen treatment. There were no significant difference in CAT, GSHPx activities, and MDA levels before and after treatment in each group. Decreased SOD activities are thought to be related with the increased superoxide anion. Decreased AOP levels may indicate impairment in the total antioxidant defence system. These NSAIDs have similar effects on free radical metabolism on human erythrocytes; despite some difference in action mechanisms.     

Antioxidant response to oxidative stress induced by smoking

Oxygen free radicals have been hypothesized to play a pivotal role in the deleterious effects of smoking on health. The present study was undertaken to examine the oxidant and antioxidant system among smokers and nonsmokers. Fourteen smokers and 11 nonsmokers were enrolled for this study. The protein carbonyl levels in smokers were found to be significantly higher than in nonsmokers. The levels of plasma ascorbic acid, free sulfhydryl group, and erythrocyte reduced glutathione were lower in smokers compared to nonsmokers. In smokers the erythrocyte activities of both glutathione peroxidase and catalase were decreased when compared to that in nonsmokers. The data from the study reemphasizes the presence of oxidative stress in smokers. The concomitant decrease in the activities of both catalase and glutathione peroxidase found in the erythrocytes of smokers raises rational grounds for expressing concern over the increased susceptibility towards oxidative stress in these subjects.     

In Vivo Effects of Meloxicam,Celecoxib, and Ibuprofen on Free Radical Metabolism in Human Erythrocytes

Abstract

One of the major groups of chemical mediators involved in the inflammatory response is the prostaglandins, which are synthesized from arachidonic acid by the enzyme cyclooxygenase. The aim of this study is to compare the in vivo effects of celecoxib, meloxicam, and ibuprofen on the activities of catalase (CAT), glutathione peroxidase (GSHPx), superoxide dismutase (SOD) as well as malondialdehyde (MDA), and antioxidant potential levels (AOP) in human erythrocytes. Patients diagnosed as osteoarthritis were included in the study. Patients were treated with Celecoxib (200 mg/d) (n = 12), Meloxicam (15 mg/d) (n = 12), and Ibuprufen (1200 mg/d) (n = 9) for 21 days. SOD, CAT, GSHPx activities, MDA, and AOP levels were investigated in human erythrocyte haemolysates. SOD activity and AOP levels were significantly decreased in all NSAID groups when we compared the values before and after 21 days of celecoxib, meloxicam, ibuprofen treatment. There were no significant difference in CAT, GSHPx activities, and MDA levels before and after treatment in each group. Decreased SOD activities are thought to be related with the increased superoxide anion. Decreased AOP levels may indicate impairment in the total antioxidant defence system. These NSAIDs have similar effects on free radical metabolism on human erythrocytes; despite some difference in action mechanisms.     

Aspirin impairs antioxidant system and causes peroxidation in human erythrocytes and guinea pig myocardial tissue

This study aims to investigate possible effects of aspirin treatment on cellular oxidant/antioxidant system. In the first part of the study, 15 guinea pigs were given aspirin at three different doses (2200, 440 and 10 mg/kg/day) for 30 days and five were fed on the same diet without aspirin. After a month, animals were killed and their hearts were removed for use in analyses. In the other part, after fasting blood samples were obtained from 11 volunteer subjects, they were given aspirin (approximately 10 mg/kg/day) for 30 days and second blood samples were obtained after 1 month. Five volunteer subjects also participated as placebo control. Oxidant/antioxidant parameters, namely superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT), malondialdehyde (MDA), nonenzymatic superoxide scavenger activity (NSSA), susceptibility to oxidation (SO) and antioxidant potential (AOP) values, were assayed in the samples. Antioxidant system was found to be impaired in the heart tissue from guinea pigs and in the erythrocytes from volunteer subjects. AOP and NSSA values were lower and MDA higher after aspirin treatment in both heart tissues and erythrocytes. In guinea pig heart tissue, SO was lower, but GSH-Px and CAT were unchanged after aspirin treatment. In human erythrocytes, SO was unchanged, but GSH-Px and CAT activities were increased after aspirin treatment. Changes in guinea pig heart tissues from animals treated with higher aspirin doses were more drastic relative to those of human erythrocytes, but no meaningful differences were observed between analysis parameters of control and lower-dose (10 mg/kg/day) aspirin-treated animals. Our results suggest that high-dose aspirin exerts significant toxicity to guinea pig myocardium and normal dose aspirin may cause peroxidation in the human erythrocytes due to its oxidant potential. We suppose that antioxidant supplementation may be beneficial for the people using aspirin for longer periods in order to prevent peroxidation damages.     

Modulation of procainamide toxicity by selenium-enriched yeast in rats

Free radical processes are proposed to play a crucial role in the development of procainamide adverse effects. Therefore, selenium, as a potent antioxidant, may modified procainamide toxicity. To test this hypothesis plasma and liver thiobarbituric acid-reacting substances (TBARS), plasma antioxidant activity (AOA), erythrocyte and liver superoxide dismutase (SOD), catalase, as well as selenium-dependent glutathione peroxidase (Se-GPX) were determined in the following four groups of rats: selenium-treated (Se), procainamide-treated (P), procainamide and selenium-treated (P + Se), and control (C). Morphological studies of leukocytes [tested for lupus erythematosus (LE) cells] and liver were also made. Atypical, i.e. enlarged and swollen, leukocytes resulting from procainamide and selenium treatment were observed. These changes were found in four out of five rats in the Se group, eight out of ten in the P group, and in seven out of ten in the P + Se group. LE-like cells were observed in two rats in the P + Se group. A statistically significant decrease in plasma and liver TBARS by 20% and 36%, respectively, increased activity of SOD by 20%, catalase by 48% and Se-GPX by 15% in erythrocytes, and decreased activity of liver SOD by 17% and catalase by 22% were found in the P + Se group as compared to the P group. These results indicated that selenium exerted antioxidant effects on the procainamide-treated rats. However, selenium did not prevent the development of disturbances in leukocyte morphology, on the contrary, it possibly promoted the conversion of leukocytes to LE cells.     

Acute effects of smoking of cigarettes with different tar content on plasma oxidant/antioxidant status

In this study, acute effects of two different types of cigarette smoking on plasma oxidant/antioxidant status were investigated. For this purpose, malondialdehyde (MDA) levels and antioxidant potential (AOP) values were measured in the plasma samples before and after cigarette smoking at fasting. After the first blood sample was obtained, second and third samples were withdrawn at 1.5 h and 3 h. In the first group, subjects smoked five cigarettes with full flavor (FF), and in the second group, five cigarettes with full-flavor low tar (FFLT). Quality classification is made mainly on the basis of tar content of the products. The cigarette with 23 mg tar is defined as FF and that with 12 mg tar as FFLT. MDA level was found to be significantly increased in the 1.5-h plasma samples of both groups, but the increase was greater in the FF group. AOP values, however, were found to be lower in the 3-h plasma samples of both groups, but the decrease was greater in the FF group compared with the FFLT group. It appears that acute smoking causes oxidant stress in blood plasma once exposed to smoke, and then this effect (MDA) begins to decrease. On the other hand, AOP is lowered due to oxidant stress created by smoke. With regard to the types of cigarettes, the FF product seems to be more oxidant than the FFLT product. Our results suggest that antioxidant supplementation might be beneficial for the smokers to cope with the oxidant load derived from cigarette smoke. It is also clearly seen from these results that cigarette manufacturers should reduce tar/nicotine ratio in their products in order to lessen the toxic effects of smoking without causing increased need to smoke.     

ACUTE EFFECTS OF SMOKING OF CIGARETTES WITH DIFFERENT TAR CONTENT ON PLASMAOXIDANT/ANTIOXIDANT STATUS

In this study, acute effects of two different types of cigarette smoking on plasma oxidant/antioxidant status were investigated. For this purpose, malondialdehyde (MDA) levels and antioxidant potential (AOP) values were measured in the plasma samples before and after cigarette smoking at fasting. After the first blood sample was obtained, second and third samples were withdrawn at 1.5 h and 3 h. In the first group, subjects smoked five cigarettes with full flavor (FF), and in the second group, five cigarettes with full-flavor low tar (FFLT). Quality classification is made mainly on the basis of tar content of the products. The cigarette with 23 mg tar is defined as FF and that with 12 mg tar as FFLT. MDA level was found to be significantly increased in the 1.5-h plasma samples of both groups, but the increase was greater in the FF group. AOP values, however, were found to be lower in the 3-h plasma samples of both groups, but the decrease was greater in the FF group compared with the FFLT group. It appears that acute smoking causes oxidant stress in blood plasma once exposed to smoke, and then this effect (MDA) begins to decrease. On the other hand, AOP is lowered due to oxidant stress created by smoke. With regard to the types of cigarettes, the FF product seems to be more oxidant than the FFLT product. Our results suggest that antioxidant supplementation might be beneficial for the smokers to cope with the oxidant load derived from cigarette smoke. It is also clearly seen from these results that cigarette manufacturers should reduce tar/nicotine ratio in their products in order to lessen the toxic effects of smoking without causing increased need to smoke.     

Induction of oxidative stress and acetylcholinesterase inhibition in organophosphorous pesticide manufacturing workers

Oxidative stress status and acetylcholinesterase (AChE) activity were studied in blood samples obtained from 45 organophosphorous (OP)-formulating pesticide workers with a minimum work history of 1 year in the age range of 23-55. Controls were age-matched workers of a food-making factory. They were evaluated for oxidative stress markers, including thiobarbituric acid-reactive substances (TBARS) indicator of lipid peroxidation (LPO), ferric-reducing ability of plasma (FRAP) indicator of total anti-oxidant capacity, total thiol (SH) groups and gamma glutamyl transpeptidase (GGT) levels in blood and AChE activity in erythrocytes. The results show marked inhibition of AChE activity, increased TBARS, decreased FRAP and decreased thiol group levels in workers. The reduction in activity of AChE correlated well with increased TBARS and decreased FRAP in OP formulators. It is concluded that OP-formulating workers are exposed to more oxidative stress. The measurement of erythrocyte AChE activity in pesticide workers who formulate OPs can be a good monitoring factor and is recommended to be performed in a regular manner.     

Oxidative effects in human erythrocytes caused by some oximes and hydroxylamine

Both oximes and hydroxylamine (HYAM) are compounds with known oxidative capacity. We tested in vitro whether acetaldoxime (AAO), cyclohexanone oxime (CHO), methyl ethyl ketoxime (MEKO) or HYAM affect haemoglobin oxidation (into HbFe³⁺), formation of thiobarbituric acid reactive substances (TBARS), and glutathione (GT) depletion in human haemolysate, erythrocytes or blood. All these parameters are known to be related to oxidative stress. Glutathione S-transferase (GST) activity was measured as it may be affected by oxygen radicals. All three oximes caused a low degree of HbFe³⁺ accumulation in erythrocytes. This was higher in haemolysates indicating that membrane transport may be limiting or that protective mechanisms within erythrocytes are more effective. HbFe³⁺ accumulation was lower for the oximes than for HYAM. AAO and HYAM caused TBARS formation in blood. For HYAM this was expected as free radicals are known to be generated during HbFe³⁺ formation. Free radical generation by AAO and HYAM in erythrocytes was confirmed by the inhibition of GST. For the other two oximes (CHO and MEKO) some special effects were found. CHO did inhibit erythrocyte GST while it did not cause TBARS formation. MEKO was the least potent oxime as it caused no TBARS formation, little HbFe³⁺ accumulation and little GST inhibition in erythrocytes. However, GT depletion was more pronounced for MEKO than for the other oximes, indicating that glutathione conjugation occurs. TBARS formation, GT depletion and GST modulation caused by the oximes and HYAM were also tested in rat hepatocytes. However, no effects were found in hepatocytes. This suggests that a factor present in erythrocytes is necessary for free radical formation. Studies with proposed metabolites of the oximes (i.e. cyclohexanone, acetaldehyde or methylethyl ketone) and addition of rat liver preparations to the erythrocyte incubations with oximes, suggest that metabolism is not a limiting factor in erythrocyte toxicity. Received: 18 August 1997 / Accepted: 21 October 1997     

Hemolytic Effects of Sodium Selenite and Mercuric Chloride in Human Blood

Many works have reported the interaction between selenium and mercury in the mammalian body and that chalcogen seems to have a protective effect against mercury toxicity. The aim of this study was to investigate the hemolytic effects of sodium selenite and/or mercuric chloride in human blood under in vitro conditions. For this, total venous blood from healthy subjects (males and females) was heparinized and incubated at 37°C for 90 min with different concentrations of sodium selenite and/or mercuric chloride. The hemolytic effects of compounds were evaluated by measuring plasma hemoglobin concentration after centrifugation. In addition, 2-thiobarbituric acid reactive substances (TBARS) from plasma and erythrocytes, as well as erythrocyte nonprotein thiols (NPSH), were also evaluated in order to investigate molecular mechanisms related to selenite- or mercury-induced hemolysis. Mercuric chloride and sodium selenite, alone (400 µM), promoted a small in vitro hemolytic effect in human erythrocytes. However, when blood was exposed to both compounds (200 µM of each), there was an extremely high synergistic hemolytic effect. The exposure of blood to sodium selenite (400 µM), mercuric chloride (400 µM), and both compounds (200 µM each) did not alter erythrocyte TBARS levels. Sodium selenite presented a high oxidant effect toward erythrocyte NPSH; however, this effect was inhibited by mercuric chloride. The current results point to a synergistic hemolytic effect of sodium selenite and mercuric chloride in human blood, suggesting new understanding on the selenium–mercury antagonism. Moreover, this observed hemolysis seems to be not related to lipoperoxidation or thiol depletion.     

Hemolytic effects of sodium selenite and mercuric chloride in human blood

Many works have reported the interaction between selenium and mercury in the mammalian body and that chalcogen seems to have a protective effect against mercury toxicity. The aim of this study was to investigate the hemolytic effects of sodium selenite and/or mercuric chloride in human blood under in vitro conditions. For this, total venous blood from healthy subjects (males and females) was heparinized and incubated at 37 degrees C for 90 min with different concentrations of sodium selenite and/or mercuric chloride. The hemolytic effects of compounds were evaluated by measuring plasma hemoglobin concentration after centrifugation. In addition, 2-thiobarbituric acid reactive substances (TBARS) from plasma and erythrocytes, as well as erythrocyte nonprotein thiols (NPSH), were also evaluated in order to investigate molecular mechanisms related to selenite- or mercury-induced hemolysis. Mercuric chloride and sodium selenite, alone (400 microM), promoted a small in vitro hemolytic effect in human erythrocytes. However, when blood was exposed to both compounds (200 microM of each), there was an extremely high synergistic hemolytic effect. The exposure of blood to sodium selenite (400 microM), mercuric chloride (400 microM), and both compounds (200 microM each) did not alter erythrocyte TBARS levels. Sodium selenite presented a high oxidant effect toward erythrocyte NPSH; however, this effect was inhibited by mercuric chloride. The current results point to a synergistic hemolytic effect of sodium selenite and mercuric chloride in human blood, suggesting new understanding on the selenium-mercury antagonism. Moreover, this observed hemolysis seems to be not related to lipoperoxidation or thiol depletion.     

Increase in Antioxidant Activity in Procainamide-Treated Rats

Abstract: Recent studies suggest that in vivo procainamide oxidation underlies induction of autoimmunity by this drug. Since drug metabolism may be accompanied by generation of reactive oxygen species, plasma and liver thiobarbituric acid reacting substances (TBARS), activity of erythrocyte and liver superoxide dismutase, catalase, selenium-dependent glutathione peroxidase (Se-GPX), and plasma antioxidant activity in procainamide treated rats were evaluated. Procainamide administration increased liver lipid peroxide levels, intensified the activity of liver catalase and erythrocyte superoxide dismutase, as well as plasma antioxidant activity. The remaining biochemical parameters in the treated rats were within control values, except for the decreased erythrocyte catalase activity. We conclude, that the increased activity of free radicals observed in the treated rats could contribute to the development of procainamide induced side effects.     

Structural component changes of erythrocytes caused by oxidative stress generated by indoxyl sulfate

Indoxyl sulfate (IS) belongs to groups of uremic toxins binding to proteins. This compound may contribute to the generation of oxidative stress in chronic kidney disease (CKD) patients. We hypothesized that a high concentration of IS in the blood may induce structural changes of erythrocyte components and thus may contribute to CKD progression.In the present study, we evaluated the influence of IS on hemolysate and membrane proteins' conformational state, lipid membrane fluidity, and internal viscosity in erythrocytes. We examined thiols, carbonyl groups, peroxides, and TBARS levels in erythrocyte incubated with IS.The treatment of erythrocytes with IS led to increase in lipid membrane fluidity, decrease in the internal viscosity of the cells and the motion of the spin labels attached to hemolysate proteins. We did not observe conformational changes in plasma membrane proteins; however, in the plasma membranes of erythrocytes incubated with IS, a decrease in the content of thiol groups and increase in the carbonyls levels and peroxides and TBARS in comparison with the control was observed.The obtained results indicate that IS induces the oxidative damage of erythrocyte components. This may be an important factor that affects the functional properties of erythrocytes in CKD patients.     

Increased erythrocyte antioxidant status protects against smoking induced hemolysis in moderate smokers

Cigarette smoking is common in societies worldwide and has been identified as injurious to human health. Human red blood cells are important targets for electrophilic and oxidant foreign compounds. In the present study, the possible role of antioxidant status on smoking-induced erythrocyte hemolysis of smokers was studied. Erythrocyte superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) activities, reduced glutathione (GSH) level, erythrocyte membrane lipid peroxidation, total cholesterol and phospholipids were determined. Further, nitrite/nitrate levels (NO(2)/NO(3)) in both plasma and erythrocyte lysate were measured. Results showed increased plasma and erythrocyte membrane lipid peroxidation and nitrite/nitrate levels in smokers. The activities of SOD, CAT and GPx were also increased with reduced glutathione (GSH) level in smokers. No significant change was observed in smokers red cell hemolysis and cholesterol/phospholipid (C/P) ratio compared to controls. Erythrocyte membrane lipid peroxidation was positively correlated with SOD (r = 0.482, p < 0.01) and GPx (r = 0.368, p < 0.018) in smokers. Increased levels of nitrite/nitrate and antioxidant status of erythrocytes might be playing a crucial role in protecting red cell from free radical damage induced by cigarette smoke.     

Marked changes in erythrocyte antioxidants and lipid peroxidation levels of rats exposed to acute, repeated and chronic restraint stress

The aim of this study was to investigate the effects of acute, repeated and chronic restraint stress on the antioxidant status and lipid peroxidation. For this purpose, 48 male Wistar rats, aged three months were used in this study. Rats were separated into six groups as follows; control (C), acute stress (AS), restrained for 7 days (1 h/day) (RS), restrained for 21 days (1 h/day) (CS1), restrained for 28 days (1 h/day) (CS2) and restrained for 21 days (1 h/day) and allowed to recovery for 7 days (CS3). Copper, zinc-superoxide dismutase (Cu, Zn-SOD), catalase (CAT) and selenium-dependent glutathione peroxidase (Se-GSH-Px) activities, corticosterone, reduced glutathione (GSH) and thiobarbituric acid-reactive substances (TBARS) levels were measured in blood samples. Corticosterone levels of all groups were found to be elevated after stress compared to group C. Cu, Zn-SOD activity was lower in all stress groups than in group C. CAT and Se-GSH-Px activities were increased in all stress groups. All stress models decreased GSH levels except for the CS3 group. TBARS levels were higher in stress groups than in C group except for AS group. The highest corticosterone level, CAT and Se-GSH-Px activity and TBARS level were seen in group RS. The lowest Cu, Zn-SOD activity and GSH level were seen in group CS2. These results may have an important implication for impaired erythrocyte antioxidant enzyme activities and glutathione levels resulting from exposure to different stress models (acute, repeated and chronic restraint stress).     

HIGH-TEMPERATURE EFFECTS ON ANTIOXIDANT SYSTEMS AND TOXIC PRODUCT FORMATION IN NUTRITIONAL OILS

In this study, effects of high-temperature heating on antioxidant defense potential (AOP) and malondialdehyde (MDA) levels were investigated in several types of oils ingested by humans. Natural olive oil, refined olive oil, sunflower oil, and soy oil were examined. High-temperature heating to 180 C significantly decreased AOP. This was accompanied by a significant increase in MDA levels. The observed changes were quantitatively greater in soy and sunflower oil compared to olive oil. The loss in antioxidant defense potential and elevation in peroxidation products may be associated with enhanced disease processes.     

Alterations in oxidative stress biomarkers associated with mild hyperlipidemia and smoking

Oxidative stress may increase the risk of atherosclerosis. The association of mild forms of hyperlipidemia, particularly primary hypertriglyceridemia, with oxidative stress has not been fully investigated. The aim of this study was to assess the alterations in oxidative stress biomarkers associated with three major types of mild untreated hyperlipidemia (hypercholesterolemia, hypertriglyceridemia and combined hyperlipidemia) in nonsmoker and smoker individuals. Five biomarkers were measured in 139 adult healthy men (83 nonsmokers and 56 smokers, ages 18-75), which included normolipidemic and hyperlipidemic subjects. Triglyceride levels were associated with a significant main effect on ferric reducing antioxidant power (FRAP) and 8-iso-prostaglandin F2α (iPF2α) levels in plasma (p<0.05 and p<0.005, respectively). Smokers with hypercholesterolemia, hypertriglyceridemia and combined hyperlipidemia had alterations in 1, 3 and 2 oxidative stress biomarkers compared to nonsmoker normolipidemics. Smokers (including normolipidemics and hyperlipidemics) had higher plasma FRAP (120.8 vs. 102.0 μM quercetin/l, p<0.05) and erythrocyte catalase activity (5125 vs. 4093 U/g Hb, p<0.01), while they had lower erythrocyte glutathione peroxidase activity (20.3 vs. 23.0 U/g Hb, p<0.05) compared to nonsmokers. These findings show that mild forms of hyperlipidemia, particularly in smokers, are associated with alterations in some oxidative stress biomarkers.