Complex of Vitamins and Antioxidants Protects Low-Density Lipoproteins in Blood Plasma from Free Radical Oxidation and Activates Antioxidants Enzymes in Erythrocytes from Patients with Coronary Heart Disease

We studied the effect of a complex containing antioxidant vitamins C and E, provitamin A, and antioxidant element selenium on the contents of primary (lipid peroxides) and secondary products (malonic dialdehyde) of free radical lipid oxidation in low-density lipoproteins isolated from the plasma of patients with coronary heart disease and hypercholesterolemia by means of preparative ultracentrifugation. Activity of key antioxidant enzymes in the blood was measured during treatment with the antioxidant preparation. Combination treatment with antioxidant vitamins and antioxidant element selenium sharply decreased the contents of primary and secondary free radical oxidation products in circulating low-density lipoproteins and increased activity of antioxidant enzymes in erythrocytes. Activities of superoxide dismutase and selenium-containing glutathione peroxidase increased 1 and 2 months after the start of therapy, respectively.     

The effects of hormone replacement therapy on lipid peroxidation and antioxidant status

OBJECTIVE: A number of studies have consistently shown a lower cardiovascular risk in women who received postmenopausal hormone replacement therapy (HRT). The aim of our study was to examine the effects of HRT on lipid peroxidation and antioxidant status, which were likely to be involved in the pathophysiology of atherosclerosis. METHODS: We measured erythrocyte and plasma thiobarbituric acid reactive substances (TBARS) levels as expression of lipid peroxidation-end product malondialdehyde, and also erythrocyte reduced glutathione (GSH) level and glutathione peroxidase (GSH-Px) activity as indicators of the antioxidant status of the 35 postmenopausal women with HRT (mean age: 51.81 +/- 4.57 yr; body mass index (BMI): 26.56 +/- 3.78 kg/m(2)) and 35 postmenopausal women without HRT (mean age: 47.50 +/- 3.64; BMI: 27.42 +/-3.43 kg/m2). RESULTS: In the group with HRT, erythrocyte and plasma TBARS levels were significantly lower than in the group without HRT (P < 0.003 and P < 0.001, respectively). Erythrocyte GSH level and GSH-Px activity was found to be increased significantly in the group with HRT in comparison with the group without HRT (P < 0.001 and P < 0.001, respectively). There was not any correlation between the erythrocyte and plasma TBARS and erythrocyte GSH levels and GSH-Px activity with duration of HRT (mean 3.5+/-1.3 yr). CONCLUSION: Our results show that HRT is beneficial in the protection against oxidative damage and can prevent atherosclerotic complications.     

Effects of vitamin E supplementation on oxidative stress in streptozotocin induced diabetic rats: investigation of liver and plasma

This experimental study was designed to investigate the effects of vitamin E supplementation, especially on lipid peroxidation and antioxidant status elements 3/4 namely, glutathione (GSH), CuZn superoxide dismutase (CuZn SOD), and glutathione peroxidase (GSH Px), both in blood and liver tissues of streptozotocin (STZ) diabetic rats. The extent to which blood can be used to reflect the oxidative stress of the liver is also investigated. In diabetic rats, plasma lipid peroxide values were not significantly different,from control,whereas erythrocyte CuZn SOD (p < 0.01), GSH Px (p < 0.001) activities and plasma vitamin E levels (p < 0.001), were significantly more elevated than controls. Vitamin E supplementation caused significant decreases of erythrocyte GSH level (p < 0.01) in control rats and of erythrocyte GSH Px activity (p < 0.05) in diabetic rats. Liver findings revealed significantly higher lipid peroxide (p < 0.001) and vitamin E (p < 0.01) levels and lower GSH (p < 0.001), CuZn SOD (p < 0.001) and GSH Px (p < 0.01) levels in diabetic rats. A decreased hepatic lipid peroxide level (p < 0.01) and increased vitamin E/lipid peroxide ratio (p < 0.001) were observed in vitamin E supplemented, diabetic rats. A vitamin E supplementation level which did not cause any increase in the concentration of the vitamin in the liver or blood, was sufficient to lower lipid peroxidation in the liver. Vitamin E/lipid peroxide ratio is suggested as an appropriate index to evaluate the efficiency of vitamin E activity,independent of tissue lipid values. Further, the antioxidant components GSH, GSH Px and CuZn SOD and the relationships among them, were affected differently in the liver and blood by diabetes or vitamin E supplementation.     

Increased erythrocyte susceptibility to lipid peroxidation in human Parkinson's disease

Recent evidence suggests that among the factors that lead to neurodegenerative changes in Parkinson's disease are stimulation of lipid peroxidation and deficiency of glutathione and glutathione peroxidase in substantia nigra. We have investigated the effect of neurodegenerative changes on plasma and erythrocytes of patients with Parkinson's disease and compared the results with those of age-matched controls. Both plasma lipid peroxide levels and erythrocyte susceptibility to lipid peroxidation were significantly increased in Parkinson's disease. Erythrocyte fragility tests revealed that in 35% of the patients there was increased fragility. In addition, erythrocyte catalase activities were not changed whereas glutathione levels and glutathione peroxidase activities were decreased in Parkinson's disease. Our results suggest that erythrocyte membrane integrity may be impaired in Parkinson's disease.     

Levels of lipid peroxidation products in a chronic inflammatory disorder

We have examined the plasma levels of the lipid peroxidation products 4-hydroxy-nonenal and malondialdehyde in a carefully controlled study of age and sex-matched subjects with rheumatoid arthritis in whom potentially confounding influences such as disease modifying anti-rheumatic drugs (DMARDs), self-medication and vitamin supplements were eliminated. The plasma concentrations of the antioxidants uric acid and vitamin E were also measured. The results reveal a strong and consistent inverse correlation between the levels of lipid peroxidation products in the plasma and erythrocyte sedimentation rate (ESR). There is no indication that vitamin E or urate function as the major antioxidant agent in arthritis, as has been suggested in more seriously affected patients. It is concluded that there is no evidence that vitamin E is more important, and urate less important as an antioxidant in mild arthritis. The correlation between lipid peroxidation and ESR suggests a more complex relationship than has been assumed.     

Antioxidant parameters and ageing in some animal species

Connection between ageing and some tissue antioxidant parameters have been studied in four experiments on different animal species. Prenatal studies on the developing chick embryos showed discrepancies between the lipid-rich liver and brain antioxidant defence. In the liver, high levels of reduced glutathione (GSH), vitamins A and E and high activities of the antioxidant enzymes glutathione peroxidase (GPX) and superoxide dismutase (SOD) were found whereas brain expressed a high vitamin C concentration. In newborn healthy calves during the first two days of life, atmospheric oxygen tension did not cause either increased lipid peroxidation as reflected in a high malondialdehyde (MDA) level or any changes in GSII, GPX, SOD and catalase (CAT) activities in red blood cells (RBC). Plasma vitamin E and carotene concentrations also did not change. In growing healthy calves during two months after birth increasing MDA, decreasing GSH, GPX and CAT are leading features, whereas plasma vitamin E and carotene concentrations significantly increased. In young (1-year-old) and old (9-year-old) dogs RBC results showed significant differences with the highest MDA and lowest GSH levels in the old males. Activity of GPX and SOD was higher in old dogs than in the young ones, especially in the females.     

Vitamin E as an antioxidant agent in CAPD patients

Oxidative stress, increased lipid peroxidation and decreased activity of antioxidant systems may contribute to the accelerated development of atherosclerosis in chronic renal failure patients during renal replacement therapy. The aim of the study was to investigate the influence of vitamin E (400 mg/day) on some antioxidant defense parameters in CAPD patients. In fourteen CAPD patients, erythrocyte antioxidant enzymes, superoxide dismutase (SOD), glutathione peroxidase (GPX) and catalase (CAT), the concentration of plasma malondialdehyde (MDA), vitamin A, vitamin C and vitamin E were investigated. The study was divided into two periods. Each period lasted six weeks. In the first period patients received orally vitamin E 400 mg/day, in the second period they did not receive vitamin E or other antioxidant drugs. Each parameter was determined at the beginning of the study and at the end of each period. Six CAPD patients were treated by erythropoietin (EPO) and received orally pyridoxine 20 mg/day and the others without EPO treatment received pyridoxine 5 mg/day. Six-week treatment by vitamin E (400 mg/day) led to the significant increase of serum vitamin E (from 33.6+/-9.0 to 49.3+/-15.5 micromol/L) and to the significant decrease of MDA (from 2.62+/-0.5 to 2.36+/-0.4 micromol/L). The mean values of erythrocyte enzymes were in or under the lower margin of normal range and were not influenced by vitamin E in CAPD patients. The results of our study showed that orally administered vitamin E is a very important antioxidant agent for CAPD patients.     

血氧饱和度降低可促进红细胞氧化损伤

研究氧化应激条件下,血氧饱和度(SO2)对红细胞氧化损伤的影响。体外将红细胞孵育至SO2分别为0.3、0.5、0.7、0.9及0.98等状态,加入终浓度为0.15mmol/L叔丁基过氧化氢(BHP)使其发生氧化应激反应。测量胞内还原性谷胱甘肽(GSH)含量反映细胞抗氧化力,以胞内高铁血红蛋白(MetHb)、膜质过氧化(TBARS)及膜上沉淀的变性珠蛋白链水平体现细胞氧化损伤程度。结果显示,BHP存在的条件下,GSH含量随SO2上升而增加;MetHb、TBARS及膜上珠蛋白链水平则随SO2的上升而下降。上述结果表明,氧化应激条件下,红细胞抗氧化力和氧化损伤与SO2密切相关,SO2的降低可促进红细胞氧化损伤。     

Antioxidant status and circulating lipids are altered in human gestational diabetes and macrosomia

Fetuses from mothers with gestational diabetes are at increased risk of developing neonatal macrosomia and oxidative stress. We investigated the modulation of antioxidant status and circulating lipids in gestational diabetic mothers and their macrosomic babies and in healthy age-matched pregnant women and their newborns. The serum antioxidant status was assessed by employing anti-radical resistance kit (KRL; Kirial International SA, Couternon, France) and determining levels of vitamin A, C, and E and the activity of superoxide dismutase (SOD). Circulating serum lipids were quantified, and lipid peroxidation was measured as the concentrations of serum thiobarbituric acid-reactive substances (TBARS). As compared with non-diabetic mothers, gestational diabetic women exhibited decreased levels of vitamin E and enhanced concentrations of vitamin C without any changes in vitamin A. Vitamin A and C levels did not change in macrosomic babies except vitamin E whose levels were lower in these infants than in the newborns of non-diabetic mothers. Gestational diabetes mellitus (GDM) and macrosomia were also associated with impaired SOD activities and enhanced TBARS levels. Globally, total serum antioxidant defense status in diabetic mothers and their macrosomic babies was diminished as compared with control subjects. Triglyceride and cholesterol concentrations did not differ significantly between gestational diabetic and control mothers; however, macrosomia was associated with enhanced plasma cholesterol and triglyceride levels. These results suggest that human GDM and macrosomia are associated with downregulation of antioxidant status, and macrosomic infants also exhibit altered lipid metabolism.     

Oxidative Stress in Atherosclerosis and Diabetes

We measured the content of lipid peroxides in plasma LDL from patients with chronic CHD not accompanied by hypercholesterolemia; CHD and hypercholesterolemia; type 2 diabetes mellitus and decompensation of carbohydrate metabolism; and CHD, circulatory insufficiency, and type 2 diabetes mellitus (without hypercholesterolemia). The content of lipid peroxides in LDL isolated from blood plasma by differential ultracentrifugation in a density gradient was estimated by a highly specific method with modifications (reagent Fe²⁺ xylene orange and triphenylphosphine as a reducing agent for organic peroxides). The content of lipid peroxides in LDL from patients was much higher than in controls (patients without coronary heart disease and diabetes). Hypercholesterolemia and diabetes can be considered as factors promoting LDL oxidation in vivo. Our results suggest that stimulation of lipid peroxidation in low-density lipoproteins during hypercholesterolemia and diabetes is associated with strong autooxidation of cholesterol and glucose during oxidative and carbonyl (aldehyde) stress, respectively. These data illustrate a possible mechanism of the progression of atherosclerosis in patients with diabetes mellitus. __________ Translated from Byulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 140, No. 7, pp. 48–51, July, 2005     

The impact of propylthiouracil therapy on lipid peroxidation and antioxidant status parameters in hyperthyroid patients

This study was performed on 17 hyperthyroid patients and 15 healthy controls. The patients were under propylthiouracil (PTU) therapy at a dosage of 3 x 100 mg/day for one month. Blood samples, taken at the beginning and on the 30th day of therapy, were analyzed for hormonal parameters (T3, T4, TSH), lipid peroxidation endproduct [thiobarbituric acid reactive substances (TBARS)] and antioxidant status parameters: glutathione (GSH), glutathione peroxidase (GSH-Px) and CuZn superoxide dismutase (CuZn SOD). Hyperthyroid patients were observed to have significantly higher TBARS, GSH and CuZn SOD levels than controls (P < 0.05, P < 0.001, P < 0.001, respectively). PTU therapy caused a relief in oxidative stress as reflected by significantly decreased TBARS levels (P < 0.001) and a selective modification in the antioxidant status parameters: significant decreases in GSH and CuZn SOD levels (P < 0.001) and a significant increase in GSH Px (P < 0.01) activity. Our findings suggest a selective modification of the antioxidative profile in hyperthyroidism. PTU should also be considered as an in vivo antioxidant, in addition to its antithyroid action.     

Increased susceptibility of serum and apo-B-containing lipoproteins to peroxidation in aged rats

Oxidative modifications of apo-B-containing lipoproteins (LDL+VLDL) appear to play a role in atherogenesis. Increased atherosclerosis is one of the major causes of morbidity and mortality during ageing. The aim of this study was to investigate the susceptibility of serum and LDL+VLDL to lipid peroxidation in 12 young (6 months) and 12 old (22 months) rats. Serum endogenous malondialdehyde (MDA) and diene conjugate (DC) levels were found to be increased by 24.9% and 30.0% respectively, in old rats. In addition, 2,2′-azobis-(2-amidinopropane) hydrochloride (AAPH)-induced lipid peroxide levels were increased in serum of old rats. Although serum vitamin E levels were significantly increased (27.4%), there was a significant decrease in cholesterol-adjusted vitamin E levels (14.3%) in old rats. Serum vitamin C and total sulphydryl levels were found to be decreased by 25.5% and 22.7% respectively. The ferric reducing ability of plasma (FRAP) was also lower (15.9%) in old rats. Endogenous DC and copper-induced MDA levels were significantly higher (65.1% and 26.7% respectively) in LDL+VLDL fractions obtained from EDTA-plasma by dextrane sulphate and MgCl₂ solution in old rats. The propagation rate and maximal amount of DC increased, but the lag phase and t _max were shortened in LDL+VLDL fractions of old rats. Our results clearly indicate that the susceptibility of whole serum and LDL+VLDL fractions to lipid peroxidation is increased in aged rats.     

Influence of apolipoprotein E genotype on blood redox status of Alzheimer's disease patients.

The blood redox status of probable Alzheimer's Disease (AD) patients and control subjects with distinct Apo E genotypes was investigated. It was assessed by measuring the levels of hydroperoxides (MDA) in plasma and erythrocytes, the levels of the antioxidant defense system (enzymatic and non-enzymatic) in plasma, erythrocytes, platelets and leukocytes, the activities of catechol-O-methyltransferase (COMT) in erythrocytes and monoamine oxidase-B (MAO-B) in platelets and also the activity of the mitochondrial respiratory chain in leukocytes. No significant differences were found between the Apo E genotype and MDA, uric acid, vitamin E and reduced-glutathione (GSH) levels in plasma; MDA, vitamin E, GSH, superoxide-dismutase (SOD), glutathione-peroxidase (GSH-Px) and COMT levels in erythrocytes; vitamin E levels in the platelets of AD patients and control subjects. However, the uric acid levels in plasma and the COMT levels in erythrocytes of AD patients and control subjects with the epsilon4 allele were significantly lower than those observed in control subjects without the epsilon4 allele. Moreover, the duraquinol oxidation level in leukocytes of AD patients with the epsilon4 allele was significantly higher than that in AD patients without the epsilon4 allele and control subjects with and without the epsilon4 allele. The meaning of these results is discussed in terms of involvement of oxidative stress in the etiopathogenesis of AD.     

Changes in blood lipid peroxidation markers and antioxidants after a single sprint anaerobic exercise

It has been well demonstrated that the principal factor responsible for oxidative damage during exercise is the increase in oxygen consumption. However, other theoretical factors (acidosis, catecholamine autoxidation, ischemia-reperfusion syndrome, etc.) that are known to induce, in vitro, oxidative damage may also be operative during short-term supramaximal anaerobic exercise. Therefore, we hypothesized that short-term supramaximal anaerobic exercise (30-s Wingate test) could induce an oxidative stress. Lipid peroxidation markers [serum lipid radical production detected by electron spin resonance (ESR) spectroscopy and plasma malondialdehyde (MDA) levels detected by the thiobarbituric acid reactive substances (TBARS) method], as well as erythrocyte antioxidant enzyme activities [glutathione peroxidase (GPx), superoxide dismutase (SOD)] and erythrocyte glutathione (GSH) levels, were measured at rest, after the Wingate test and during the 40 min of recovery. The recovery of exercise was associated with a significant increase (x2.7) in lipid radical production detected by ESR spectroscopy, as well as with changes in the erythrocyte GSH level (−13.6%) and SOD activity (−11.7%). The paradoxical decrease in plasma TBARS (−23.7%) which was correlated with the peak power developed during the Wingate test (r=−0.7), strongly suggests that such exercise stimulates the elimination of MDA. In conclusion, this study demonstrates that short-term supramaximal anaerobic exercise induces an oxidative stress and that the plasma TBARS level is not a suitable marker during this type of exercise. Electronic Publication     

Lipid peroxidation in cats experimentally infected with <Emphasis Type="Italic">Trypanosoma evansi</Emphasis>

The objective of this study was to evaluate the lipid peroxidation and the susceptibility of erythrocytes to in vitro peroxidation as indicators of oxidative damage in erythrocytes and their roles in the pathogenesis of anemia during experimental Trypanosoma evansi infection in cats. Animals were divided into two groups: control and infected with T. evansi. Seven cats were infected with 10⁸ trypomastigotes each, and parasitemia was estimated daily for 49 days by microscopic examination of smears. Hematological and biochemical parameters were evaluated for monitoring of the disease. Plasma lipid peroxidation (Thiobarbituric Acid Reactive Substances (TBARS)) and the susceptibility of erythrocytes to in vitro peroxidation were evaluated. Blood samples for analysis were collected at days 21 and 49 post-inoculation. TBARS level, indicated by MDA concentration, was higher in the infected group than in the control group in both analyzed periods, as well as the in vitro erythrocyte peroxidation (P < 0.001). The infected cats had variable degrees of regenerative anemia, which could be explained by the damage in erythrocyte membrane caused by lipid peroxidation.     

Vitamin combinations reduce oxidative stress and improve antioxidant status in patients with iron deficiency anemia

The purpose of the present study was to investigate whether oxidative stress occurs at the clinical onset of iron deficiency anemia and to find the influence of iron therapy and antioxidant vitamins on the oxidative stress parameters. A comparison was made with two other categories of anaemia, pernicious anaemia and haemolytic anaemia that are not characterized with iron deficiency. Oxidative stress was measured through the level of plasma lipid peroxidation (MDA) and the activities of ceruloplasmin (CP), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px); important extracellular and intracellular antioxidants. Significantly increased lipid peroxidation was demonstrated in the plasma of patients with iron deficiency anemia (P=0.005). While the activity of erythrocyte antioxidant enzyme GSH-Px remained unaltered, SOD was significantly decreased (P <0.05), CAT and plasma CP were significantly increased (P <0.001). Repletion of iron deficient patients with iron promotes oxidative stress: MDA was found to remain high, the activities of SOD and GSH-Px remained lower and CAT remained very high as before iron treatment. When iron deficient patients were treated with iron along with the antioxidant vitamins A, E and C, the oxidative stress was reduced and the activity of SOD was normalized. The combination of Vitamins A+E and Vitamin C is more effective than Vitamin C in reversing antioxidant status. In conclusion, our results demonstrated that increased oxidative stress is present in patients with iron deficiency anemia which appears to be compromised by imbalance in antioxidant defense systems. The repletion of iron deficient patients with iron promotes the oxidative stress. Patients with iron deficiency anemia after iron treatment actually are at risk of oxidative injury. Iron in the presence of the antioxidant vitamins A+E and ascorbic acid reduced the oxidative stress.     

An increase in lipoprotein oxidation and endogenous lipid peroxides in serum of obese women

Endogenous malondialdehyde and diene conjugate levels, the susceptibility of apolipoprotein B-containing lipoproteins to copper-induced lipid peroxidation, and antibody titer against oxidized low-density lipoproteins were increased, but serum antioxidant activity was unchanged in obese women. Serum cholesterol, low-density lipoproteincholesterol, and trigliceride levels were also elevated, but high-density lipoprotein-cholesterol levels remained unchanged in obese women. In vitro, oxidation of apolipoprotein B-containing lipoproteins and levels of antibody against oxidized low-density lipoprotein correlated with body mass index, serum total cholesterol, and low-density lipoproteincholesterol levels in obese women. These results indicate that obesity is associated with increases in endogenous lipid peroxides, oxidation of low-density lipoproteins, and lipids in serum. Received: 14 May 2002 / Accepted: 27 November 2002 Correspondence to ü. Mutlu-Türkoğlu     

Trimetazidine as Indirect Antioxidant

One-month therapy with trimetazidine sharply decreased the content of free radical oxidation products, lipid peroxides and malonic dialdehyde, in atherogenic low-density lipoproteins in patients with coronary heart disease. Activity of glutathione peroxidase utilizing lipid peroxides in the plasma markedly increased during trimetazidine therapy. The data suggest that trimetazidine not directly interacting with free radicals attenuates the adverse effects of intensive free radical oxidation in coronary heart disease. This effect is mediated via activation of antioxidant enzymes, which diminishes negative consequences of ischemia.     

Intensification of free radical oxidation of low-density lipoproteins in the plasma of patients with ischemic heart disease receiving beta-hydroxy-beta-methylglutaryl-coenzyme A reductase inhibitor cerivastatin and inhibition of low-density lipoprotein peroxidation with antioxidant probucol

Inhibitors of the key enzyme of cholesterol biosynthesis beta-hydroxy-beta-methylglutaryl-coenzyme A reductase (statins) decrease cholesterol content in atherogenic low-density lipoproteins in patients with coronary heart disease and hypercholesterolemia, but inhibited biosynthesis of ubiquinone Q10 protecting low-density lipoproteins from free radical oxidation. Cerivastatin in a daily dose of 0.4 mg markedly increased the content of lipid peroxides in low-density lipoproteins. However, complex therapy with cerivastatin and antioxidant probucol (250 mg/day) was accompanied by a sharp decrease in the content of lipid peroxides in low-density lipoproteins in patients with coronary heart disease in vivo. These data indicate that antioxidant agents should be used in combination with inhibitors of beta-hydroxy-beta-methylglutaryl-coenzyme A reductase (hypolipidemic preparations) for the therapy of patients with coronary heart disease.     

Abnormal lipid metabolism and oxidative stress in hemodialysis patients

Oxidative stress is enhanced in patients with end-stage renal disease (ESRD) undergoing hemodialysis (HD). Bioincompatibility represents an important source of reactive oxygen species. HD patients exhibit altered antioxidative defenses, and antioxidative vitamins such as vitamin E and C are altered in uremia. Frequently, HD patients also suffer from atherosclerotic cardiac disease. We previously reported that low-density lipoprotein (LDL) of HD patients is rich in malondialdehyde (MDA), an end product of lipid peroxidation. MDA-rich LDL is thought to be an atherogenic lipoprotein because of its enhancement of macrophage foam-cell formation. We conducted a controlled study for 2 years comparing the effects of a vitamin E-coated cellulose membrane dialyzer and an ordinary cellulose membrane dialyzer on lipid metabolism and the progress of atherosclerosis. LDL MDA and oxidized LDL (ox-LDL) were measured in HD patients by using these two types of dialyzers. Plasma vitamin E and lipid concentrations were also evaluated. Aortic calcification index (ACI) was evaluated by CT scan to assess the progress of atherosclerosis before and every year after initiation of the treatment. The use of a vitamin E-coated cellulose membrane dialyzer for 6 months, 1 year, and 2 years resulted in a significant reduction in LDL-MDA and ox-LDL compared with that obtainal with the use of the ordinary cellulose membrane dialyzer. The treatment with a vitamin E-coated dialyzer significantly reduced the percent increase in ACI after 24 months as compared with control. There were no significant differences in plasma vitamin E and lipid concentrations between the two groups. These results suggest that oxidative stress could be one of the factors stimulating abnormal lipid metabolism and atherosclerosis in ESRD patients.