Plasma Antioxidant Levels Research Articles

Grape seed proanthocyanidins prevent plasma postprandial oxidative stress in humans.

Postprandial hyperlipemia is a well-defined risk factor for atherosclerosis. A reasonable contributing mechanism could involve the postprandial increase of plasma lipid hydroperoxides (LPO) affecting the oxidant/antioxidant balance and increasing the susceptibility of LDL to oxidation. Wine has been shown to prevent both these events. The present study was designed to investigate the effect of supplementing a meal with grape seed proanthocyanidins (the main phenolic antioxidant of red wine) on plasma postprandial oxidative stress. In two different sessions, 8 healthy volunteers consumed the same test meal rich in oxidized and oxidizable lipids without (control) or with 300 mg of a proanthocyanidin-rich grape seeds extract (GSE). Lipid hydroperoxide concentration, antioxidant status, and LDL resistance to oxidative modification were measured in postprandial plasma. The content of LPO in chylomicrons was 1.5-fold higher after the control meal than after the GSE-supplemented meal. Plasma LPO increased only after consumption of the control meal. The plasma antioxidant capacity increased in the postprandial phase only following the GSE supplemented meal. LDL isolated 3 h after the control meal tended to be more susceptible to oxidative modification (but the difference did not reach statistical significance). An opposite trend was observed following the GSE supplemented meal. In conclusion, the supplementation of a meal with GSE minimizes the postprandial oxidative stress by decreasing the oxidants and increasing the antioxidant levels in plasma, and, as a consequence, enhancing the resistance to oxidative modification of LDL.

Neuroprotection in HIV-positive drug users: implications for antioxidant therapy.

Impaired neuroprotection resulting from oxidative stress has been implicated in neurodegeneration in a number of pathologic conditions of the brain, including both subcortical and cortical type dementias. Production of excessive oxidative stress, moreover, can lead to elevated levels of certain proinflammatory cytokines that are considered to be contributing factors to neuronal injury and are evident in HIV-related dementia as well as in other neurodegenerative conditions. Inhibitors of oxidative damage could thus be promising therapeutic agents for preventing progressive nerve cell death and slowing the advance of neurodegenerative disease. The potential of antioxidant therapy to provide neuroprotection is substantiated by studies demonstrating reduced oxidative stress with supplementation and lower risk for cognitive impairment with higher plasma antioxidant levels.

Effects of β-carotene, vitamin C and E on antioxidant status in hyperlipidemic smokers

Smoking can accelerate the consumption of the stored antioxidant vitamins and increase the oxidative stress in the hyperlipidemic patients. The study investigated the effects of combined β-carotene, vitamin C, and vitamin E on plasma antioxidant levels, erythrocyte antioxidative enzyme activities, and LDL lipid peroxides. Male hyperlipidemic smokers (35–78 years old) were randomly divided into two antioxidant supplemented groups: intervention 1 (I1, n = 22) (15 mg β-carotene/day, 500 mg vitamin C/day, and 400 mg α-tocopherol equivalent/day) and intervention 2 (I2, n = 20) (30 mg β-carotene/day, 1000 mg vitamin C/day, and 800 mg α-tocopherol equivalent/day). After 6-week supplementation, plasma β-carotene, vitamin C, vitamin E, and erythrocyte glutathione levels increased significantly by 200%, 98%, 129%, and 39%, respectively, in the I1 group, and by 209%, 216%, 197%, and 32%, respectively, in the I2 group. Plasma Fe +2 concentrations and Fe +2/Fe +3 decreased significantly in both groups. Except erythrocyte glutathione peroxidase activity in the I1 group, erythrocyte catalase, glutathione peroxidase, and superoxide dismutase activities increased significantly in both groups. Lipid peroxides in LDL decreased significantly by 56% and 72% in the I1 and I2 groups, respectively. However, the levels of plasma iron, erythrocyte glutathione, and LDL lipid peroxides, and the activities of erythrocyte antioxidative enzymes did not differ between two groups. In conclusion, combined antioxidant supplements increased plasma antioxidant levels and antioxidative enzyme activities, and lowered LDL lipid peroxides in male hyperlipidemic smokers. Higher dosage of the supplements did not have an additive effect.

Higher oxidation and lower antioxidant levels in peripheral blood plasma and bone marrow plasma from advanced cancer patients.

Bone marrow (BM) is an important tissue in the generation of immunocompetent and peripheral blood cells. The precursors of hematopoietic cells in BM undergo continuous proliferation and differentiation and are highly vulnerable to acute and chronic oxidative stress. Little is known about the oxidant and antioxidant status in the BM of untreated patients with nonhematologic tumors. In this study, oxidative stress was evaluated in peripheral blood plasma (PBP) and BM plasma (BMP) from lung carcinoma (LC) and breast carcinoma (BC) patients. The sample included 13 consecutive untreated LC patients, 15 BC patients, and 11 healthy controls. Luminol-dependent chemiluminescence was used to evaluate oxygen radical generation by peripheral blood neutrophils. Lipid oxidation, assessed by 2-thiobarbituric acid-reactive substances (TBARS), and alpha-tocopherol, beta-carotene, and total ubiquinol-10 levels were determined in PBP and BMP. In LC and BC patients, neutrophil chemiluminescence was higher (128% and 264%, respectively) than in controls (P < 0.05). In cancer patients, TBARS levels were higher in both PBP (51% and 243% for LC and BC patients, respectively) and BMP (66% and 305% for LC and BC patients, respectively) than in plasma from controls (P < 0.01). alpha-Tocopherol and total ubiquinol-10 levels were significantly lower in BMP from BC patients compared with controls. In BC patients, alpha-tocopherol content in PBP was significantly lower than in controls. Untreated cancer patients presented an imbalance between oxidant generation and lipid-soluble antioxidant levels in favor of the former.

Lymphocyte oxidative DNA damage and plasma antioxidants in Alzheimer disease.

A large body of experimental evidence suggests that in Alzheimer disease (AD) pathogenesis an important role is played by oxidative stress, but there is still a lack of data on in vivo markers of free radical-induced damage. To evaluate levels of 8-hydroxy-2'-deoxyguanosine (8-OHdG), a marker of oxidative damage to DNA, in peripheral lymphocytes; to measure plasma concentrations of several nonenzymatic antioxidants; and to assess the relationships between any observed changes in lymphocyte DNA 8-OHdG content and plasma antioxidant levels in patients with AD and healthy aged control subjects. Forty elderly outpatients with AD and 39 healthy age- and sex-matched controls were studied. The level of 8-OHdG was determined in DNA extracted from lymphocytes and plasma levels of vitamin C, vitamin A, vitamin E, and carotenoids (zeaxanthin, beta-cryptoxanthin, lycopene, lutein, and alpha- and beta-carotene) were measured by high-performance liquid chromatography. Lymphocyte DNA 8-OHdG content was significantly higher and plasma levels of antioxidants (with the exception of lutein) were significantly lower in patients with AD compared with controls. In patients with AD, a significant inverse relationship between lymphocyte DNA 8-OHdG content and plasma levels of lycopene, lutein, alpha-carotene, and beta-carotene, respectively, was observed. Markers of oxidative damage are increased in AD and correlate with decreased levels of plasma antioxidants. These findings suggest that lymphocyte DNA 8-OHdG content in patients with AD reflects a condition of increased oxidative stress related to a poor antioxidant status.

Antioxidant nutrient supplementation and brachial reactivity in patients with coronary artery disease

Epidemiologic studies have shown a correlation between antioxidant intake and coronary artery disease (CAD); however, the results of clinical trials have been inconsistent. We evaluated the effect of combined antioxidant supplementation on endothelial function and its correlation with change in low-density lipoprotein cholesterol (LDLC) oxidation in patients with established CAD. In a double-blind, placebo-controlled 12-week trial, 18 nonsmoking, nondiabetic patients (mean age 62.4 ± 8.1 years) were randomized to receive placebo or antioxidant supplementation consisting of (a) 400 IU of vitamin E, 500 mg of vitamin C, and 12 mg of β-carotene; or (b) 800 IU of vitamin E, 1000 mg of vitamin C, and 24 mg of β-carotene daily. Endothelial function was evaluated on the basis of percent and absolute changes in brachial artery diameter in response to reactive hyperemia induced by occlusion-release. Baseline and 12-week values of LDL oxidation (measured on the basis of lag phase), endothelial function, dietary composition, serum antioxidants, and lipids were measured. We noted a significant between-group difference at 12 weeks for change in plasma concentrations of α-tocopherol, vitamin C, and β-carotene between the placebo and antioxidant groups (p <.05). Both placebo and treatment groups demonstrated a significant improvement in lag phase; however, the treatment group achieved a greater, although nonsignificant, magnitude of change compared with the placebo group (181.3 ± 177.8 minutes vs 80.6 ± 63.0 minutes, P =.06). Within-group change in brachial reactivity from baseline to follow-up in the treatment group did not reach statistical significance (1.7% ± 3.2% and 0.07 mm ± 0.13 mm, P =.08 and P =.09, respectively), whereas an improved change in brachial reactivity was observed in the placebo group (2.2% ± 1.9%, 0.09 mm ± 0.06 mm, P <.05). No significant correlation was found between change in lag phase and change in endothelial function. On adjustment for confounders, antioxidant supplementation was found not to be a significant predictor of brachial reactivity. We conclude that antioxidant supplementation did not significantly alter brachial reactivity, despite significantly increased plasma levels of antioxidants and improved lag phase. These data should be confirmed in larger-scale trials and examined in studies evaluating individual dietary antioxidant supplementation. (J Lab Clin Med 2002;139:133-9)

The effects of lipid-lowering therapy on low-density lipoprotein auto-antibodies: relationship with low-density lipoprotein oxidation and plasma total antioxidant status.

Oxidized low-density lipoprotein (Ox-LDL) is believed to play an important role in the progression of atherosclerosis. Oxidative modification of low-density lipoprotein (LDL) is a prerequisite for rapid accumulation of LDL in macrophages and for the formation of foam cells. Because of high antioxidant levels in plasma, LDL oxidation is suggested to occur mainly in the subendothelial space of the arterial wall, where there is the concomitant presence of large amounts of reactive oxygen species generated by endothelial cells and activated leukocytes. After Ox-LDL formation, antibodies against this form of LDL may occur. Auto-antibodies against Ox-LDL (AuAb-Ox-LDL) show directly in in-vivo LDL oxidation. Many studies have indicated that the amount of antibodies in serum is positively correlated to the rate of progression of atherosclerotic plaques. In this study the effect of lipid-lowering therapy on the levels of AuAb-Ox-LDL in patients with dyslipidemia was determined using atorvastatin (10 mg/day), and the relationship between the antibodies and plasma total antioxidant status (TAS) and LDL oxidation capacity was also investigated. Serum levels of AuAb-Ox-LDL, lipids, lipoproteins, TAS and susceptibility of LDL to oxidation were determined using lag time in 44 patients with dyslipidemia (29 with hypercholesterolemia and 15 with mixed-type hyperlipidemia). After lipid-lowering therapy, serum levels of AuAb-Ox-LDL were found to be significantly decreased, by 18.7%, while lag time and plasma TAS were increased (31.3% and 7.6% respectively) in patients with dyslipidemia. The percentage change in lag time was found to be negatively correlated to the percentage change in AuAb-Ox-LDL (r = -0.31, P < 0.05). The percentage change in lag time also showed a positive correlation with the percentage change in TAS (r = 0.58, P < 0.01). AuAb-Ox-LDL levels decreased by 21.7% in patients with hypercholesterolemia and by 12.6% in patients with mixed-type hyperlipidemia. Also AuAb-Ox-LDL levels in patients with hypercholesterolemia were higher than in those with mixed-type hyperlipidemia (367 +/- 294 compared with 300 +/- 176 mU/l). It was concluded that lipid-lowering therapy may contribute to the reduction in levels of AuAb-Ox-LDL and the increase in the antioxidant capacity of plasma LDL and TAS. It was also suggested that the measurement of antibodies against Ox-LDL during lipid-lowering therapy may be used as an important marker for representing in-vivo LDL oxidation and atherosclerotic processes.

Influence of b-Resorcylidene Aminoguanidine on Selected Metabolic Parameters and Antioxidant Status of Rats with Diabetes Mellitus.

We studied the effects of administration of b-resorcylidene aminoguanidine (RAG) to Wistar strain rats with experimental diabetes mellitus (DM) induced by streptozotocin. The effects studied included antioxidant levels in plasma and the liver, oxidative damage of lipids represented by the formation of substances reacting with thiobarbituric acid (TBARP) and selected biochemical indicators. The administration of RAG did not significantly affect antioxidant status of diabetic rats or hemoglobin glycation and plasma concentration of fructosamine. In diabetic rats, application of RAG decreased formation of TBARP in plasma but not in the liver. Moderate steatosis of liver and increased plasma levels of triacylglycerols in diabetic rats were significantly improved by application of RAG.

Ozone causes lipid peroxidation but little antioxidant depletion in exercising and nonexercising hamsters.

Ozone (O(3)), a major component of urban air pollution, is a strong oxidizing agent that can cause lung injury and inflammation. In the present study, we investigated the effect of inhalation of O(3) on levels of F(2)-isoprostanes in bronchoalveolar lavage fluid (BALF) and on levels of antioxidants in the BALF and plasma of hamsters. Because antioxidants, including urate, ascorbate, GSH, and vitamin E, defend the lungs by reacting with oxidizing agents, we expected to find a decrease in antioxidant levels after O(3) exposure. Similarly, we expected an increase in the levels of F(2)-isoprostanes, which are lipid peroxidation products. Exposure to 1.0 or 3.0 parts/million (ppm) O(3) for 6 h resulted in an increase in BALF neutrophil numbers, an indicator of acute inflammation, as well as elevation of BALF F(2)-isoprostanes. The higher dose of O(3) caused an increase in the BALF level of urate and a decrease in the plasma level of ascorbate, but 1.0 ppm O(3) had no effect on BALF or plasma antioxidant levels. Exposure to 0.12 ppm O(3) had no effect on BALF neutrophils or F(2)-isoprostanes nor on BALF and plasma antioxidants. We also investigated the effect of O(3) exposure of hamsters during exercise on F(2)-isoprostane and antioxidant levels. We found that exposure to 1.0 ppm O(3) during 1 h of exercise on a laddermill increased BALF levels of F(2)-isoprostanes but had no effect on BALF neutrophils or on BALF and plasma antioxidants. These results indicate that O(3) induces inflammation and biomolecule oxidation in the lungs, whereas extracellular antioxidant levels are relatively unchanged.

Employee Exposure to Chromium and Plasma Lipid Oxidation

Exposure to chromium increases free-radical species in the body, which has an adverse biologic effect. In view of evidence that the oxidation of low-density lipoproteins is important in the pathogenesis of atherosclerosis, the authors measured plasma lipid oxidation and antioxidant levels in 11 welders chronically exposed to chromium and compared them with levels in 15 matched controls. Exposure level was determined by urinalysis. Plasma lipid peroxidation and susceptibility to oxidation were determined by measuring generated thiobarbituric acid reactive substance (TBARS) and lipid peroxides. Total plasma antioxidant status and serum paraoxonase activity were also measured. The Kruskal-Wallis test was used to test for statistical significance. There was no significant difference between the groups with regard to lipid peroxidation, plasma lipid susceptibility to oxidation, total plasma antioxidant status, or serum paraoxonase. Three workers with urinary chromium levels over the biologic exposure index limit (> 10.0 microg/g creatinine) had higher plasma lipid peroxidation and lipid susceptibility to oxidation compared with the rest of the study group. The results suggest that welders exposed to chromium have increased plasma lipid oxidation. The small numbers of subjects and those with elevated urinary chromium limit the power of this preliminary study. Further studies of the association of chromium with plasma lipid oxidation are warranted.

Beneficial effects of α-lipoic acid and ascorbic acid on endothelium-dependent, nitric oxide-mediated vasodilation in diabetic patients: relation to parameters of oxidative stress

The impairment of nitric oxide (NO)-mediated vasodilation in diabetes has been attributed to increased vascular oxidative stress. Lipoic acid has been shown to have substantial antioxidative properties. The aim of this study was to assess the effect of lipoic acid on NO-mediated vasodilation in diabetic patients in comparison with the well-recognized effect of ascorbic acid. Using venous occlusion plethysmography, we examined the effects of lipoic acid (0.2 mM) and ascorbic acid (1 and 10 mM) on forearm blood flow responses to acetylcholine, sodium nitroprusside and concomitant infusion of the NO-inhibitor, N G-monomethyl-L-arginine, in 39 diabetic patients and 11 control subjects. Plasma levels of antioxidants and parameters of lipid peroxidation were measured and correlated to endothelial function tests. Lipoic acid improved NO-mediated vasodilation in diabetic patients, but not in controls. NO-mediated vasodilation was improved by ascorbic acid at 10 mM, but not 1 mM. Improvements of endothelial function by ascorbic acid and lipoic acid were closely related. The beneficial effects of lipoic acid were positively related to plasma levels of malondialdehyde and inversely related to levels of ubiquinol-10. These findings support the concept that oxidative stress contributes to endothelial dysfunction and suggest a therapeutic potential of lipoic acid particularly in patients with imbalance between increased oxidative stress and depleted antioxidant defense.

Interaction between chemokines and oxidative stress: possible pathogenic role in acute coronary syndromes

OBJECTIVESWe sought to study the relationships between chemokines and oxidative stress in acute coronary syndrome.BACKGROUNDIn view of existing knowledge on the participation of leukocytes and oxidative stress in the pathogenesis of acute coronary syndrome, we hypothesized that chemokines may play a role in recruiting and activating leukocytes in this disorder.METHODSThe levels of chemokines and oxidative stress were studied in 38 patients with stable and 38 with unstable angina and in 20 controls. In separate in vitro experiments the effect of chemokines on reactive oxygen species in monocytes and the effect of antioxidants on chemokine levels in these cells were also studied.RESULTS1) Angina patients had raised serum levels of chemokines in both cross-sectional and longitudinal testing, with particularly high levels of interleukin (IL)-8, monocyte chemoattractant protein (MCP)-1 and macrophage inflammatory peptide (MIP)-1-alpha in unstable disease. 2) T cells, and particularly monocytes, seem to contribute to the raised IL-8, MCP-1 and MIP-1-alpha levels in unstable angina. 3) Concomitantly, and significantly correlated with MCP-1 and IL-8 levels, stable and particularly unstable angina patients had decreased plasma levels of antioxidants and increased lipid peroxidation, suggesting enhanced oxidative stress. 4) Monocyte chemoattractant protein-1 enhanced the generation of O2−in monocytes from unstable angina patients, and the antioxidant glutathione-monoethyl ester suppressed the production of IL-8 and MCP-1 in these cells.CONCLUSIONSOur findings suggest an interaction between chemokines and oxidative stress in unstable angina. This interaction may represent a vicious circle involved in the pathogenesis of acute coronary syndromes.

The effect of pharmacological doses of different antioxidants on oxidation parameters and atherogenesis in hyperlipidaemic rabbits

The oxidation hypothesis of atherosclerosis implies that antioxidants are able to inhibit lipoprotein oxidation in the arterial wall and thereby retard atherogenesis. Since most of the animal studies performed have used very high doses of antioxidants, it is to date unknown whether antioxidants are effective antiatherosclerotic agents when given in pharmacological doses. Here we addressed this question using homozygous Watanabe heritable hyperlipidaemic (WHHL) rabbits as an animal model of atherosclerosis. The rabbits were divided into four groups, each consisting of ten animals. They received either a standard diet or a diet containing 4.3 mg ubiquinone-10, or 4.3 mg vitamin E or 15 mg probucol/kg body weight daily. After 12 months, the extent of aortic atherosclerosis was assessed as the intima thickness, media thickness and intima-to-media ratio in 14 cross sections equally distributed over the whole aorta. To evaluate the antioxidant effects of the diet, lipophilic and hydrophilic antioxidants, lipids, fatty acids and plasma oxidizability were measured after 0, 3 and 6 months of feeding. We found that supplementation with probucol significantly decreased aortic intima-to-media ratio compared to controls. The antiatherosclerotic action of probucol was accompanied by its beneficial action on plasma oxidizability and some plasma antioxidants. No decrease in aortic atherosclerosis was measured in ubiquinone-10- and vitamin E-supplemented rabbits, despite the fact that both antioxidants decreased plasma oxidizability and ubiquinone-10 increased the plasma levels of antioxidants. Taken together, these data suggest that pharmacological doses of probucol retard atherogenesis in WHHL rabbits by an antioxidant mechanism, while ubiquinone-10 and vitamin E at these dosages are ineffective in this highly hyperlipidaemic model. The measurement of some oxidation-related parameters in plasma, such as lipophilic antioxidants, polyunsaturated fatty acids and lipoprotein oxidizability, may be useful in assessing the risk of atherogenesis in humans.

Consumption of tomato products with olive oil but not sunflower oil increases the antioxidant activity of plasma

Health benefits of lycopene from tomato products have been suggested to be related to its antioxidant activity. Dietary fat may influence the absorption and hence the plasma levels and antioxidant activity of lycopene. In the present study, we have compared the effect of consumption of tomato products with extra-virgin olive oil vs. tomato products plus sunflower oil on plasma lycopene and antioxidant levels. Results show that the oil composition does not affect the absorption of lycopene from tomato products because similar levels of plasma lycopene (mean ± SD) were obtained on feeding tomatoes (providing approximately 46 mg lycopene/d) for 7 d with either olive oil (0.66 ± 0.26 vs 1.20 ± 0.20 μmol/l, p < .002) or sunflower oil (0.67 ± 0.27 vs. 1.14 μmol/l, p < .001). However, consumption of tomato products with olive oil significantly raised the plasma antioxidant activity (FRAP) from 930 ± 150 to 1118 ± 184 μmol/l, p < .01) but no effect was observed when the sunflower oil was used. The change (supplementation minus start values) in FRAP following the consumption of tomato products with oil was significantly higher for olive oil (190 ± 101) than for sunflower oil (−9.6 ± 99, p < .005). In conclusion, the results of the study show that consumption of tomato products with olive oil but not with sunflower oil improves the antioxidant activity of the plasma.

Attenuated Development of Hypertension by Antioxidant Vitamins in Stroke-Prone Shr Is Associated with Increased Vascular Superoxide Dismutase Activity and Decreased Oxidative Stress.

P34 Oxidative stress has been implicated in the pathophysiology of cardiovascular diseases. We investigated effects of antioxidant vitamins and tempol, superoxide dismutase (SOD) mimetic, on vascular superoxide anion (×O 2 - ) concentration, NADPH oxidase activity, SOD activity, plasma antioxidant levels and blood pressure in stroke-prone SHR (SHRSP). 16 week-old SHRSP on a high salt diet (4%NaCl) were divided into 4 groups: control (C), Vit C (1000mg/day), Vit E (1000 U/day) and tempol (1 mmol/d). Systolic blood pressure (SBP) and antioxidant status were measured weekly for 6 weeks. Aortic ×O 2 - concentration and NADPH oxidase activity were measured by luminometry using lucigenin (5 μmol/L) and aortic SOD activity and total plasma antioxidant status were measured using a spectrophotometric assay system. SBP and plasma antioxidant levels were similar in all groups prior to treatment. Table demonstrates results after 6 weeks treatment. Data are means ± SEM. Data from this study demonstrate that antioxidant vitamins and tempol attenuate the development of hypertension in SHRSP. This is associated with decreased vascular ×O2- production, increased activity of SOD and increased plasma antioxidant concentrations. We demonstrate the novel findings that Vits E and C induce their antioxidant effects, in part, by stimulating SOD activity. Thus increased oxidative stress is an important factor underlying vascular changes associated with severe hypertension in SHRSP.

Autoantibody against oxidized low-density lipoproteins may be enhanced by cigarette smoking

A total of 59 healthy male subjects (32 smokers and 27 nonsmokers) who had no reported systemic disease and did not take alcohol and vitamin supplementation were included. The levels of autoantibody to oxidized low-density lipoproteins (ox-LDL) in smokers and age-matched nonsmokers were compared. The plasma levels of antioxidants that can affect the formation of ox-LDL were also measured, and correlation analyses between anti ox-LDL IgG and plasma antioxidants, controlling for age and body mass index (BMI), were performed. Plasma α-tocopherol and uric acid concentrations of nonsmokers (2.78±1.09 μg/mg total lipid and 6.96±1.69 mg/dl, respectively) were significantly higher than those of smokers (1.68±0.48 μg/mg total lipid and 6.15±1.14 mg/dl, respectively) ( P<0.05). Although plasma ascorbate and retinol levels were not significantly different between smokers and nonsmokers, smokers older than 45 years old had significantly lower plasma ascorbate levels (0.32±0.17 mg/dl) than age-matched nonsmokers (0.53±0.14 mg/dl) ( P=0.036). Higher level of plasma anti ox-LDL IgG was noted in the group of smokers compared with nonsmokers (515±409 mU/ml vs. 407±268 mU/ml, respectively) under the statistic method of Chi-Square test ( P=0.049). A significant negative correlation was found between plasma anti ox-LDL IgG and α-tocopherol in the combined population as well as in the smoker group ( r=−0.26, p=0.047; r=−0.48, p=0.006; respectively). However, there was no correlation between plasma anti ox-LDL IgG and the levels of other antioxidants. These results suggest that reduced concentrations of α-tocopherol are associated with cigarette smoking. The significantly negative correlation between plasma anti ox-LDL IgG and α-tocopherol in the entire study population as well as in the smoker group suggests that plasma α-tocopherol may be partially effective if not totally at protecting LDL from oxidative damage caused by cigarette smoking and dietary supplementation with α-tocopherol may provide a protective effect against LDL oxidation, especially in smokers.

Reduced plasma antioxidants levels and increased oxidative DNA damage in inflammatory bowel diseases

Reduced plasma antioxidants levels and increased oxidative DNA damage in inflammatory bowel diseases

A Case-Control Study of Plasma Antioxidant (Pro-)Vitamins in Relation to Respiratory Symptoms in Non-Smokers

The aim of this study was to investigate the relations between plasma levels of antioxidants, beta-carotene and alpha-tocopherol, and chronic respiratory symptoms in Dutch adults who never smoked or were long-term former smokers. Cases (who reported one or more respiratory symptoms) and controls were selected from a population-based cross-sectional study. Plasma concentrations of antioxidants were determined in 491 cases and 496 controls. ORs for the presence of chronic respiratory symptoms were estimated for quintiles of plasma antioxidant concentration after adjustment for age, gender, and body mass index. The OR of respiratory symptoms in all but the highest quintile of plasma beta-carotene decreased and were slightly below one. We saw no meaningful relation with plasma alpha-tocopherol.

Ascorbate and glutathione regulation in hibernating ground squirrels

Ground squirrels withstand up to 90% reductions in cerebral blood flow during hibernation as well as rapid reperfusion upon periodic arousals from torpor. Metabolic suppression likely plays a primary adaptive role which allows hibernating species to tolerate such phenomena. However, several other aspects of hibernation physiology are also consistent with tolerance to dramatic fluctuations in cerebral blood flow, suggesting that multiple neuroprotective adaptations may work in concert during hibernation. The purpose of the present work was to study the dynamics of the low molecular weight antioxidants, ascorbate and glutathione (GSH), during hibernation. Alterations in concentrations of ascorbate during hibernation and arousal in two species of hibernating ground squirrels suggest that it could play a protective role during hibernation or arousal. Samples were collected during the hibernation season from arctic ground squirrels (AGS; Spermophilus parryii) and 13-lined ground squirrels (TLS; S. tridecemlineatus) during prolonged torpor and in squirrels that did not hibernate or had not been hibernating for several weeks. We determined antioxidant levels in plasma, cerebrospinal fluid (CSF), and in frontal cortex, hippocampus and cerebellum using high-performance liquid chromatography (HPLC). Plasma ascorbate concentrations increased dramatically (3–4-fold) in both species during hibernation and rapidly returned to prehibernation levels upon arousal. By contrast, plasma GSH concentrations fell slightly or remained stable during hibernation. Ascorbate levels in the CSF doubled in hibernating AGS (not determined in TLS), while brain ascorbate content fell slightly (10–15%) in both species. Substantial increases in plasma and CSF ascorbate concentrations suggest that this antioxidant could play a protective role during hibernation and reperfusion upon arousal from hibernation.

Erythrocyte susceptibility to lipid peroxidation in patients with coronary atherosclerosis.

In recent years it has been reported that free oxygen radicals play an important role in the pathogenesis of degenerative diseases and that antioxidant vitamins such as vitamins E or C prevent their harmful effects. In this study, we evaluated the following: Erythrocyte susceptibility to lipid peroxidation; the role of erythrocyte glutathione (GSH) as an antioxidant; plasma lipid fractions; and the relationship between plasma lipid peroxides and antioxidant vitamin levels. Thiobarbituric acid-reactive substance (TBARS) levels were measured to determine the levels of plasma lipid peroxides and the susceptibility to lipid peroxidation when erythrocytes were stressed by hydrogen peroxide for 2 h in vitro. Erythrocyte TBARS production was significantly higher in patients with coronary atherosclerosis than in the controls. On the other hand, the levels of plasma high-density lipoproteins, vitamin C, vitamin E and erythrocyte GSH were significantly lower, and the levels of plasma total cholesterol, triglycerides, low-density lipoproteins and TBARS were significantly higher in the patients with coronary atherosclerosis than in the controls. In conclusion, our results indicate that erythrocytes from patients with coronary atherosclerosis are more susceptible to oxidation than those of controls and that these patients have lowered antioxidant capacity as revealed by decreased plasma levels of vitamins C and E.