Effects Of Antioxidant Vitamins Research Articles

Effect of dietary vitamin E supplementation on the shelf life of cured pork sausage

This study examined the shelf life of cured sausage under different packaging conditions from vitamin E supplemented pigs. One group ( n=6) of crossbred pigs received a normal fattening diet containing 20 ppm α-tocopherol for 39 days before slaughter. Another group was fed a diet containing 410 ppm α-tocopherol during the same period. After slaughter, cured sausages were produced, packaged under three different atmospheric conditions, ripened for 4 weeks and then stored for 8 weeks (9 °C; 200 lux). The α-tocopherol content was recorded in the fat, liver, muscles and the sausage. TBARS, L*, a*, b* values and antioxidative capacity were evaluated in the sausage during storage. The results showed a transfer of vitamin E into tissues and sausage but no detectable effect on TBARS and colour stability. However, antioxidative effects of vitamin E were seen by provocation. Probably the effect of vitamin E in the sausage was masked by nitrite in the curing salt. The oxygen content of the packs had an influence on TBARS and colour stability.

Antioxidant vitamins and risk of cardiovascular disease. Review of large-scale randomised trials.

People who consume a diet rich in fruit and vegetables have lower risks of cancer, cardiovascular disease and all-cause mortality. Many prospective cohort studies have reported inverse associations between dietary intake or blood levels of beta-carotene and risks of cancer. Several large-scale trials were set up to assess whether beta-carotene supplementation might reduce the risk of cancer. Subsequently, evidence emerged from basic research which indicated that oxidative modification of low-density lipoprotein cholesterol increases its atherogenicity. The evidence from basic research, and epidemiological evidence for a possible protective effect of antioxidant vitamins for cardiovascular disease was strongest for vitamin E. More recently, further trials were set up to examine if supplementation with anti-oxidant vitamins might also reduce the risk of cardiovascular disease. This review summarises the available randomised evidence from published trials of beta-carotene supplementation involving 70,000 people from 3 large-scale trials in healthy populations and on vitamin E supplementation involving 29,000 patients at high-risk of cardiovascular disease from 5 large-scale trials. The results of these trials have been disappointing and failed to confirm any protective effect of these vitamins for either cancer or for cardiovascular disease.

Antioxidant effects of vitamins C and E are associated with altered activation of vascular NADPH oxidase and superoxide dismutase in stroke-prone SHR.

Ascorbic acid (vitamin C) and alpha-tocopherol (vitamin E) have antioxidant properties that could improve redox-sensitive vascular changes associated with hypertension. We determined whether vitamins C and E influence vascular function and structure in hypertension by modulating activity of NADPH oxidase and superoxide dismutase (SOD). Adult stroke-prone spontaneously hypertensive rats (SHRSP) were divided into 3 groups: control (C; n=6), vitamin C-treated (vit C, 1000 mg/day; n=7), and vitamin E-treated (vit E, 1000 IU/day; n=8). All rats were fed 4% NaCl. Blood pressure was measured weekly. After 6 weeks of treatment, the rats were killed, and mesenteric arteries were mounted as pressurized preparations. Vascular O(2)(-) generation and NADPH oxidase activity were measured by chemiluminescence. Vascular SOD activity and plasma total antioxidant status (TAS) were determined spectrophotometrically. Blood pressure increased from 212+/-7 to 265+/-6 mm Hg in controls. Treatment prevented progression of hypertension (vit C, 222+/-6 to 234+/-14 mm Hg; vit E, 220+/-9 to 227+/-10 mm Hg). Acetylcholine-induced vasodilation was improved (P<0.05), and media-to-lumen ratio was reduced (P<0.05) in the treated rats. O(2)(-) was lower in vitamin-treated groups compared with controls (vit C, 10+/-4 nmol. min(-1). g(-1) dry tissue weight; vit E, 9.6+/-3.5 nmol. min(-1). g(-1) dry tissue weight; C, 21+/-9 nmol. min(-1). g(-1) dry tissue weight; P<0.05). Both vitamin-treated groups showed significant improvement (P<0.01) in TAS. These effects were associated with decreased activation of vascular NADPH oxidase (vit C, 46+/-10; vit E, 50+/-9; C, 70+/-16 nmol. min(-1). g(-1) dry tissue weight, P<0.05) and increased activation of SOD (vit C, 12+/-2; vit E, 8+/-1; C, 4.6+/-1 U/mg; P<0.05). Our results demonstrate that vitamins C and E reduce oxidative stress, improve vascular function and structure, and prevent progression of hypertension in SHRSP. These effects may be mediated via modulation of enzyme systems that generate free radicals.

Effects of antioxidant vitamins on anti-IgE-induced mediator release from human basophils.

Effects of antioxidant vitamins on anti-IgE-induced mediator release from human basophils.

Vitamin E Supplementation Improves Cell-Mediated Immunity and Oxidative Stress of Asian Men and Women

Vitamin E is an efficient antioxidant and a modulator of the immune system. Although racial differences in both baseline vitamin E level and immunologic subsets are known, no reliable data exist for the Asian population. Furthermore, the extent of the effect of alpha-tocopherol in protecting lymphocyte cells against oxidative stress and its association with cell-mediated immunity have not been elucidated. This study was undertaken to investigate the immunologic and antioxidant effects of vitamin E in healthy ethnic Chinese men and women. Volunteers < 35 y old (n = 26) were supplemented with 233 mg/d dl-alpha-tocopherol for 28 d. The in vitro proliferative response to phytohemagglutinin (PHA) or lipopolysaccharide (LPS) of T-lymphocytes was determined in the study group before and after vitamin E supplementation. Cell-mediated immunity subsets and hydrogen peroxide production in T-lymphocytes were investigated by flow cytometry. The oxidant-antioxidant balance in plasma and urine was studied by spectrophotometric and gas chromatography-mass selective detection methods. The antioxidant properties of vitamin E were established (P: < 0.01) by the elevation of plasma vitamin E, together with depression in both plasma malondialdehyde and urinary DNA adduct 8-hydroxy-2'-deoxyguanosine after supplementation. Our data suggest a specific requirement for vitamin E in total-T and T-helper cell proliferation. We present the first evidence of the beneficial effects of supplemental vitamin E in healthy Chinese individuals on cell-mediated immunity and oxidative stress.

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.

Effects of antioxidant vitamins A, C, E and trace elements Cu, Se on CuZn SOD, GSH‐Px, CAT and LPO levels in chicken erythrocytes

The biologically damaging effects of reactive oxygen species are controlled in vivo by a wide spectrum of antioxidant defence mechanisms. Dietary constituents of antioxidant vitamins and trace elements may play an important role in protecting against oxidant damage. The effects of supplementation of vitamins A, C, E and trace elements Cu and Se on the activities of antioxidant enzymes and lipid peroxide levels in chicken erythrocytes were investigated depend on the time. CuZnSOD activity and plasma Cu levels in the Cu group were increased by 39 and 37 per cent respectively. CuZnSOD activity in vitamin C groups was also increased by 20 per cent. The GSH-Px activity in Se, Se+E and Se+Cu groups was raised by 35, 46 and 69 per cent respectively. Also, the GSH-Px activity in the vitamin C group was increased by 33 per cent. Catalase activity in all of these groups was not significantly different when compared with controls (p<0·01). The maximum decrease in LPO levels of 42 per cent was obtained for the Se+E group. Copyright © 2000 John Wiley & Sons, Ltd.

Effects of antioxidant vitamins A, C, E and trace elements Cu, Se on CuZn SOD, GSH-Px, CAT and LPO levels in chicken erythrocytes.

The biologically damaging effects of reactive oxygen species are controlled in vivo by a wide spectrum of antioxidant defence mechanisms. Dietary constituents of antioxidant vitamins and trace elements may play an important role in protecting against oxidant damage. The effects of supplementation of vitamins A, C, E and trace elements Cu and Se on the activities of antioxidant enzymes and lipid peroxide levels in chicken erythrocytes were investigated depend on the time. CuZnSOD activity and plasma Cu levels in the Cu group were increased by 39 and 37 per cent respectively. CuZnSOD activity in vitamin C groups was also increased by 20 per cent. The GSH-Px activity in Se, Se+E and Se+Cu groups was raised by 35, 46 and 69 per cent respectively. Also, the GSH-Px activity in the vitamin C group was increased by 33 per cent. Catalase activity in all of these groups was not significantly different when compared with controls (p<0.01). The maximum decrease in LPO levels of 42 per cent was obtained for the Se+E group.

Protective effect of vitamin E on gastric mucosal injury in rats with biliary obstruction.

Patients with liver disease display increased susceptibility to gastric mucosal damage. A role of free radicals has been suggested in the development of gastric mucosal damage in normal subjects. The effects of antioxidant vitamin E treatment on the liver and stomach in cirrhotic rats were examined. Fifty rats were divided into three groups. Cirrhosis was induced by bile duct ligation in 40 of 50 rats. Controls underwent a sham operation. Gastric mucosal lesions were produced by intragastric administration of 1 mL of 95% ethanol in all three groups. Twenty bile duct-ligated rats were injected intramuscularly with vitamin E (100 mg/kg/day). Liver and stomach histology, and stomach malondialdehyde and glutathione levels were determined. Portal hypertension was measured. Macroscopic and microscopic gastric mucosal injury were significantly greater in the control and common bile duct-ligated groups than in the vitamin E-pretreated group (P<0.05). The tissue malondialdehyde and glutathione levels were significantly decreased in the vitamin E-administrated group compared with the common bile duct-ligated group (P<0.001). Vitamin E administration may be cytoprotective for both the liver and gastric mucosa in bile duct-ligated rats.

Antioxidative efficacy of parallel and combined supplementation with coenzyme Q10 and d-α-Tocopherol in mildly hypercholesterolemic subjects: a randomized placebo-controlled clinical study

It has been claimed that coenzyme Q10 (Q10) would be an effective plasma antioxidant since it can regenerate plasma vitamin E. To test separate effects and interaction between Q10 and vitamin E in the change of plasma concentrations and in the antioxidative efficiency, we carried out a double-masked, double-blind clinical trial in 40 subjects with mild hypercholesterolemia undergoing statin treatment. Subjects were randomly allocated to parallel groups to receive either Q10 (200 mg daily), d-α-tocopherol (700 mg daily), both antioxidants or placebo for 3 months. In addition we investigated the pharmacokinetics of Q10 in a separate one-week substudy. In the group that received both antioxidants, the increase in plasma Q10 concentration was attenuated. Only vitamin E supplementation increased significantly the oxidation resistance of isolated LDL. Simultaneous Q10 supplementation did not increase this antioxidative effect of vitamin E. Q10 supplementation increased and vitamin E decreased significantly the proportion of ubiquinol of total Q10, an indication of plasma redox status in vivo. The supplementations used did not affect the redox status of plasma ascorbic acid. In conclusion, only vitamin E has antioxidative efficiency at high radical flux ex vivo. Attenuation of the proportion of plasma ubiquinol of total Q10 in the vitamin E group may represent in vivo evidence of the Q10-based regeneration of the tocopheryl radicals. In addition, Q10 might attenuate plasma lipid peroxidation in vivo, since there was an increased proportion of plasma ubiquinol of total Q10.

The antioxidant effects of vitamin C and vitamin E on oxidative stress

Objective: To determine the antioxidant effect of high dose Vitamin C (Vit C), Vitamin E (Vit E) and Vit C+ Vit E on acute hyperoxic lung injury, using plasma and lung tissue malonyldialdehyde (MDA) levels, as indicators and to compare the degree of peroxidation with histopathological lung changes in a rat model. Design: Randomized, prospective laboratory study. Setting: Animal research laboratory in Aegean University. Subjects: 90 adult male Swiss-albino rats (150-160 g). Intervention: The rats were randomly allocated to one of five groups. Saline was administered intraperitoneally (IP) to group I (normoxic control, n=10) and group II (hyperoxic control, n=20). Vit C (150 mg/kg, n=20), Vit E (100 mg/kg, n=20) and Vit C plus Vit E (150 mg/kg plus 100 mg/kg, n=20) were administered IP to group III, IV and V, respectively. The rats were then exposed to 90% or higher concentrations of oxygen in an isolator for 24 hours. Measurement: Blood samples and lung tissues were taken after 24 hours of their exposure t...

The antioxidant effects of vitamin C and vitamin E on oxidative stress

The antioxidant effects of vitamin C and vitamin E on oxidative stress

Effect of Antioxidant Vitamin E as a Protective Factor in Experimental Atherosclerosis in Rhesus Monkeys

Atherosclerosis has been known for many years, yet its etiology remains unknown. Hypercholesterolemia is a major risk factor for atherosclerosis. The mechanism by which it triggers endothelial injury is not known. Since the role of the antioxidant vitamin E on experimental atherosclerosis is inconsistent, the present study was undertaken to evaluate platelet lipid peroxidation and the role of vitamin E (α-tocopherol) as protective factor in atherosclerosis in rhesus monkeys. A significant decrease in serum cholesterol and serum triglyceride levels was found in the group of animals which were reverted to stock diet along with vitamin E injections after 9 months of atherogenic diet feeding. Decreases in malonyldialdehyde levels and antioxidant enzyme activities were less significant in animals continued on an atherogenic diet feeding along with vitamin E as compared with animals fed a stock diet with vitamin E supplementation. The overall observations in this study suggest that antioxidant status and lipid peroxidation could be partly restored with vitamin E supplementation in experimental atherosclerosis. Damage to endothelial cells destroys their antithrombotic status and leads to fatal thrombosis. α-Tocopherol offers the best hope, but the question is how much of it should be administered for the prevention of atherosclerosis.

Copper-induced LDL peroxidation: interrelated dependencies of the kinetics on the concentrations of copper, hydroperoxides and tocopherol

Excessive uptake of oxidized low density lipoprotein plays a role in the onset of atherosclerosis. Lipid-associated antioxidants, the most abundant of which is tocopherol (vitamin E), are therefore believed to have anti-atherogenic properties. By contrast, hydroperoxides enhance the peroxidation of low density lipoprotein. We demonstrate that none of these compounds markedly affect the maximal rate of oxidation of low density lipoprotein, whereas the lag preceding rapid oxidation is prolonged by tocopherol but shortened by hydroperoxides. The corresponding ‘prolongation’ and ‘shortening’ can be compensated by each other in low density lipoprotein preparations enriched with both these compounds. The dependence of the balance between the effects of tocopherol and hydroperoxides on the copper concentration indicates that the antioxidative effect of vitamin E increases with the oxidative stress.

Dietary vitamin E supplementation does not inhibit Candida albicans intestinal translocation in rats.

Candida albicans translocation was determined in rats receiving a normal or vitamin E-supplemented and deficient diet submitted to mesenteric ischemia and reperfusion (MIR). The antioxidant effect of vitamin E on lipid peroxidation was also assessed. The animals were divided into six groups submitted to different diets for 30 d. Groups N, NI, NC and NIC were submitted to a normal diet and used as controls, and groups VITE and DEFE received a vitamin E-supplemented and vitamin E-deficient diet, respectively. Groups NIC, VITE and DEFE were submitted to MIR, inoculated with Candida albicans and sacrificed 24 h after the surgical procedure. The antioxidant effect of vitamin E was determined in the liver and gut mucosa using the TBARS method. Candida albicans translocation was assessed in lymph node, liver and kidney specimens. The results showed that lipid peroxidation was lower (p < 0.05) in the vitamin E-supplemented group. However, vitamin E supplementation did not protect the rats against Candida albicans translocation (the translocation in the Group VITE was 100% for lymph nodes).

Effect of antioxidant vitamins on transplant atherosclerosis in the Zucker rat model: Evidence for oxidative stress in the pathophysiology?

Effect of antioxidant vitamins on transplant atherosclerosis in the Zucker rat model: Evidence for oxidative stress in the pathophysiology?

Effect of antioxidant vitamins on transplant atherosclerosis in the Zucker rat model: Evidence for oxidative stress in the pathophysiology?

152 Oxidative stress is central to the pathophysiology of atherosclerosis. Hyperlipidemia and hyperglycemia trigger endothelial generation of reactive oxidant species, activating nuclear transcription factors (NFκB) which induce genes involved in atherosclerosis such as VCAM-1 and MCP-1. Phenolic antioxidants such as vitamin E restore endothelial redox state, while vitamin C protects against peroxidative damage and is the most effective endogenous antioxidant known. The effect of antioxidants on the pathophysiology of TxCAD is unknown. We hypothesized that TxCAD induced by metabolic abnormalities, as we have previously reported in the Zucker fat rat transplant model, will be attenuated by antioxidant vitamins. Methods: We compared the effects on TxCAD of: α-tocopherol (vitamin E) 40 mg/kg/day, L-ascorbic acid(vitamin C) 10 g/kg chow, and vehicle (control) 0.2 ml, HCO polyethylene 60-hydrogenated castor oil. Treatment was begun two weeks prior to transplant surgery, and continued until the 60-day endpoint. Vitamin C was administered by dietary supplementation of standard laboratory chow, and Vitamin E and vehicle by tail-vein injection on alternate days. Plasma concentrations of vitamins were measured prior to transplantation to ensure adequacy of dosing, and at 30-day and 60-day time points. Sections of the transplant heart were stained with elastic van Geisson, and severity of intimal thickening graded(1-4) by a cardiac pathologist blinded to the treatment groups. The total numbers of vessels seen in each section were counted, and the frequency of TxCAD expressed as a percentage of the total count. Results:TableConclusions: TxCAD frequency and severity were significantly lower in vitamin C-treated rats; vitamin E appeared to have no effect despite plasma concentrations 4-fold higher than controls. This discordant effect is consistent with the known action of the tocopherol radical as a pro-oxidant in the absence of sufficient co-factors (e.g., vitamin C, co-enzymc Q) rendering it capable of initiating lipid peroxidation. The results suggest a role for oxidative stress in the disease process, and that vitamin C supplementation might be effective in preventing TxCAD in patients.

Comparative effects of antioxidant vitamins C, E and β-carotene on cell proliferation and apoptosis in a gastric epithelial cell line

Comparative effects of antioxidant vitamins C, E and β-carotene on cell proliferation and apoptosis in a gastric epithelial cell line

Effect of antioxidant vitamins on the transient impairment of endothelium-dependent brachial artery vasoactivity following a single high-fat meal

Effect of antioxidant vitamins on the transient impairment of endothelium-dependent brachial artery vasoactivity following a single high-fat meal

Effect of cholesterol-rich diets with and without added vitamins E and C on the severity of atherosclerosis in rabbits

Oxysterols as oxidation products of cholesterol are considered an atherogenic factor in the development of atherosclerosis in the arteries of cholesterol-fed rabbits. We compared the atherogenic effects of diets enriched either with 0.5% oxidized cholesterol (OC; characterized by high amounts of oxysterols) or with pure cholesterol (PC). The effects of antioxidant vitamins E and C added to the PC diet were also evaluated in view of their antioxidative properties for lipoproteins and cholesterol and how this could affect the severity of atherosclerosis. Four groups of rabbits were fed the following for 11 wk: 1) a nonpurified stock diet, 2) this stock diet plus 0.5% OC, 3) the stock diet plus 0.5% PC, and 4) the stock diet plus 0.5% PC and 1000 mg vitamin E and 500 mg vitamin C/kg diet (PC + antioxidants). The OC and PC diets were equally hyperlipidemic and hypercholesterolemic. The severity of atherosclerotic lesions was highest with the OC diet and lowest with the PC + antioxidants diet. The plasma oxysterol concentration was proportional to the severity of atherosclerosis in all three groups of cholesterol-fed rabbits. beta-Very-low-density-lipoprotein modification was minimized by vitamins E and C as indicated by its polyacrylamide gel electrophoretic pattern and its increased binding to the rabbit liver membrane in vitro. This study indicated that OC and PC were equally atherogenic but that the addition of antioxidants to the PC diet significantly reduced its severity, even when hypercholesterolemia persisted. This indicated that atherogenesis can result from an excessive accumulation of oxidation products of cholesterol in the plasma.