Α-tocopherol Supplementation Research Articles

Effect of dietary high-oleic acid sunflower seed, palm oil and vitamin E supplementation on broiler performance, fatty acid composition and oxidation susceptibility of meat

1. A study was conducted to evaluate the effect of inclusion of two fat sources: high-oleic acid sunflower seed (HOASS; 0, 50, 100, 150 and 200 g/kg diet) and palm oil (PO), and dietary supplementation of vitamin E (α-tocopheryl acetate, 200 mg/kg diet) on performance, fatty acid composition and susceptibility to oxidation of white and dark chicken meat during refrigerated storage. Female chicks (3 to 6 weeks) were given one of 5 diets containing 90 g/kg of added fat with increasing monounsaturated fatty acid (MUFA) content, adjusted by progressively replacing PO by HOASS. 2. Body weight gain and gain:food ratio of birds were depressed in diets containing the highest proportions of HOASS (150 and 200 g/kg). Relative abdominal fat was reduced in birds fed diets including HOASS, except in the diet containing 100 g HOASS/kg. The inclusion of α-tocopheryl acetate improved body weight gain and gain:food ratio. 3. According to the fatty acid profile of the diets, saturated and polyunsaturated fatty acid (SFA and PUFA, respectively) contents were significantly reduced and MUFA content was significantly increased in white and dark chicken meats when the saturated oil, PO, was replaced progressively by HOASS in the diet. The inclusion of α-tocopheryl acetate increased PUFA content in both meats. 4. After 4 and 7 d of refrigerated storage, white and dark meat samples obtained from birds fed on diets containing HOASS had significantly lower thiobarbituric acid reacting substance (TBARS) values than those derived from the PO diet. The addition of α-tocopheryl acetate significantly reduced the lipid oxidation in white and dark meat. 5. Overall, the results showed that increasing MUFA content of chicken meat by replacing dietary PO with HOASS (up to 100 g/kg) did not adversely affect broiler performance and reduced the susceptibility of meat to oxidation during refrigerated storage. Dietary α-tocopherol supplementation improved chicken performance and was effective in protecting lipid meat from oxidation.

Alpha-Tocopherol Distribution in Lipoproteins and Anti-Inflammatory Effects Differ between CHD-Patients and Healthy Subjects

Objective: The purpose of this study was to investigate the dose-dependent effects of RRR-α-tocopherol supplementation in coronary heart disease (CHD) patients and healthy subjects on plasma α-tocopherol levels, plasma lipoprotein distribution, LDL oxidation, and inflammatory plasma markers.Methods: 12 patients with coronary heart disease and 12 healthy subjects were supplemented with increasing dosages of RRR-α-tocopherol at 100, 200 and 400 mg/day for a period of 3 weeks per dose. Lipoproteins were separated by FPLC and ultracentrifugation. α-Tocopherol was measured by HPLC. Resistance of LDL to oxidation was determined by reading the absorption at 234 nm after CuCl2-induced oxidation. Clinical chemistry and inflammatory markers were measured on automated analysis systems.Results: Plasma α-tocopherol concentrations at baseline were comparable between CHD-patients and healthy subjects (21.7 ± 4.7 μmol/L and 25.8 ± 7.6 μmol/L, respectively). CHD-patients showed a significant increase (59%) of plasma α-tocopherol concentrations to 34.6 ± 9.8 μmol/L at a dosage of 100 mg/day RRR-α-tocopherol, whereas healthy subjects showed a significant (54%) increase to 39.7 ± 6.1 μmol/L only with 400 mg/day RRR-α-tocopherol. In addition, CHD-patients showed a significantly increased enrichment of α-tocopherol in VLDL. Supplementation (200 mg/day) caused a significant decrease of the acute phase plasma proteins C-reactive protein (CRP) (−65%) and fibrinogen (−24%).Conclusion: Our data demonstrate that CHD-patients require lower dosages of α-tocopherol supplementation than healthy subjects to exert biological effects on plasma lipoproteins and acute phase response.

Role of α-tocopherol on antioxidant status in liver, lung and kidney of PCB exposed male albino rats

Polychlorinated biphenyls (PCB) are widespread, lipophilic environmental pollutants which have been identified as contaminants in almost every component of the global ecosystem including fish, wildlife, and human adipose tissue, breast milk, and serum. Several studies have shown that PCBs can cause oxidative damage to biomolecules, in the form of lipid peroxidation, modulation of antioxidant enzymes, and oxidative stress. In the present study, we have sought to investigate the effects of α-tocopherol (vitamin E) on antioxidant status of PCB-induced toxicity in male Wistar rats. The protective effect of α-tocopherol (50 mg/kg body weight/day) was tested in PCB-induced toxicity in rat liver, lung, and kidney. We report here that the oral supplementation of α-tocopherol was found to maintain the cellular redox status by maintaining the activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase accompanied with glutathione and vitamin E levels and down regulation in the levels of lipid peroxides, hydroxyl radical and hydrogen peroxides generation in PCB treated rats. Therefore, our present study demonstrates the PCB-induced deficits in antioxidant enzyme activities and increase in reactive oxygen species and lipid peroxidation levels in liver, kidney, and lung which can be overcome through simultaneous supplementation with α-tocopherol.

α-Tocopherol supplementation restores the reduction of erythrocyte glucose-6-phosphate dehydrogenase activity induced by forced training

Background Erythrocyte glucose-6-phosphate dehydrogenase (G6PD) activity is closely related to free radical production. α-Tocopherol (alpha-T) is implicated with the reduction of lipid peroxidation. Aim To investigate the effect of training and alpha-T supplementation on the erythrocyte G6PD activity. Methods Blood was obtained from 10 basketball players pre-game (group A), post-game (group B) and after 30 days on alpha-T ( dl-alpha-tocopheryl-acetate, 200 mg 24 h −1 orally) supplementation pre- (group C) and post-training (group D). alpha-T and catecholamines were evaluated with HPLC methods and creatine kinase, lactate dehydrogenase, total antioxidant status (TAS) and G6PD activity with commercial kits. Results TAS was increased in the groups with alpha-T addition (groups C and D). Post-exercise, TAS and G6PD activity were remarkably higher (2.10 ± 0.13 mmol l −1, 7.92 ± 1.5 U g −1 Hb, respectively) in group D than those in group B (0.92 ± 0.10 mmol l −1, 4.8 ± 1.4 U g −1 Hb, p < 0.01, respectively). G6PD activity positively correlated with TAS ( r = 0.64, p < 0.001) in all the studied groups. Conclusions Supplementation with alpha-T may protect G6PD activity from reduction induced by forced training.

Status of Lipid Peroxidation in Normal Cycling and 慣-Tocopherol Supplemented Anestrus Buffalo Heifers (Bubalus bubalis)

The present study was undertaken to analyze the status of erythrocytic malonyl dialdehyde (MDA) as an index of lipid peroxidation in normal cycling and α-tocopherol supplemented anestrus buffalo heifers. Before supplementation, the blood samples were collected at weekly interval in anestrus and normal cycling buffalo heifers and data from four samples was pooled to establish pre-supplementation base line. Thereafter, the blood samples from anestrus and α-tocopherol supplemented anestrus buffalo heifers were taken at fortnightly interval for 12 weeks during supplementation and for four weeks during the post-supplementation period. The pre-supplementation endogenous erythrocytic MDA, 0.3% H 2 O 2 induced-erythrocytic MDA and 1.5% H 2 O 2 induced-erythrocytic MDA levels (nmol/g Hb) increased significantly (p<0.05) in anestrus heifers (372.3±5.0, 564.4±5.7, 862.4±8.5) when compared to normal cycling animals (289.6±3.0, 508.2±6.0, 777.7±4.9). Oral supplementation of 3,000 mg of a-tocopherol per week per animal in anestrus heifers resulted in a progressive and significant (p<0.01) decline in erythrocytic MDA levels. These observations implied that supplementation of α-tocopherol to anestrus buffalo heifers ameliorated their antioxidant status by alleviating the effects of oxidative stress.

EFFECT OF DIFFERENT LEVELS OF DIETARY α-TOCOPHEROL ON OVARIAN MATURATION AND REPRODUCTIVE PERFORMANCE OF BROODSTOCK LITOPENAEUS VANNAMEI (BOONE)

Effects of 4 grade levels of dietary α-tocopherol (37.82, 115.64, 349.42 and 522.56 mg kg−1 diet) on ovarian maturation and reproductive performance of broodstock shrimp, Litopenaeus vannamei were investigated. The α-tocopherol concentrations in hepatopancreas, ovaries, eggs and muscle of female shrimp increased significantly as dietary α-tocopherol levels increased. Survival, spermatophore weight, sperm count, gonadosomatic index (GSI), hepatosomatic index (HSI), fecundity and egg diameter were not significantly affected by dietary α-tocopherol levels. Average daily spawns, hatching rate and fertilization rate significantly increased as dietary α-tocopherol levels increased. Results of this study confirmed the importance of supplementation of α-tocopherol to broodstock diets fed to L. vannamei, and suggested that at least 350 mg α-tocopherol kg−1 of diet was needed to achieve significantly better ovarian maturation and reproductive performance.

The Efficacy and Safety of Multivitamin and Mineral Supplement Use To Prevent Cancer and Chronic Disease in Adults: A Systematic Review for a National Institutes of Health State-of-the-Science Conference

Multivitamin and mineral supplements are the most commonly used dietary supplements in the United States. To synthesize studies on the efficacy and safety of multivitamin/mineral supplement use in primary prevention of cancer and chronic disease in the general population. English-language literature search of the MEDLINE, EMBASE, and Cochrane databases through February 2006 and hand-searching of pertinent journals and articles. Randomized, controlled trials in adults were reviewed to assess efficacy, and randomized, controlled trials and observational studies in adults or children were reviewed to assess safety. Paired reviewers extracted data and independently assessed study quality. 12 articles from 5 randomized, controlled trials that assessed efficacy and 8 articles from 4 randomized, controlled trials and 3 case reports on adverse effects were identified. Study quality was rated fair for the studies on cancer, cardiovascular disease, cataracts, or age-related macular degeneration and poor for the studies on hypertension. In a poorly nourished Chinese population, combined supplementation with beta-carotene, alpha-tocopherol, and selenium reduced the incidence of and mortality rate from gastric cancer and the overall mortality rate from cancer by 13% to 21%. In a French trial, combined supplementation with vitamin C, vitamin E, beta-carotene, selenium, and zinc reduced the rate of cancer by 31% in men but not in women. Multivitamin and mineral supplements had no significant effect on cardiovascular disease or cataracts, except that combined beta-carotene, selenium, alpha-tocopherol, retinol, and zinc supplementation reduced the mortality rate from stroke by 29% in the Linxian study and that a combination of 7 vitamins and minerals stabilized visual acuity loss in a small trial. Combined zinc and antioxidants slowed the progression of advanced age-related macular degeneration in high-risk persons. No consistent adverse effects of multivitamin and mineral supplements were evident. Only randomized, controlled trials were considered for efficacy assessment. Special nutritional needs, such as use of folic acid by pregnant women to prevent birth defects, were not addressed. Findings may not apply to use of commercial multivitamin supplements by the general U.S. population. Evidence is insufficient to prove the presence or absence of benefits from use of multivitamin and mineral supplements to prevent cancer and chronic disease.

Antioxidant vitamins supplementation and mortality: A randomized trial in head and neck cancer patients

There has been concern that long-term supplementation with high-dose antioxidant vitamins, especially vitamin E (alpha-tocopherol), may increase all-cause mortality. We conducted a randomized controlled trial with alpha-tocopherol (400 IU/day) and beta-carotene (30 mg/day) supplements among 540 head and neck cancer patients treated by radiation therapy. Supplementation with beta-carotene was discontinued during the trial. The supplements were given during radiation therapy and for 3 additional years. During the follow-up (median 6.5 years), 179 deaths were recorded. All death certificates were obtained. All-cause and cause-specific mortality rates were compared between the 2 arms of the trial by Cox regression. All-cause mortality was significantly increased in the supplement arm: hazard ratio: 1.38, 95% confidence interval 1.03-1.85. Cause-specific mortality rates tended to be higher in the supplement arm than in the placebo arm. Our results concur with previous reports to suggest that high-dose vitamin E could be harmful.

Assessment of Tocopherol Metabolism and Oxidative Stress in Familial Hypobetalipoproteinemia

Vitamin E supplementation has been recommended for persons with familial hypobetalipoproteinemia (FHBL), a rare disorder of lipoprotein metabolism that leads to low serum alpha-tocopherol and decreased LDL-cholesterol and apolipoprotein (apo) B. We examined the effect of truncated apoB variants on vitamin E metabolism and oxidative stress in persons with FHBL. We studied 9 individuals with heterozygous FHBL [mean (SE) age, 40 (5) years; body mass index (BMI), 27 (10) kg/m2] and 7 normolipidemic controls [age, 41 (5) years; BMI, 25 (2) kg/m2]. We also studied 3 children-2 with homozygous FHBL (apoB-30.9) and 1 with abetalipoproteinemia-who were receiving alpha-tocopherol supplementation. We used HPLC with electrochemical detection to measure alpha- and gamma-tocopherol in serum, erythrocytes, and platelets, and gas chromatography-mass spectrometry to measure F2-isoprostanes and tocopherol metabolites in urine as markers of oxidative stress and tocopherol intake, respectively. Compared with controls, persons with FHBL had significantly lower fasting plasma concentrations of total cholesterol [2.4 (0.2) vs 4.7 (0.2) mmol/L], triglycerides [0.5 (0.1) vs 0.9 (0.1) mmol/L], LDL-cholesterol [0.7 (0.1) vs 2.8 (0.3) mmol/L], apoB [0.23 (0.02) vs 0.84 (0.08) g/L], alpha-tocopherol [13.6 (1.0) vs 28.7 (1.4) micromol/L], and gamma-tocopherol [1.0 (0.1) vs 1.8 (0.3) micromol/L] (all P < 0.03). Erythrocyte alpha-tocopherol was decreased [5.0 (0.2) vs 6.0 (0.3) micromol/L; P < 0.005], but we observed no differences in lipid-adjusted serum tocopherols, erythrocyte gamma-tocopherol, platelet alpha- or gamma-tocopherol, urinary F2-isoprostanes, or tocopherol metabolites. Taken together, our findings do not support the recommendation that persons with heterozygous FHBL receive vitamin E supplementation.

The Effect of α-tocopherol on Cholesterol and Lipoproteins Levels in Rats

The effect of the α-tocopherol on the reduction of plasma cholesterol, HDL, and LDL have been investigated in rats. No significant differences were observed on the rate of body weight gain, food intake, and food efficiency of rats fed with diet supplemented with α-tocopherol. There were significant decreases in serum cholesterol, and LDL+VLDL of animals fed α-tocopherol supplementation compared to control. In contrast the HDL cholesterol showed no significant decrease in animal groups fed α-tocopherol compared to control group. The lowest bile acid levels were in feces of control group, and the highest levels were for the groups fed α-tocopherol supplementation.

Protective effect of vitamin E supplements on experimental atherosclerosis is modest and depends on preexisting vitamin E deficiency

Vitamin E has failed to protect humans from cardiovascular disease outcome, yet its role in experimental atherosclerosis remains less clear. A previous study ( Proc. Natl. Acad. Sci. USA 97:13830–13834; 2000) showed that vitamin E deficiency caused by disruption of the α-tocopherol transfer protein gene ( Ttpa) is associated with a modest increase in atherosclerosis in apolipoprotein E gene deficient ( Apoe −/−) mice. Here we confirm this finding and report that in Apoe −/− Ttpa −/− mice dietary α-tocopherol (αT) supplements restored circulating and aortic levels of αT, and decreased atherosclerosis in the aortic root to a level comparable to that seen in Apoe −/− mice. However, such dietary supplements did not decrease disease in Apoe −/− mice, whereas dietary supplements with a synthetic vitamin E analog (BO-653), either alone or in combination with αT, decreased atherosclerosis in Apoe −/− and in Apoe −/− Ttpa −/− mice. Differences in atherosclerosis were not associated with changes in the arterial concentrations of F 2-isoprostanes and cholesterylester hydro(pero)xides, nor were they reflected in the resistance of plasma lipids to ex vivo oxidation. These results show that vitamin E at best has a modest effect on experimental atherosclerosis in hyperlipidemic mice, and only in situations of severe vitamin E deficiency and independent of lipid oxidation in the vessel wall.

Lack of effect of α-tocopherol on in vitro angiogenesis

Oxidative stress and angiogenesis are important elements in the pathogenesis of atherosclerosis and cancer. Because of its antioxidant properties, α-tocopherol has long proposed as prevention of diseases associated with oxidative stress. We explore whether α-tocopherol modulates some cell responses induced by angiogenic and proliferative stimuli. For this purpose, we evaluate the effect in human vein endothelial cells (HUVECs), of α-tocopherol treatment (5–40 μmol/L) for 72 h on the production of reactive oxygen species (ROS), induction of matrix metalloproteinases (MMPs), expression of vascular endothelial–cadherin (VE-cadherin) and α 2-integrin, cell migration, cell proliferation, and tube formation. α-Tocopherol significantly inhibits intracellular ROS production induced by TNF-α ( P < 0.01) or PMA ( P < 0.001). However, α-tocopherol does not interfere with mRNA expression of VE-cadherin, α 2-integrin, MMP-1, MMP-2, and MMP-9. Similarly, α-tocopherol does not modulate cell migration and capillary-like tube formation although at the concentration of 20 and 40 μmol/L it potentiated PMA-induced DNA synthesis ( P < 0.05). Our results suggest that although α-tocopherol supplementation reduces endothelial cell oxidative stress, it does not alter the cell response to angiogenic stimuli.

An in vivo and in vitro study of erythrocyte membrane acetylcholinesterase, (Na +, K +)-ATPase and Mg 2+-ATPase activities in basketball players on α-tocopherol supplementation. The role of l-carnitine

Vitamin E (alpha-tocopherol, alpha-Te) and carnitine reduce lipid peroxidation. THE AIM WAS TO: To investigate the erythrocyte membrane acetylcholinesterase (AChE), Na+, K+-ATPase and Mg2+-ATPase activities in basketball players with or without alpha-Te supplementation, before and after training. In vitro, we aimed to find out any additional effect of L-carnitine (L-C) on the modulated enzyme activities. Blood was obtained from 10 players before (group A), after exercise (group B) and after 1 month on alpha-Te (200 mg/24 h orally) supplementation before (group C) and after the game (group D). Lactate, pyruvate, muscle enzyme activities and total antioxidant status (TAS) were measured with commercial kits. Catecholamines and alpha-Te were determined with HPLC methods and membrane enzyme activities spectrophotometrically. Lactate, pyruvate, muscle enzymes and catecholamine levels were increased (P<0.001) in all groups after training. Alpha-Te levels and Mg2+-ATPase activity remained unaltered before and after exercise. TAS was decreased in the groups after the game. AChE activity was increased in group B (P<0.01) and decreased in group D (P<0.01). After the exercise, Na+, K+-ATPase activity was increased in group B and remained unaltered in group D. In vitro incubation of membranes from group D with L-C resulted in a partially restoration of the membrane AChE activity, whereas Na+, K+-ATPase and Mg2+-ATPase activities were found unchanged. Alpha-Te supplementation in basketball players results in an increase of TAS and AChE activity, whereas the other enzyme activities were found unchanged. L-C addition may restore AChE activity, which was modulated by training in players on alpha-Te.

Does Pharmaconutrition with L-Arginine and/or α-Tocopherol Improve the Gut Barrier in Bile Duct Ligated Rats?

Background/Aim: Nitric oxide supplementation and antioxidant therapy modulate gut barrier function, but the relationships between enhanced nitric oxide production, antioxidant administration, and biliary obstruction remain unclear. We evaluated the role of nitric oxide and α-tocopherol supplementation in bile duct ligated rats. Methods: Fifty male Wistar albino rats underwent sham operation (group I; control animals) or bile duct ligation (groups II, III, IV, and V). The ligation groups received the following regimens: standard pellet diet (group II), pellet diet plus intramuscularly administerd α-tocopherol (group III), and L-arginine-enriched pellet diet without (group IV) or with (group V) α-tocopherol. Nitric oxide, malondialdehyde, and α-tocopherol concentrations were assessed at the end of 3 weeks. Liver and intestinal samples were scored histologically. Mesenteric lymph node and liver cultures were assessed for bacterial translocation. Results: The liver malondialdehyde concentration was highest in group III. The nitric oxide content in the liver was higher in groups III and V, as were the blood α-tocopherol levels. Bacterial translocation was evident following bile duct ligation, but did not differ among the treatment groups. Intestinal histology revealed that group III had the lowest villus height, that group V had the least villus count, and that group II had the highest mucous cell count. The fibrosis scores were higher in groups IV and V. Conclusions: An obvious effect of α-tocopherol (with or without L-arginine) on the gut barrier could not be demonstrated. Moreover, the L-arginine-enriched diet promoted fibrosis in the liver. Thus, while biliary duct obstruction triggers bacterial translocation, nitric oxide and/or α-tocopherol supplementation did not seem to improve the gut barrier in our model.

Cigarette smokers differ in their handling of natural ( RRR) and synthetic ( all rac) α-tocopherol: A biokinetic study in apoE4 male subjects

We have compared the biokinetics of deuterated natural ( RRR) and synthetic ( all rac) α-tocopherol in male apoE4-carrying smokers and nonsmokers. In a randomized, crossover study subjects underwent two 4-week treatments (400 mg/day) with undeuterated RRR- and all rac-α-tocopheryl acetate around a 12-week washout. Before and after each supplementation period subjects underwent a biokinetic protocol (48 h) with 150 mg deuterated RRR- or all rac-α-tocopheryl acetate. During the biokinetic protocols, the elimination of endogenous plasma α-tocopherol was significantly faster in smokers ( P < 0.05). However, smokers had a lower uptake of deuterated RRR than nonsmokers, but there was no difference in uptake of deuterated all rac. The supplementation regimes significantly raised plasma α-tocopherol ( P < 0.001) with no differences in response between smokers and nonsmokers or between α-tocopherol forms. Smokers had significantly lower excretion of α-carboxyethyl-hydroxychroman than nonsmokers following supplementation ( P < 0.05). Nonsmokers excreted more α-carboxyethyl-hydroxychroman following RRR than all rac; however, smokers did not differ in excretion between forms. At baseline, smokers had significantly lower ascorbate ( P < 0.01) and higher F 2-isoprostanes ( P < 0.05). F 2-isoprostanes in smokers remained unchanged during the study, but increased in nonsmokers following α-tocopherol supplementation. These data suggest that apoE4-carrying smokers and nonsmokers differ in their handling of natural and synthetic α-tocopherol.

The effect of dietary supplementation with blueberry, α-tocopherol or astaxanthin on oxidative stability of Arctic char ( Salvelinus alpinus) semen

The objective was to determine the oxidative stability of Arctic char ( Salvelinus alpinus) semen following dietary supplementation with lowbush blueberry ( Vaccinium angustifolium) product, α-tocopherol, α-tocopherol + blueberry product, or α-tocopherol + astaxanthin. Sperm lipid peroxidation was initiated by challenging with ferrous sulphate/ascorbic acid (Fe ++/Asc) at level of 0.04/0.2 mmol/L. Addition of blueberry, α-tocopherol, or both to char diets inhibited semen lipid peroxidation by: (a) decreasing the rate of sperm lipid peroxidation, an effect which was more pronounced with α-tocopherol treatments; and (b) increasing the antioxidant potential of seminal plasma, based on the lipid peroxidation process of sperm and an in vitro chicken brain tissue model. Dietary supplementation with astaxanthin and α-tocopherol had the same effect as the supplementation with α-tocopherol alone on inhibiting the lipid peroxidation process of sperm and chicken brain. Catalase-like activity increased significantly in sperm of fish fed α-tocopherol, blueberry, or both. There was a negative correlation ( r = −0.397, P < 0.05) between catalase-like activity in sperm cells and the rate of sperm lipid peroxidation. Seminal plasma α-tocopherol levels increased significantly in fish supplemented with α-tocopherol alone or in combination with blueberry or astaxanthin. There were negative correlations between seminal plasma α-tocopherol levels and lipid peroxidation rates of sperm cells ( r = −0.625, P < 0.01) and brain tissue ( r = −0.606, P < 0.01). In conclusion, dietary supplementation of blueberry product or α-tocopherol inhibited lipid peroxidation in Arctic char semen. Further experiments are needed to test the effect of dietary blueberry and antioxidants on Arctic char semen quality during liquid and cryopreserved storage.

Combined antioxidant (β-carotene, α-tocopherol and ascorbic acid) supplementation increases the levels of lung retinoic acid and inhibits the activation of mitogen-activated protein kinase in the ferret lung cancer model

Interactions among beta-carotene (BC), alpha-tocopherol (AT) and ascorbic acid (AA) led to the hypothesis that using a combination of these antioxidants could be more beneficial than using a single antioxidant alone, particularly against smoke-related lung cancer. In this investigation, we have conducted an animal study to determine whether combined BC, AT and AA supplementation (AOX) protects against 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)-induced lung carcinogenesis in smoke-exposed (SM) ferrets. Ferrets were treated for 6 months in the following four groups: (i) control, (ii) SM + NNK, (iii) AOX and (iv) SM + NNK + AOX. Results showed that the combined AOX supplementation (i) prevented the SM + NNK-decreased lung concentrations of retinoic acid (RA) and BC; (ii) inhibited the SM + NNK-induced phosphorylation of Jun N-terminal kinase (JNK), extracellular-signal-regulated protein kinase (ERK) and proliferating cellular nuclear antigen proteins in the lungs of ferrets; and (iii) blocked the SM + NNK-induced up-regulation of total p53 and Bax proteins, as well as phosphorylated p53 in the lungs of ferrets. In addition, there were no lesions observed in the lung tissue of ferrets in the control and/or the AOX groups after 6 months of intervention, but combined AOX supplementation resulted in a trend toward lower incidence of both preneoplastic lung lesions and lung tumor formation in SM + NNK + AOX group of ferrets, as compared with the SM + NNK group alone. These data indicate that combined AOX supplementation could be a useful chemopreventive strategy against lung carcinogenesis through maintaining normal tissue levels of RA and inhibiting the activation of mitogen-activated protein kinase pathways, cell proliferation and phosphorylation of p53.

α-Tocopherol supplementation reduces the elevated 8-hydroxy-2-deoxyguanosine blood levels induced by training in basketball players

The aim of the present study was to investigate the effect of alpha-tocopherol (alpha-Te) supplementation on DNA oxidative damage induced by heavy training in basketball players. Blood was obtained from 10 players before (group A) and after training (group B) and after 1 month on alpha-Te (200 mg/day, orally) supplementation, before (group C) and after training (group D). Total antioxidant status (TAS), muscle enzyme activities and the biomarker of DNA oxidation, 8-hydroxy-2-deoxyguanosine (8-OHdG), were measured using commercial kits. alpha-Te and catecholamine blood levels were determined using HPLC methods. TAS was higher in the groups with alpha-Te (groups C and D). Levels of 8-OHdG and muscle creatine kinase (CK) and lactate dehydrogenase (LDH) were remarkably lower (0.20+/-0.03 ng/mL, 120+/-15 U/L and 430+/-90 U/L, respectively) in the group with alpha-Te (group D) than in group B (0.42+/-0.05 ng/mL, 286+/-12 U/L and 688+/-88 U/L, respectively; p<0.001). 8-OHdG levels were negatively correlated to TAS and positively to CK levels. alpha-Te supplementation may reduce DNA oxidation induced by training by protecting muscle cell "death" from glutamate entry and/or by elevation of TAS via amelioration of lipid peroxidation.

Highlights from the Literature

Highlights from the Literature

Assessment of the antioxidative potential of dietary supplementation with α-tocopherol in low-nitrite salami-type sausages

The objective of this study was to determine the effects of dietary α-tocopherol supplementation to pigs on the lipid stability of nitrite-reduced salami-type sausages (custom-produced for this study). Fourteen crossbred pigs were divided into two equal groups. The control group (CG) was fed a basal diet containing 34 ppm α-tocopherol, and the experimental group (EG), a diet supplemented with 364 ppm α-tocopherol, both for 35 days. After slaughter, salami-type sausages were produced with the addition of different nitrite levels in the curing salt (100, 50, 25 and 0 ppm), ripened for four weeks, sliced, and packaged under a protective atmosphere (80 parts N 2 to 20 parts CO 2). The packed products were stored for eight weeks under simulation of the usual conditions in self-service shelves with permanent lighting (9 °C, 200 lux). The sausages were regularly assessed for their oxidative status (thiobarbituric acid-reactive substances, fatty acid pattern) and the amount of α-tocopherol, and by sensory evaluation. In the EG sausages, α-tocopherol concentrations were twice as high and TBARS were lower than in the CG sausages. The α-tocopherol in EG prevented the loss of unsaturated fatty acids during storage. Sausages of EG containing 100 ppm nitrite had the longest sensory stability. However, the biochemical parameters did not indicate that nitrite had any effect on the antioxidative potential of the sausages.