Vitamin E and relationships among tocopherols in human plasma, platelets, lymphocytes, and red blood cells

Plasma, RBC, platelets, and lymphocytes from human subjects on graded intakes of vitamin E were analyzed for tocopherols to determine which humoral compartment most closely followed changes in the dietary intake. Relative merits of the various blood elements to reflect changes in vitamin E intake were calculated by the sensitivity concept of Mandel and Stiehler (ie, rate of change of tocopherol levels with dose divided by the standard deviation). Sensitivities of alpha-tocopherol levels of the various blood components to vitamin E intake decreased in the order platelets greater than RBC greater than plasma lipids greater than plasma greater than lymphocytes. Changes in tocopherol levels in platelets most closely followed changing dietary intakes of vitamin E when compared with data from RBC, lymphocytes, and plasma. Furthermore, for studying the effects of diets on vitamin E status, tocopherol levels of platelets appear to be a better measure than tocopherol levels of either RBC, lymphocytes, or plasma lipids.     

Changes in vitamin E concentrations in human plasma and platelets with age

It has been postulated that vitamin E compounds (tocopherols) can retard the aging process. Therefore, changes in concentrations of tocopherols in human plasma and platelets with aging were studied. Fasting blood samples were obtained from 48 healthy male volunteers aged 24-91 years. Concentrations of the tocopherols in plasma and platelets were determined by a liquid chromatographic method. Alpha and gamma tocopherols were the major forms of vitamin E found in both plasma and platelets. The concentrations of alpha and total tocopherols in plasma did not change significantly with age. However, the plasma gamma tocopherol and the platelet alpha, gamma, and total tocopherol concentrations decreased significantly with age. The platelet to plasma ratios of tocopherol concentrations also decreased with age.     

Vitamin E deficiency in Uganda African subjects

• 1.1) The incidence of vitamin E deficiency was estimated in 490 Uganda African subjects.
• 2.2) 15 per cent. of the control group were deficient and similar values were found in diabetic subjects, cardiac failure subjects and primagravidae. There was a significant increase in the incidence of deficiency in cases of severe hookworm infection.
• 3.3) It is suggested that the possible role of vitamin E deficiency in the aetiology of cardiac disease of obscure origin and of cirrhosis should be borne in mind.
     

Changes in vitamin E concentrations in human plasma and platelets with age.

It has been postulated that vitamin E compounds (tocopherols) can retard the aging process. Therefore, changes in concentrations of tocopherols in human plasma and platelets with aging were studied. Fasting blood samples were obtained from 48 healthy male volunteers aged 24-91 years. Concentrations of the tocopherols in plasma and platelets were determined by a liquid chromatographic method. Alpha and gamma tocopherols were the major forms of vitamin E found in both plasma and platelets. The concentrations of alpha and total tocopherols in plasma did not change significantly with age. However, the plasma gamma tocopherol and the platelet alpha, gamma, and total tocopherol concentrations decreased significantly with age. The platelet to plasma ratios of tocopherol concentrations also decreased with age.     

Vitamin E in fortified cow milk uniquely enriches human plasma lipoproteins

BACKGROUND: Milk fat may contribute to atherogenesis in humans. OBJECTIVE: We sought to offset the atherogenic potential of milk fat by adding polyunsaturated fat and vitamin E to milk. DESIGN: We measured plasma lipids, lipoproteins, and tocopherol and LDL oxidation in normolipemic adults. In experiment 1 (n = 48), we compared delivery of 100 mg all-rac-alpha-tocopheryl acetate/d in capsules, skim milk, and 1%-fat milks containing soybean oil, milk fat, or both (1:1). In experiment 2 (n = 24), we compared delivery of natural (RRR-alpha-tocopheryl acetate) and synthetic (all-rac-alpha-tocopheryl acetate) vitamin E in milk with delivery of all-rac-alpha-tocopheryl acetate in orange juice (200 mg/d in each group). In experiment 3 (n = 7), we compared delivery of 30 mg all-rac-alpha-tocopheryl acetate/d in milks with and without added vitamins A and D. RESULTS: Enrichment of milk fat with soybean oil did not alter plasma lipoproteins. Microdispersion of vitamin E in milks increased the molar ratio of plasma tocopherol to cholesterol by >2-fold compared with the molar ratio after consuming vitamin E capsules, whereas the molar ratios were comparable after ingestion of orange juice and capsules. Synthetic and natural vitamin E performed comparably. The enhanced plasma vitamin E:cholesterol attributed to milk increased protection of LDL against oxidation. Vitamins A and D did not affect vitamin E delivery by milk. CONCLUSIONS: Milk augments vitamin E transport by human lipoproteins at intakes of 100-200 but not 30 mg/d. This augmentation is independent of the presence and type of fat in milk, its vitamin A and D contents, and whether the vitamin E is natural or synthetic.     

Basal and stimulated plasma leptin in diabetic subjects

OBJECTIVE: To determine whether leptin secretion is impaired in diabetes, we compared basal and stimulated plasma leptin levels in diabetic subjects and healthy controls. RESEARCH METHODS AND PROCEDURES: Blood samples for assay of leptin and other hormones were obtained at baseline in 54 diabetic patients and 65 controls, and 8 hours, 16 hours, and 40 hours following ingestion of dexamethasone (4 mg) in 6 healthy and 12 controls. C-peptide status was defined as "negative" if < or =0.1 ng/mL or "positive" if > or =0.3 ng/mL, in fasting plasma. RESULTS: Basal plasma leptin levels were 19.7+/-2.2 ng/mL in nondiabetic subjects, 13.4+/-1.5 ng/ml in C-peptide negative (n = 28) and 26.1+/-3.7 ng/mL in C-peptide positive (n = 26, p = 0.001) diabetic patients. Dexamethasone increased leptin levels of controls (n = 6) to 145+/-17% of baseline values at 8 hours (p = 0.03), 224+/-18% at 16 hours (p = 0.01), and 134+/-18% at 40 hours (p=0.05). The corresponding changes were 108+/-13%, 126+/-23%, and 98+/-16% in C-peptide negative (n=6), and 121+/-10%, 144+/-16% (p=0.03), and 147+/-23% (p=0.11) in C-peptide positive (n = 6) diabetic patients, respectively. The peak stimulated leptin levels were lower in the diabetic patients, compared with controls. Plasma insulin increased (p = 0.02) in controls, but not in the diabetic patients, following dexamethasone. DISCUSSION: Although diabetic patients have normal plasma leptin levels under basal conditions, their leptin responses to glucocorticoid are impaired, probably because of the concomitant insulin secretory defect. A subnormal leptin secretory response could worsen obesity and insulin resistance in diabetes.     

Selenium and vitamin E status of healthy and institutionalized elderly subjects: analysis of plasma, erythrocytes and platelets

Levels of selenium in whole blood, plasma, erythrocytes and platelets, glutathione peroxidase (EC 1.11.1.9; GSH-Px) activity in erythrocytes and platelets and vitamin E, low-density-lipoprotein (LDL)-cholesterol and vitamin E: LDL cholesterol in plasma were measured in seventy-five healthy subjects aged less than 65 years and twenty-eight healthy and twenty-three institutionalized elderly people aged greater than 65 years. Healthy elderly subjects had significantly lower levels of Se in whole blood and plasma when compared with younger subjects. Other measurements of Se status were not significantly different. In the healthy subjects plasma levels of vitamin E and LDL-cholesterol increased with age to 60 years and decreased above 80 years. Vitamin E: LDL cholesterol values were not affected by age. Measurements of Se and vitamin E status in the institutionalized elderly compared with the healthy elderly were all reduced with the exception of platelet Se levels and erythrocyte GSH-Px activity. Ageing per se had minimal effect on Se and vitamin E status but intercurrent illness and decreased food intake can lead to reduced levels in the elderly.     

Vitamin E supplementation enhances cell-mediated immunity in healthy elderly subjects

The effect of vitamin E supplementation on the immune response of healthy older adults was studied in a double-blind, placebo-controlled trial. Subjects (n = 32) resided in a metabolic research unit and received placebo or vitamin E (800 mg dl-alpha-tocopheryl acetate) for 30 d. Alpha-tocopherol content of plasma and peripheral blood mononuclear cells (PBMCs), delayed-type hypersensitivity skin test (DTH), mitogen-stimulated lymphocyte proliferation, as well as interleukin (IL)-1, IL-2, prostaglandin (PG) E2, and serum lipid peroxides were evaluated before and after treatment. In the vitamin E-supplemented group 1) alpha-tocopherol content was significantly higher (p less than 0.0001) in plasma and PBMCs, 2) cumulative diameter and number of positive antigen responses in DTH response were elevated (p less than 0.05), 3) IL-2 production and mitogenic response to optimal doses of concanavalin A were increased (p less than 0.05), and 4) PGE2 synthesis by PBMCs (p less than 0.005) and plasma lipid peroxides (p less than 0.001) were reduced. Short-term vitamin E supplementation improves immune responsiveness in healthy elderly individuals; this effect appears to be mediated by a decrease in PGE2 and/or other lipid-peroxidation products.     

Comparison of eicosapentaenoic acid concentrations in plasma between patients with ischemic stroke and control subjects

Objectiveω-3 fatty acids, including eicosapentaenoic acid (EPA), prevent ischemic stroke. However, the clinical importance of EPA for ischemic stroke and its subtype has not been fully elucidated.MethodsIn a cross-sectional study, we determined whether ω-3 fatty acids were predictive factors for ischemic stroke. We compared common clinical parameters among 65 patients with ischemic stroke and 65 control subjects. The parameters included blood chemistry data; concentrations of EPA, docosahexaenoic acid, and arachidonic acid (AA); EPA/AA ratio; smoking; alcohol intake; fish consumption more than four times per week; and the incidence of underlying diseases. The comparisons were performed using the Mann-Whitney U test, and multiple logistic regression analysis was applied to the significant factors in the non-parametric test. We also applied the same approach to the ischemic stroke subtypes, cardioembolism and large-artery atherosclerosis.ResultsIn the multiple logistic regression analysis after the Mann-Whitney U test, a lower EPA concentration was one of the significant risk factors for ischemic stroke, as were a lower body mass index, lower high-density lipoprotein cholesterol, and smoking (sensitivity 0.846, specificity 0.831, positive predictive value 0.833). In the analysis of subtypes, a lower EPA/AA ratio and a lower body mass index were the significant risk factors for cardioembolism (sensitivity 0.800, specificity 0.733, positive predictive value 0.750). However, large-artery atherosclerosis was not related to the EPA concentration or the EPA/AA ratio.ConclusionsIn this study, the plasma EPA concentration and the EPA/AA ratio were potential predictive risk factors for ischemic stroke, especially for cardioembolism. Further prospective studies are necessary.     

Vitamin E binding proteins in human serum.

The distribution of vitamin E in human serum lipoprotein fraction was investigated by measuring the amount of vitamin E in various protein fractions prepared by ultracentrifugation, gel filtration and electrophoresis. The larger part of the total serum vitamin E (up to 44%) was present in the alpha1-lipoproteins, while the beta-lipoproteins contained smaller concentrations (up to 26%).     

Vitamin E: absorption, plasma transport and cell uptake

PURPOSE OF REVIEW: Large-scale clinical trials have failed to demonstrate a benefit for vitamin E supplementation in cardiovascular prevention. This contrasts with previous epidemiological studies indicating that individuals with high vitamin E status benefit from protection against chronic illnesses, including cardiovascular diseases. These conflicting results suggest that the metabolism of supplemental versus naturally delivered vitamin E and their potential roles, other than a potent antioxidant action, are not fully understood. The purpose of this review is to provide an update on current knowledge on the intestinal absorption of vitamin E, its plasma transport and its supply to cells. The review will also discuss the intravascular metabolism of intravenously delivered vitamin E. RECENT FINDINGS: Although the luminal digestion of vitamin E is fairly well understood, several pathways regulating net vitamin E absorption remain to be elucidated. In several cell types, cholesterol and vitamin E share common mechanisms for cellular uptake (scavenger receptor B type I and LDL receptors) and efflux (ABCA1 transporters). The role of specific binding proteins in alpha-tocopherol intracellular trafficking is increasingly being understood, leading to new insights into the non-antioxidant functions of vitamin E. SUMMARY: Substantial progress has been made in characterizing the plasma transport of vitamin E and its delivery to cells. Mechanisms regulating the balance between the cellular uptake and efflux of vitamin E are under investigation. Vitamin E is not only an antioxidant but may also modulate pathways of cell signalling and gene expression. The translation of this new knowledge into clinical studies will help define future indications for vitamin E supplementation.     

Interactions between vitamins C and E in human subjects

Despite convincing in vitro evidence, a vitamin C-E interaction has not been confirmed in vivo. This study was designed to examine the effects of supplementation with either vitamin C or E on their respective plasma concentrations, other antioxidants, lipids and some haemostatic variables. Fasting blood was collected before and after intervention from thirty healthy adults in a double-blinded crossover study. Baselines for measured variables were established after 2 weeks of placebo supplementation, followed by daily supplementation with 73.5 mg RRR-alpha-tocopherol acetate or 500 mg ascorbic acid, and placebo, for 6 weeks. A 2 month washout preceded supplement crossover. Mean values showed that plasma lipid standardised alpha-tocopherol increased with ascorbic acid supplementation: from 4.09 (sem 0.51) to 4.53 (sem 0.66) micromol/mmol total cholesterol plus triacylglycerol (P < 0.05), and plasma ascorbic acid increased from 62.8 (sem 14.9) to 101.3 (sem 22. 2) micromol/l (P < 0.005). Supplementation with (RRR)-alpha-tocopherol acetate increased plasma alpha-tocopherol from 26.8 (sem 3.9) to 32.2 (sem 3.8) micromol/l (P < 0.05), and lipid-standardised alpha-tocopherol from 4.12 (sem 0.48) to 5.38 (sem 0.52) micromol/mmol (P < 0.001). Mean plasma ascorbic acid also increased with vitamin E supplementation, from 64.4 (sem 13.3) to 76. 4 (sem 18.4) micromol/l (P < 0.05). Plasma ferric reducing (antioxidant) power and glutathione peroxidase (U/g haemoglobin) increased in both groups, while urate, total cholesterol and triacylglycerol levels decreased (P < 0.05 throughout). Results are supportive of an in vivo interaction between vitamins C and E.     

Vitamin E and prevention of heart disease in high-risk patients

Several observational studies have suggested that high intake of vitamin E may slow the development and progression of atherosclerosis. Some clinical trials also reported beneficial effects of vitamin E supplementation in the secondary prevention of cardiovascular events. However, results of recent large, multicenter clinical trials reported that vitamin E supplementation was not effective in reducing the incidence of cardiovascular events in high-risk patients.     

2,3,7,8-四氯二苯-p-二英对雌性小鼠血浆维生素A、E的影响

目的了解2,3,7,8-四氯二苯-p-二(口恶)英(TCDD)对雌鼠血浆维生素A、E水平的影响.方法将实验昆明种雌性小鼠24只,随机分为染毒高(100 μg/kg)、中(10 μg/kg)、低(1 μg/kg)剂量和空白对照4组,腹腔注射染毒.48 h后对实验小鼠取血,离心后取上层血浆,用无水乙醇沉淀蛋白,加环己烷萃取后,使用荧光分光光度仪在不同波长下测定其荧光值,计算出维生素A、E浓度,进行统计分析.结果对照及染毒剂量低、中、高4组中小鼠血浆维生素A的平均水平差异无显著性(P＞0.05);血浆维生素E的平均水平差异有显著性(P＜0.05),对照组与低剂量组之间维生素E的浓度水平差异无显著性,但与中、高剂量组之间维生素E的浓度水平差异都有显著性(P＜0.05).结论在此实验条件下,尚不能够认为TCDD对雌鼠血浆维生素A的水平有影响,但对维生素E的水平有一定影响.     

2,3,7,8-四氯二苯-p-二(口恶)英对雌性小鼠血浆维生素A、E的影响

目的了解2,3,7,8-四氯二苯-p-二(口恶)英(TCDD)对雌鼠血浆维生素A、E水平的影响.方法将实验昆明种雌性小鼠24只,随机分为染毒高(100 μg/kg)、中(10 μg/kg)、低(1 μg/kg)剂量和空白对照4组,腹腔注射染毒.48 h后对实验小鼠取血,离心后取上层血浆,用无水乙醇沉淀蛋白,加环己烷萃取后,使用荧光分光光度仪在不同波长下测定其荧光值,计算出维生素A、E浓度,进行统计分析.结果对照及染毒剂量低、中、高4组中小鼠血浆维生素A的平均水平差异无显著性(P＞0.05);血浆维生素E的平均水平差异有显著性(P＜0.05),对照组与低剂量组之间维生素E的浓度水平差异无显著性,但与中、高剂量组之间维生素E的浓度水平差异都有显著性(P＜0.05).结论在此实验条件下,尚不能够认为TCDD对雌鼠血浆维生素A的水平有影响,但对维生素E的水平有一定影响.     

Determination of alpha-tocopherol in plasma, platelets and erythrocytes of type I and type II diabetic patients by high-performance liquid chromatography

Vitamin E (alpha-tocopherol) concentrations of plasma, platelets and erythrocytes were determined by HPLC in insulin-dependent (type I) and age-matched non-insulin-dependent (type II) diabetic patients and in two control groups. Plasma alpha-tocopherol levels were significantly increased in diabetic patients compared to control groups. Platelet and erythrocyte alpha-tocopherol levels were not significantly different in type I and type II diabetics as compared to their respective control groups, but differed from one another. Plasma vitamin E concentrations showed a significant correlation with plasma cholesterol and apoprotein B concentrations in different groups. The alpha-tocopherol/cholesterol and alpha-tocopherol/apoprotein B ratios in plasma were higher in diabetic patients, as were triglyceride contents. Platelet vitamin E levels were not significantly correlated with plasma concentrations. These findings suggest that vitamin E activity is altered in diabetic patients but that no diet supplementation seems necessary.     

Vitamin plasma levels in long-term enteral feeding patients

Plasma levels of vitamins were determined in eight patients who were nourished with long-term enteral feeding using commercial formulas. The type and quantity of the formula were individually tailored to the patients' needs. Caloric intake (mean +/- SEM) amounted to 1564 +/- 97 kcal/day. Vitamins intake from the formulas, expressed as percent of Recommended Daily Allowances (RDA), was as follows: pantothenic acid, 222 +/- 44%; vitamin B12, 206 +/- 34%; vitamin C, 376 +/- 51%; thiamine, 207 +/- 34%; niacin, 207 +/- 34%; riboflavin, 207 +/- 34%; pyridoxine, 222 +/- 17%; biotin, 113 +/- 13%; vitamin A, 93 +/- 4%; and folic acid, 104 +/- 14%. Plasma levels of thiamine, riboflavin, pyridoxine, pantothenic acid, folic acid, and vitamin B12 were within normal limits in all patients. Two patients had lower than normal plasma levels of nicotinic acid despite the high intake. Plasma biotin levels were above normal in all patients, with a mean of 931 +/- 140 pg/ml (N: 200-500 pg/ml). Ascorbic acid levels were within or above normal, but no correlation with intake was found. Carotene levels were measured in five patients and found to be below the lower limit of normal, a reflection of lack of intake from the enteral formulas. The plasma vitamin A levels were normal in all patients. It is concluded that feeding with commercial enteral formulas results in normal plasma levels of vitamins in patients maintained on these formulas for over 6 months. The excessive amounts of vitamins in the formulas do not result in elevated plasma levels, except for Biotin.