Vitamin E Deficiency
Receptors, Adrenergic, alpha
Hypoxia-Inducible Factor 1, alpha Subunit
Chromatography, High Pressure Liquid
alpha7 Nicotinic Acetylcholine Receptor
Receptors, Adrenergic, alpha-1
Alkyl and Aryl Transferases
Molecular Sequence Data
Dose-Response Relationship, Drug
Receptors, Adrenergic, alpha-2
Integrin alpha Chains
alpha 1-Antitrypsin Deficiency
Hepatocyte Nuclear Factor 1-alpha
All-rac-alpha-tocopherol acetate is a better vitamin E source than all-rac-alpha-tocopherol succinate for broilers. (1/780)The difference in bioavailabilities of the acetate and succinate esters of all-rac-alpha-tocopherol was investigated in a feeding experiment with broilers. The experiment was initiated with 96 12-d-old male Cobb broilers and lasted for 4 wk. The two sources of vitamin E were fed to eight groups of broilers at four different dietary levels (50, 100, 150 and 200 mg/kg feed, including the naturally occurring alpha-tocopherol). A total collection of droppings for determination of apparent tocopherol absorption were performed at two separate time periods (d 28-34 and d 35-41). There were no differences among the eight experimental groups with respect to animal performance or feed intake. At all dietary levels, the apparent absorption coefficient for all-rac-alpha-tocopherol succinate was significantly lower than that of the acetate ester. The mean (+/- SD) apparent absorption coefficient for all-rac-alpha-tocopherol succinate was 58.0 +/- 5.4 compared with 70. 8 +/- 5.6 for all-rac-alpha-tocopherol acetate. Furthermore, the apparent absorption coefficients for both esters was significantly lower in the first collection period (d 28-34) than in the second collection period (d 35-41). This difference in the apparent absorption coefficient between the succinate and the acetate ester was accompanied by significant differences in alpha-tocopherol concentrations in plasma, breast muscle, liver and adipose tissue of the broilers, which were lower in those fed the succinate ester. Based on a comparison of plasma and tissue responses, the succinate ester was utilized only 69-76% as efficiently as the acetate ester. In vitro studies showed a significantly higher capacity of pancreatic carboxyl ester hydrolase to hydrolyze alpha-tocopherol acetate compared to alpha-tocopherol succinate. This difference in intestinal hydrolysis of the two vitamin E sources may explain the observed differences in biopotency. (+info)
Effects of UV light and tumor promoters on endogenous vitamin E status in mouse skin. (2/780)Recent reports indicate that both orally administered and topically applied alpha-tocopherol (vitamin E, TH) prevent UVB-induced skin carcinogenesis in mice. Because UVB exposure causes the formation of oxidants associated with tumor promotion, epidermal TH status may be an important determinant of susceptibility to photocarcinogenesis. To test this hypothesis, we studied the status of epidermal TH in C3H mice following exposure to single and repeated UVB exposures at doses typical of chronic photocarcinogenesis protocols. Exposure of mice to a single 13 kJ/m(2) dose over 60 min resulted in no acute depletion of epidermal TH and a modest increase in TH within 6-12 h. Daily exposure to 6.5 kJ/m(2) over 30 min resulted in a gradual increase in epidermal TH, which reached 5-fold after five daily exposures. The increase in epidermal TH was accompanied by an increase in the TH oxidation products alpha-tocopherolquinone (TQ) and alpha-tocopherolhydroquinone (THQ). We also studied the effect of the prooxidant chemical tumor promoter benzoyl peroxide and the prooxidant azo initiators azobis(amidinopropane HCl) and azobis(2, 4-dimethylvaleronitrile). Topical application of these prooxidant chemicals acutely oxidized epidermal TH to TQ and THQ. Topical treatments with the phorbol ester tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) increased epidermal TH levels without producing a significant accumulation of TH oxidation products. The results indicate that UVB and tumor promoting chemicals all exert qualitatively different effects on epidermal TH status and that UVB and TPA trigger an adaptive response involving epidermal TH accumulation. (+info)
Vitamin E reduces chromosomal damage and inhibits hepatic tumor formation in a transgenic mouse model. (3/780)We have previously shown that chronic activation of mitogenic signaling induced by over-expression of c-myc and transforming growth factor-alpha (TGFalpha) transgenes in mouse liver induces a state of oxidative stress. We therefore proposed that increased reactive oxygen species (ROS) generation might be responsible for the extensive chromosomal damage and acceleration of hepatocarcinogenesis characteristic for TGFalpha/c-myc mice. In this study, we show that vitamin E (VE), a potent free radical scavenging antioxidant, is able to protect liver tissue against oxidative stress and suppress tumorigenic potential of c-myc oncogene. Dietary supplementation with VE, starting from weaning, decreased ROS generation coincident with a marked inhibition of hepatocyte proliferation while increasing the chromosomal as well as mtDNA stability in the liver. Similarly, dietary VE reduced liver dysplasia and increased viability of hepatocytes. At 6 mo of age, VE treatment decreased the incidence of adenomas by 65% and prevented malignant conversion. These results indicate that ROS generated by over-expression of c-myc and TGFalpha in the liver are the primary carcinogenic agents in this animal model. Furthermore, the data demonstrate that dietary supplementation of VE can effectively inhibit liver cancer development. (+info)
Effects of vitamin E and selenium supplementation on esophageal adenocarcinogenesis in a surgical model with rats. (4/780)Two well-known antioxidative nutrients, vitamin E and selenium, were used in this study to investigate possible inhibitory action against the formation of esophageal adenocarcinoma (EAC) in rats. In this model, carcinogenesis is believed to be driven by oxidative stress. Male Sprague-Dawley rats (8 weeks old) were divided into four groups and received esophagoduodenal anastomosis (EDA) surgery plus iron supplementation (12 mg/kg/week). Vitamin E and selenium were supplemented in the diet in the forms of alpha-tocopheryl acetate (750 IU/kg) and sodium selenate (1.7 mg Se/kg), which were 10 times the regular amounts in the basic AIN93M diet. At 40 weeks after surgery, all the EDA groups had lower body weights than the non-operated control group. Iron nutrition (hemoglobin, total serum iron and transferrin saturation) was normal as a result of iron supplementation after EDA. Vitamin E supplementation maintained the normal plasma level of alpha-tocopherol in EDA rats, but not those of gamma-tocopherol and retinol. Selenium supplementation increased the serum and liver selenium contents of the EDA rats. Histopathological analysis showed that selenium supplementation increased the incidence of EAC and the tumor volume. The selenium level in the tumor is higher than that in the duodenum of the same animal. Vitamin E supplementation, however, inhibited carcinogenesis, especially in the selenium-supplemented group. We believe that vitamin E exerts its effect through its antioxidative properties, and a high dose of inorganic selenium may promote carcinogenesis by enhancing oxidative stress. (+info)
Oxidation of plasma proteins is not increased after supplementation with eicosapentaenoic and docosahexaenoic acids. (5/780)BACKGROUND: It is generally thought that as the intake of dietary polyunsaturated fatty acids increases, so should that of alpha-tocopherol, to protect the polyunsaturated fatty acids from increased in vivo peroxidation. However, there are little quantitative data about the concentration of alpha-tocopherol that is necessary when eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are consumed. OBJECTIVE: The purpose of this study was to measure changes produced in 2 indexes of lipid oxidation after supplementation with EPA and DHA from fish oil and 3 doses of RRR-alpha-tocopheryl acetate in postmenopausal women. DESIGN: Daily supplements of fish oil providing 2.5 g EPA and 1.8 g DHA and 0, 100, 200, or 400 mg alpha-tocopheryl acetate were given to 46 postmenopausal women in a 4-treatment, 4-period crossover design. RESULTS: The supplements increased plasma concentrations of EPA, DHA, and alpha-tocopherol. The fish-oil supplement increased the plasma concentration of thiobarbituric acid-reactive substances (TBARS) (P: = 0.0001) but not that of oxidatively modified protein, as indicated by the carbonyl content. The alpha-tocopheryl acetate and fish-oil supplements had no significant effect on plasma concentrations of TBARS or oxidized protein. CONCLUSIONS: Although these data show a small but statistically significant increase in oxidative stress on the basis of plasma TBARS concentrations after the consumption of EPA and DHA, the clinical relevance of this change is questionable. In addition, as supplements of alpha-tocopheryl acetate were added to the diet, neither the plasma TBARS concentration nor the protein oxidation changed. Consequently, the results of this study indicate that there is no basis for vitamin E supplementation after consumption of EPA and DHA. (+info)
Altered susceptibility to ischemia-reperfusion injury in isolated-perfused hearts of short-term diabetic rats associated with changes in non-enzymatic antioxidants. (6/780)The effects of short-term (2-week) diabetes on myocardial ischemia-reperfusion (I-R) injury and associated changes in myocardial non-enzymatic antioxidant level were examined. Isolated-perfused hearts prepared from control and diabetic rats were subjected to increasing periods of ischemia and reperfusion, and myocardial I-R injury was assessed by measuring the extent of lactate dehydrogenase (LDH) leakage and contractile force recovery. While a brief period (20 min) of post-ischemic reperfusion caused a smaller extent of LDH leakage, the prolonged period (40 min) of reperfusion produced a greater degree of I-R injury in diabetic hearts, as indicated by the impaired recovery of contractile force. The apparent protection against I-R injury in diabetic hearts during the early phase of post-ischemic reperfusion was associated with increases in myocardial reduced glutathione/ascorbic acid and a-tocopherol levels, with the effect on a-tocopherol being most prominent. Insulin treatment could reverse the diabetes-associated changes in susceptibility to myocardial I-R injury and antioxidant response. The ensemble of results indicates that the myocardium isolated from short-term diabetic rat can produce a beneficial antioxidant response to I-R challenge, which may, in turn, be attributable to the decreased susceptibility to I-R injury observable during the early phase of reperfusion. (+info)
Differential effects among thiazolidinediones on the transcription of thromboxane receptor and angiotensin II type 1 receptor genes. (7/780)Peroxisome proliferator-activated receptor (PPAR)-gamma ligands thiazolidinediones (TZDs) have recently been reported to be anti-hypertensive and anti-atherosclerotic. We have previously shown that one of the TZDs troglitazone significantly suppressed the transcription of both thromboxane receptor (TXR) and angiotensin II type 1 receptor (AT1R) genes in vascular smooth muscle cells (VSMCs) by activating PPAR-gamma. In the present study, we compared the effects of troglitazone and other TZDs on the transcription of these genes. TXR and AT1R mRNAs in rat VSMCs were determined by semi-quantitative RT-PCR. Luciferase chimeric constructs containing either the 989-bp rat TXR gene promoter or the 1,969-bp rat AT1R gene promoter were transiently transfected into VSMCs. The cells were incubated with troglitazone, RS-1455 (a derivative of troglitazone which does not contain the hindered phenol resembling alpha-tocopherol), pioglitazone, or rosiglitazone for 12 h before harvesting. mRNA expression levels of TXR and AT1R were significantly decreased by troglitazone in contrast to rosiglitazone. TXR gene and AT1R gene transcription was significantly suppressed by troglitazone in a dose-dependent manner, while RS-1455 was less potent. Pioglitazone and rosiglitazone weakly suppressed the transcription of both genes in a manner almost similar to RS-1455. We have shown that troglitazone suppresses transcription of both the TXR and AT1R genes more potently than other TZDs. The structure of troglitazone and RS-1455 is identical except the hindered phenol, which is recently recognized to function as an antioxidant. Moreover, we have shown that the potency for activating PPAR-gamma is almost identical between troglitazone and RS-1455. We therefore speculate that the strong transcriptional suppression of the TXR and AT1R genes by troglitazone may be mediated in part by its antioxidant effect. (+info)
Evidence of a lysosomal pathway for apoptosis induced by the synthetic retinoid CD437 in human leukemia HL-60 cells. (8/780)The novel synthetic retinoid 6-[3-(1-adamantyl)-4-hydroxyphenyl]-2-naphtalene carboxylic acid (AHPN/CD437) has been proven to be a potent inducer of apoptosis in a variety of tumor cell types. However, the mechanism of its action remains to be elucidated. Recent studies suggest that the lysosomal protease cathepsin D, when released from lysosomes to the cytosol, can initiate apoptosis. In this study, we examined whether cathepsin D and free radicals are involved in the CD437-induced apoptosis. Exposure of human leukemia HL-60 cells to CD437 resulted in rapid induction of apoptosis as indicated by caspase activation, phosphatidylserine exposure, mitochondrial alterations and morphological changes. Addition of the antioxidants alpha-tocopherol acetate effectively inhibited the CD437-induced apoptosis. Measurement of the intracellular free radicals indicated a rise in oxidative stress in CD437-treated cells, which could be attenuated by alpha-tocopherol acetate. Interestingly, pretreatment of cells with the cathepsin D inhibitor pepstatin A blocked the CD437-induced free radical formation and apoptotic effects, suggesting the involvement of cathepsin D. However, Western blotting revealed no difference in cellular quantity of any forms of cathepsin D between control cells and CD437-treated cells, whereas immunofluorescence analysis of the intracellular distribution of cathepsin D showed release of the enzyme from lysosomes to the cytosol. Labeling of lysosomes with lysosomotropic probes confirmed that CD437 could induce lysosomal leakage. The CD437-induced relocation of cathepsin D could not be prevented by alpha-tocopherol acetate, suggesting that the lysosomal leakage precedes free radical formation. Furthermore, a retinoic acid nuclear receptor (RAR) antagonist failed to block these effects of CD437, suggesting that the action of CD437 is RAR-independent. Taken together, these data suggest a novel lysosomal pathway for CD437-induced apoptosis, in which lysosomes are the primary target and cathepsin D and free radicals act as death mediators. (+info)
Causes and risk factors:
1. Poor diet: A diet that is lacking in vitamin E can lead to a deficiency. Foods that are low in vitamin E include processed foods, sugary drinks, and refined carbohydrates.
2. Malabsorption: Certain medical conditions, such as celiac disease, can lead to malabsorption of nutrients, including vitamin E.
3. Pregnancy and lactation: Pregnant and breastfeeding women have a higher requirement for vitamin E, and a deficiency can occur if they do not consume enough.
4. Chronic diseases: Certain chronic diseases, such as Crohn's disease, can increase the risk of vitamin E deficiency.
5. Genetic disorders: Some genetic disorders, such as abetalipoproteinemia, can lead to a deficiency in vitamin E.
1. Fatigue and weakness
2. Muscle weakness
3. Loss of appetite
4. Nerve damage
5. Poor wound healing
6. Increased risk of infections
7. Decreased immune function
9. Skin problems, such as acne and dermatitis
10. Eye problems, such as cataracts and retinal degeneration.
Vitamin E deficiency is diagnosed based on a combination of clinical symptoms, medical history, and laboratory tests, including:
1. Blood tests: Measurement of serum vitamin E levels can help determine if there is a deficiency.
2. Dietary assessment: A dietitian or nutritionist may evaluate the patient's diet to identify any potential sources of vitamin E deficiency.
3. Physical examination: A healthcare provider may perform a physical examination to look for signs of vitamin E deficiency, such as skin problems or muscle weakness.
Treatment and Prevention:
1. Dietary changes: Increasing the intake of foods rich in vitamin E, such as nuts, seeds, and vegetable oils, can help prevent and treat vitamin E deficiency.
2. Supplementation: Vitamin E supplements can be used to treat and prevent vitamin E deficiency. The recommended daily intake of vitamin E varies by age and sex, but generally ranges from 5-15 mg/day.
3. Addressing underlying causes: If the deficiency is caused by an underlying medical condition, such as Crohn's disease or abetalipoproteinemia, treating the condition can help resolve the deficiency.
4. Supportive care: Patients with severe vitamin E deficiency may require supportive care, such as intravenous nutrition or respiratory support, to manage their symptoms.
Prognosis and Complications:
The prognosis for vitamin E deficiency is generally good if the underlying cause is identified and treated promptly. However, untreated severe vitamin E deficiency can lead to complications such as:
1. Skin problems: Vitamin E deficiency can cause skin problems, such as acne, dermatitis, and wound healing difficulties.
2. Muscle weakness: Vitamin E is important for muscle function, and deficiency can lead to muscle weakness and wasting.
3. Neurological problems: Vitamin E deficiency can cause neurological problems, such as peripheral neuropathy and seizures.
4. Increased risk of infections: Vitamin E is important for immune function, and deficiency can increase the risk of infections.
5. Reproductive problems: Vitamin E deficiency can cause reproductive problems, such as infertility and miscarriage.
The main symptom of abetalipoproteinemia is a complete absence of chylomicrons, which are small particles that carry triglycerides and other lipids in the bloodstream. This results in low levels of triglycerides and other lipids in the blood, as well as an impaired ability to absorb vitamins and other nutrients from food.
Abetalipoproteinemia is usually diagnosed during infancy or early childhood, when symptoms such as fatigue, weakness, and poor growth become apparent. The disorder can be identified through blood tests that measure lipid levels and genetic analysis.
Treatment for abetalipoproteinemia typically involves a combination of dietary changes and supplements to ensure adequate nutrition and prevent complications such as malnutrition and liver disease. In some cases, medications may be prescribed to lower triglyceride levels or improve the absorption of fat-soluble vitamins.
The prognosis for abetalipoproteinemia varies depending on the severity of the disorder and the presence of any complications. In general, early diagnosis and appropriate treatment can help to manage symptoms and prevent long-term health problems. However, some individuals with abetalipoproteinemia may experience ongoing health issues throughout their lives.
People with AATD have low levels of functional AAT in their blood, which can lead to premature lung disease and liver disease. The most common form of AATD is caused by the Pi*Z phenotype, which results from a missense mutation in the SERPINA1 gene. This mutation leads to misfolding and accumulation of AAT in the liver, where it is normally broken down and secreted into the bloodstream.
The most common symptoms of AATD are:
* Chronic obstructive pulmonary disease (COPD)
* Lung fibrosis
* Liver cirrhosis
The diagnosis of AATD is based on a combination of clinical symptoms, laboratory tests, and genetic analysis. Treatment for AATD typically involves managing the underlying symptoms and preventing complications. For example, individuals with COPD may receive bronchodilators and corticosteroids to help improve lung function and reduce inflammation. Liver disease may be treated with medications to slow the progression of cirrhosis or with liver transplantation in severe cases.
The goal of genetic counseling for AATD is to provide information about the risk of transmitting the disorder to offspring and to discuss options for prenatal testing and family planning. Prenatal testing can be performed on a fetus by analyzing a sample of cells from the placenta or amniotic fluid. Carrier testing can also be performed in individuals who have a family history of AATD.
The prognosis for AATD varies depending on the severity of the mutation and the specific symptoms present. With appropriate management, many individuals with AATD can lead active and productive lives. However, the disorder can be severe and life-threatening in some cases, especially if left untreated or if there is a delay in diagnosis.
Currently, there is no cure for AATD, and treatment is focused on managing symptoms and preventing complications. However, research into the genetics of AATD is ongoing, and new developments in gene therapy and other areas may provide hope for improved treatments and outcomes in the future.
Alpha-tocopherol transfer protein
Vitamin E deficiency
NAD(P)H dehydrogenase (quinone 1)
William H. Harris (orthopaedic surgeon)
List of antioxidants in food
Wheat germ oil
Herbert McLean Evans
Complications of diabetes
James Edward Cottrell
List of food additives
Zinc transporter ZIP12
List of MeSH codes (D03)
Maret G. Traber
Vitamin E (Alpha-Tocopherol): MedlinePlus Drug Information
Grant Abstract: Alpha-Tocopherol Modulation of Xenobiotic Metabolism
MedlinePlus - Search Results for: ".Alpha.-Tocopherol" OR Cholecalciferol OR "Omega-3" Fatty Acids
DailyMed - BAL-CARE DHA ESSENTIAL- beta carotene, ascorbic acid, cholecalciferol, .alpha.-tocopherol acetate, dl-, thiamine...
Effect of in vitro vitamin E (alpha-tocopherol) su... - BV FAPESP
"Foliar applications of alpha-tocopherol improves the composition of fr" by MUHAMMAD SADIQ, NUDRAT AISHA AKRAM et al.
The effect of long-term beta-carotene and vitamin A administration on serum concentrations of alpha-tocopherol. | Cancer...
Serum Metabolomic Profiling of All-Cause Mortality: A Prospective Analysis in the Alpha-Tocopherol, Beta-Carotene Cancer...
NDC Active Ingredient .alpha.-tocopherol Acetate, Dl
NHANES 2001-2002: Dietary Interview - Individual Foods Data Documentation, Codebook, and Frequencies
Possible adverse effect of high delta-alpha-tocopherol intake on hepatic iron overload: enhanced production of vitamin C and...
DC Practice Blog: Supplemental alpha-tocopherol: A Perspective on Approaching an Evidence-based Project
DailyMed - NOVADHA BABY DHA- omega-3 fatty acids, cholecalciferol, and .alpha.-tocopherol liquid
Tocotrienols, but not Alpha-Tocopherol, Necessary for Bone Calcification in Growing Female Rats | Osteoporosis-Studies
Solgar Vitamin E 268 MG (400 IU) Mixed (d-Alpha Tocopherol & Mixed Tocopherols), - namastewest.com
All news articles for September 2022
Preventing Chronic Disease | Nutritional Assessment of Free Meal Programs in San Francisco - CDC
Spontaneous disappearance of Helicobacter pylori antibodies in patients with advanced atrophic corpus gastritis
Infant formula, MEAD JOHNSON, PREGESTIMIL, with iron, powder, not reconstituted Nutrition
The effect of alpha-tocopherol, gamma-tocopherol and beta-carotene on oxidant-induced injury of proliferating human intestinal...
"HPLC Analysis of Blood and Liver Tissue for Free Alpha-tocopherol" by John C. Meadows, Gaylin L. Nickell et al.
Alpha-tocopherol quinine ameliorates spatial memory deficits by reducing beta-amyloid oligomers, neuroinflammation and...
DailyMed - RESTful Web Services - /uniis
DailyMed - ANTI-BACTERIAL HAND SANITIZER WITH GOAT MILK CREAMY COCONUT AND OATS- alcohol liquid
SkinCeuticals Antioxidant Lip Repair (0.34 fl. oz.) - Dermstore
Kerassentials Reviews - Do NOT Buy Before Reading this!
NIH Guide: LINKING ENVIRONMENTAL AGENTS, OXIDATIVE DAMAGE AND DISEASE
Cardiovascular Archives - The James Lind Library The James Lind Library
Antioxidants | The Nutrition Source | Harvard T.H. Chan School of Public Health
- The effect of alpha-tocopherol, gamma-tocopherol and beta-carotene on oxidant-induced injury of proliferating human intestinal CaCo-2 cells. (dundee.ac.uk)
- The group that most stands out is that of the tocopherols that has 4 members: alpha tocopherol, beta tocopherol, gamma tocopherol and delta tocopherol, the first being the best known and which seems to be more active. (botanical-online.com)
- tocopherol Acetate. (ndclist.com)
- The effect of long-term beta-carotene and vitamin A administration on serum concentrations of alpha-tocopherol. (aacrjournals.org)
- A short-term study recently suggested that two of these nutrients, beta-carotene and alpha-tocopherol, may have an adverse interaction, with beta-carotene supplementation leading to markedly decreased serum concentrations of alpha-tocopherol. (aacrjournals.org)
- We have analyzed the effect of beta-carotene supplementation on serum concentrations of alpha-tocopherol in 2319 participants enrolled in the Carotene and Retinol Efficacy Trial who have taken beta-carotene and vitamin A for up to 6 years. (aacrjournals.org)
- Using standard high pressure liquid chromatography techniques, with attention to quality control, these samples were analyzed for beta-carotene and alpha-tocopherol. (aacrjournals.org)
- After up to 6 years of supplementation with beta-carotene (30 mg/day) and vitamin A (25,000 international units/day) we found a small but statistically significant increase in the serum concentration of alpha-tocopherol in participants taking the active agents. (aacrjournals.org)
- We conclude that long-term supplementation with the combination of beta-carotene and vitamin A does not decrease serum concentrations of alpha-tocopherol. (aacrjournals.org)
- The trial, dubbed the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study (ATBC Study), was carried out by the U.S. National Cancer Institute and the National Public Health Institute of Finland. (medicinenet.com)
- The aim of this study was to determine if high doses of delta - alpha-tocopherol supplementation in iron overload would ameliorate the oxidative stress . (bvsalud.org)
- Equivalent evidence reporting both risk and benefit associated with 22.5 to 800 IU/d for 1.4 to 9.4 years, and increased risk of mortality observed with α-tocopherol supplementation >150 IU/day. (dietitians.ca)
- Alpha-tocopherol (α-Toc), so-called vitamin E, is a low molecular weight lipophilic antioxidant that generally protects plants from stress-induced cellular oxidation. (tubitak.gov.tr)
- Possible adverse effect of high delta-alpha-tocopherol intake on hepatic iron overload: enhanced production of vitamin C and the genotoxin, 8-hydroxy-2'- deoxyguanosine. (bvsalud.org)
- A positive correlation existed between vitamin C and 8-OHdG, suggesting possible delta - alpha-tocopherol toxicity . (bvsalud.org)
- In fact, the name of vitamin E, tocopherol , derives from the Greek toco (= birth) an d phereon (= carry out). (botanical-online.com)
- The necessary daily doses of this vitamin (RDA) for adults are 11-15 mg of vitamin E (alpha-tocopherol) (or its equivalent to 22.5 IU) daily. (botanical-online.com)
- In the Finnish study, vitamin E was tested in the form of alpha tocopherol. (medicinenet.com)
- We use a soy-free, mixed tocopherols source that matches the composition of Vitamin E found in foods. (ritual.com)
- Ascorbic Acid, Cholecalciferol, .alpha. (ndclist.com)
- Taking the Dietary Reference Intake (DRI) course in the past proved helpful as I was able to easily retrieve required information on α-tocopherol. (dietitians.ca)
- Foliar applications of alpha-tocopherol improves the composition of fr" by MUHAMMAD SADIQ, NUDRAT AISHA AKRAM et al. (tubitak.gov.tr)
- Oxidative liver damage, as determined by serum AST and ALT levels, was not attenuated by alpha-tocopherol . (bvsalud.org)
- My objectives were to weigh the potential risks versus benefits of supplemental α-tocopherol in primary and secondary prevention of cardiovascular disease (CVD) to determine specific practice considerations for supplemental α-tocopherol including the type of supplement, dose and duration. (dietitians.ca)
- Thus, not enough evidence to support recommending supplemental α-tocopherol for primary prevention of CVD. (dietitians.ca)
- COMT and Alpha-Tocopherol Effects in Cancer Prevention: Gene-Supplement Interactions in Two Randomized Clinical Trials. (cdc.gov)
- The natural d form of alpha-tocopherol is more active than its synthetic dl-alpha-tocopherol racemic mixture. (bvsalud.org)
- Comparison of effects of alpha-tocopherol and matching placebo on chest pain in patients with heart disease. (jameslindlibrary.org)
- Four groups of 20 male Wistar albino rats were studied group 1 (control) was fed normal diet , group 2 (Fe) 0.75% Ferrocene iron , group 3 (FV gp) 0.75% Ferrocene/ delta - alpha-tocopherol (10x RDA), group 4 (V gp) normal diet / delta - alpha-tocopherol . (bvsalud.org)
- HPLC Analysis of Blood and Liver Tissue for Free Alpha-tocopherol" by John C. Meadows, Gaylin L. Nickell et al. (mst.edu)
- HPLC Analysis of Blood and Liver Tissue for Free Alpha-tocopherol," Trace Substances in Environmental Health: Proceedings of University of Missouri's Annual Conference , University of Missouri--Columbia, Jan 1982. (mst.edu)
- Group III - Calen™ with chlorhexidine at 0.4% with the addition of 20% (weight) of alhatocopherol compound and Group IV - Calen™ with chlorhexidine at 0.4% with the addition of 10% (weight) alphatocopherol. (bvsalud.org)
- The aim of this study was to evaluate the pH of calcium hydroxide (Calen TM ) when associated or not with chlorhexidine 0.4%, and when associated with chlorhexidine with the addition of 20% or 10% of alphatocopherol (Aché TM ), assessed in several periods of time. (bvsalud.org)
- The mean (SD) serum concentration of 1.77 (0.50) μmol L(-1) for retinol and 30.81 (6.46) μmol L(-1) for α-tocopherol indicates an adequate biochemical status. (nih.gov)
- Serum haemoglobin, alpha-tocopherol, retinol and magnesium levels were significantly decreased in stunted children compared with the controls. (who.int)
- Define how a-tocopherol modulates hepatic cytochrome P450 enzymes (CYPs) involved in the metabolism of therapeutic drugs. (nih.gov)
- Determine the ability of a-tocopherol to modulate hepatic transport proteins known to be involved in the biliary excretion of a-tocopherol and/or therapeutic drugs. (nih.gov)
- It is therefore suggested that alpha-TTP may play a major role in supplying alpha-tocopherol to the foetus prior to delivery and is likely involved in maintaining adequate alpha-tocopherol levels in the foetus. (nih.gov)
- The objective of this research is to define hepatic pathways for a-tocopherol catabolism and its disposition, as well as to specifically address a-tocopherol interactions with pharmacologic agents and their metabolizing systems. (nih.gov)
- Expression of alpha-TTP has not only been described in animal model liver, but also in diverse other tissues such as rat brain or pregnant mouse uterus, the latter finding stressing the importance of alpha-TTP for embryogenesis and foetal development. (nih.gov)
- In this study, we report the identification of alpha-TTP in human liver by anti-human alpha-TTP monoclonal antibodies made in rat and the cellular localization of alpha-TTP in term human placenta. (nih.gov)
- Search Results for: ".ALPHA. (nih.gov)
- The supplemented group was administered with a retinyl palmitate capsule and, 24 h after the first collection, the second colostrum sample was obtained in the two groups for analysis of α-tocopherol. (nih.gov)
- Alpha-tocopherol transfer protein is specifically localized at the implantation site of pregnant mouse uterus. (nih.gov)