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Tocopherols (or TCP) are a class of chemical compounds of which many have vitamin E activity. It is a series of organic compounds consisting of various methylated phenols. Because the vitamin activity was first identified in 1936 from a dietary fertility factor in rats, it was given the name "tocopherol" from the Greek words "τόκος" [birth], and "φέρειν", [to bear or carry] meaning in sum "to carry a pregnancy," with the ending "-ol" signifying its status as a chemical alcohol.
alpha-Tocopherol is the main source found in supplements and in the European diet, where the main dietary sources are olive and sunflower oils, while gamma-tocopherol is the most common form in the American diet due to a higher intake of soybean and corn oil.
Tocotrienols, which are related compounds, also have vitamin E activity. All of these various derivatives with vitamin activity may correctly be referred to as "vitamin E". Tocopherols and tocotrienols are fat-soluble antioxidants but also seem to have many other functions in the body.
Vitamin E exists in eight different forms, four tocopherols and four tocotrienols. All feature a chromanol ring, with a hydroxyl group that can donate a hydrogen atom to reduce free radicals and a hydrophobic side chain which allows for penetration into biological membranes.
The tocotrienols have the same methyl structure at the ring and the same Greek letter-methyl-notation, but differ from the analogous tocopherols by the presence of three double bonds in the hydrophobic side chain. The unsaturation of the tails gives tocotrienols only a single stereoisomeric carbon (and thus two possible isomers per structural formula, one of which occurs naturally), whereas tocopherols have 3 centers (and eight possible stereoisomers per structural formula, again, only one of which occurs naturally).
Each form has a different biological activity. In general, the unnatural l-isomers of tocotrienols lack almost all vitamin activity, and half of the possible 8 isomers of the tocopherols (those with 2S chirality at the ring-tail junction) also lack vitamin activity. Of the stereoisomers which retain activity, increasing methylation, especially full methylation to the alpha-form, increases vitamin activity. In tocopherols, this is due to the preference of the tocophrol binding protein for the alpha-tocopherol form of the vitamin.
As a food additive, tocopherol is labeled with these E numbers:E306 (tocopherol), E307 (α-tocopherol/alpha-tocopherol), E308 (γ-tocopherol/gamma-tocopherol), and E309 (δ-tocopherol/delta-tocopherol). These are all approved in the USA, EU and Australia and New Zealand for use as antioxidants.
Alpha-tocopherol is the form of vitamin E that is preferentially absorbed and accumulated in humans. The measurement of "vitamin E" activity in international units (IU) was based on fertility enhancement by the prevention of miscarriages in pregnant rats relative to alpha-tocopherol.
Although the mono-methylated form ddd-gamma-tocopherol is the most prevalent form of vitamin E in oils, there is evidence that rats can methylate this form to the preferred alpha-tocopherol, since several generations of rats retained alpha-tocopherol tissue levels, even when fed only gamma-tocopherol through their lives.
There are three stereocenters in alpha-tocopherol, so this is a chiral molecule. The eight stereoisomers of alpha-tocopherol differ in the arrangement of groups around these stereocenters. In the image of RRR-alpha-tocopherol below, all three stereocenters are in the R form. However, if the middle of the three stereocenters were changed (so the hydrogen was now pointing down and the methyl group pointing up), this would become the structure of RSR-alpha-tocopherol. These stereoisomers can also be named in an alternative older nomenclature, where the stereocenters are either in the d or l form.
1 IU of tocopherol is defined as ⅔ milligrams of RRR-alpha-tocopherol (formerly named d-alpha-tocopherol or sometimes ddd-alpha-tocopherol). 1 IU is also defined as 1 milligram of an equal mix of the eight stereoisomers, which is a racemic mixture called all-rac-alpha-tocopheryl acetate. This mix of stereoisomers is often called dl-alpha-tocopheryl acetate, even though it is more precisely dl,dl,dl-alpha-tocopheryl acetate). However, 1 IU of this racemic mixture is not now considered equivalent to 1 IU of natural (RRR) α-tocopherol, and the Institute of Medicine and the USDA now convert IU's of the racemic mixture to milligrams of equivalent RRR using 1 IU racemic mixture = 0.45 "milligrams α-tocopherol".
Tocotrienols, although less commonly known, also belong to the vitamin E family. Tocotrienols have four natural 2' d-isomers (they have a stereoisomeric carbon only at the 2' ring-tail position). The four tocotrienols (in order of decreasing methylation: d-alpha, d-beta, d-gamma, and d-delta-tocotrienol) have structures corresponding to the four tocopherols, except with an unsaturated bond in each of the three isoprene units that form the hydrocarbon tail, whereas tocopherols have a saturated phytyl tail (the phytyl tail of tocopherols gives the possibility for 2 more stereoisomeric sites in these molecules that tocotrienols do not have). Tocotrienol has been subject to fewer clinical studies and seen less research as compared to tocopherol. However, there is growing interest in the health effects of these compounds.
During feeding experiments with rats Herbert McLean Evans concluded in 1922 that besides vitamins B and C, an unknown vitamin existed. Although every other nutrition was present, the rats were not fertile. This condition could be changed by additional feeding with wheat germ. It took several years until 1936 when the substance was isolated from wheat germ and the formula C29H50O2 was determined. Evans also found that the compound reacted like an alcohol and concluded that one of the oxygen atoms was part of an OH (hydroxyl) group. As noted in the introduction, the vitamin was given its name by Evans from Greek words meaning "to bear young" with the addition of the -ol as an alcohol. The structure was determined shortly thereafter in 1938.
Recommended amounts 
The U.S. Dietary Reference Intake (DRI) Recommended Daily Amount (RDA) for a 25-year-old male for Vitamin E is 15 mg/day. The DRI for vitamin E is based on the alpha-tocopherol form because it is the most active form as originally tested. Results of two national surveys, the National Health and Nutrition Examination Survey (NHANES III 1988-91) and the Continuing Survey of Food Intakes of Individuals (1994 CSFII) indicated that the dietary intakes of most Americans do not provide the recommended amounts of vitamin E. However, a 2000 Institute of Medicine (IOM) report on vitamin E states that intake estimates of vitamin E may be low because energy and fat intake is often underreported in national surveys and because the kind and amount of fat added during cooking is often not known. The IOM states that most North American adults get enough vitamin E from their normal diets to meet current recommendations. However, they do caution individuals who consume low fat diets because vegetable oils are such a good dietary source of vitamin E. "Low-fat diets can substantially decrease vitamin E intakes if food choices are not carefully made to enhance alpha-tocopherol intakes". Vitamin E supplements are absorbed best when taken with meals.
Because vitamin E can act as an anticoagulant and may increase the risk of bleeding problems, many agencies have set an upper tolerable intake level (UL) for vitamin E at 1,000 mg (1,500 IU) per day.
alpha-Tocopherol Equivalents 
For dietary purposes, vitamin E activity of Vitamin E Isomers is expressed as a-tocopherol equivalents (a-TEs). One a-TE is defined by the biological activity of 1 mg (natural) d-alpha-Tocopherol in the resorption-gestation test. According to listings by FAO and others beta-tocopherol should be multiplied by 0.5, gamma-tocopherol by 0.1, and a-tocotrienol by 0.3. The IU is converted to aTE by multiplying it with 0.67.
In general, food sources with the highest concentrations of vitamin E are vegetable oils, followed by nuts and seeds including whole grains. Adjusting for typical portion sizes, however, for many people in the United States the most important sources of vitamin E include commercial breakfast cereal and tomato sauce. Although originally extracted from wheat germ oil, most natural vitamin E supplements are now derived from vegetable oils, usually soybean oil.
- Wheat germ oil (215.4 mg)
- Sunflower oil (55.8 mg)
- Almond oil (39.2 mg)
- Sunflower seed (35.17 mg)
- Almond (26.2 mg)
- Hazelnut (26.0 mg)
- Walnut oil (20.0 mg)
- Peanut oil (17.2 mg)
- Olive oil (12.0 mg)
- Poppyseed oil (11.4 mg)
- Peanut (9.0 mg)
- Pollard (2.4 mg)
- Maize (2.0 mg)
- Poppy seed (1.8 mg)
- Asparagus (1.5 mg)
- Oats (1.5 mg)
- Chestnut (1.2 mg)
- Coconut (1.0 mg)
- Tomatoes (0.9 mg)
- Walnut (0.7 mg)
- Carrots (0.6 mg)
- Goat's milk (0.1 mg)
A 100 g serving of certain fortified breakfast cereals may contain 24 mg (or more) vitamin E.
Vitamin E deficiency causes neurological problems due to poor nerve conduction. These include neuromuscular problems such as spinocerebellar ataxia and myopathies. Deficiency can also cause anemia, due to oxidative damage to red blood cells.
Commercial vitamin E supplements can be classified into several distinct categories:
- Fully synthetic vitamin E, "dl-alpha-tocopherol", the most inexpensive, most commonly sold supplement form usually as the acetate ester;
- Semi-synthetic "natural source" vitamin E esters, the "natural source" forms used in tablets and multiple vitamins. These are highly fractionated d-alpha tocopherol or its esters, often made by synthetic methylation of gamma and beta d,d,d tocopherol vitamers extracted from plant oils.
- Less fractionated "natural mixed tocopherols" and high d-gamma-tocopherol fraction supplements
Synthetic all-racemic 
Synthetic vitamin E derived from petroleum products is manufactured as all-racemic alpha tocopheryl acetate with a mixture of eight stereoisomers. In this mixture, one alpha-tocopherol molecule in eight molecules are in the form of RRR-alpha-tocopherol (12.5% of the total).
The 8-isomer all-rac vitamin E is always marked on labels simply as dl-tocopherol or dl-tocopheryl acetate, even though it is (if fully written out) actually dl,dl,dl-tocopherol. The present largest manufacturers of this type are DSM and BASF.
(An earlier semisynthetic vitamin E actually contained 50% d,d,d-alpha tocopherol moiety and 50% l,d,d-alpha-tocopherol moiety, as synthesized by an earlier process which started with a plant sterol intermediate with the correct chirality in the tail, and thus resulted in a racemic mixture at only one chiral center. This form, known as 2-ambo tocopherol, is no longer made.)
Natural alpha-tocopherol is the RRR-alpha (or ddd-alpha) form. The synthetic dl,dl,dl-alpha ("dl-alpha") form is not as active as the natural ddd-alpha ("d-alpha") tocopherol form. This is mainly due to reduced vitamin activity of the 4 possible stereoisomers which are represented by the l or S enantiomer at the first stereocenter (an S or l configuration between the chromanol ring and the tail, i.e., the SRR, SRS, SSR, and SSS stereoisomers). The 3 unnatural "2R" stereoisomers with natural R configuration at this 2' stereocenter, but S at one of the other centers in the tail (i.e., RSR, RRS, RSS), appear to retain substantial RRR vitamin activity, because they are recognized by the alpha-tocopherol transport protein, and thus maintained in the plasma, where the other four stereoisomers (SRR, SRS, SSR, and SSS) are not. Thus, the synthetic all-rac-α-tocopherol in theory would have approximately half the vitamin activity of RRR-alpha-tocopherol in humans. Experimentally, the ratio of activities of the 8 stereoisomer racemic mixture to the natural vitamin, is 1 to 1.36 in the rat pregnancy model (suggesting a measured activity ratio of 1/1.36 = 74% of natural, for the 8-isomer racemic mix).
Although it is clear that mixtures of stereoisomers are not as active as the natural RRR-alpha-tocopherol form, in the ratios discussed above, specific information on any side effects of the seven synthetic vitamin E stereoisomers is not readily available.
Manufacturers also commonly convert the phenol form of the vitamins (with a free hydroxyl group) to esters, using acetic or succinic acid. These tocopheryl esters are more stable and are easy to use in vitamin supplements. Alpha tocopheryl esters are de-esterified in the gut and then absorbed as the free tocopherol. Tocopheryl nicotinate and tocopheryl linolate esters are also used in cosmetics and some pharmaceuticals.
An initial study in humans saw large variability between different people's absorption of all these forms of vitamin E, with no statistically significant differences seen between tocopheryl esters and the free tocopherol. Later studies saw no difference between the rate of absorption of these forms of vitamin E and found that tocopheryl esters and free tocopherol had the same bioavailability. The esterase activity responsible for releasing the free tocopherol may be reduced in children with cystic fibrosis.
Mixed tocopherols 
"Mixed tocopherols" in the US contain at least 20% w/w other natural R, R,R- tocopherols, i.e. R, R,R-alpha-tocopherol content plus at least 25% R, R,R-beta-, R, R,R-gamma-, R, R,R-delta-tocopherols.
Some brands may contain 200% w/w or more of the other tocopherols and measurable tocotrienols. Some mixed tocopherols with higher gamma-tocopherol content are marketed as "High Gamma-Tocopherol." The label should report each component in milligrams, except R, R,R-alpha-tocopherol may still be reported in IU. Mixed tocopherols can also be found in other nutritional supplements.
Age-related macular degeneration (AMD) is the leading cause of visual impairment and blindness in the United States and the developed world among people 65 years and older. It has been shown that vitamin E alone does not attenuate the development or progression of AMD.
Alternative medicine 
Excessive intake of vitamin E may increase risk of bleeding, and a 2005 meta-analysis found that high-dosage vitamin E supplements may increase all-cause mortality. A Cochrane review of 2007 also found an increase in mortality, of 4% (Relative Risk 1.04, 95% confidence interval 1.01-1.07).
Proponents of megavitamin, orthomolecular, and naturally based therapies have for the last two thirds of a century advocated and used the natural tocopherols, often mixed tocopherols with an additional 25%-200% w/w d-beta-, d-gamma-, and d-delta-tocopherol. Studies on vitamin E have largely concentrated on use of either a synthetic all-racemic ("d, l-") alpha tocopheryl ester (acetate or succinate) or a semi-synthetic d-alpha tocopheryl ester (acetate or succinate).
Alzheimer's disease 
Alzheimer's disease is a wasting disease of the brain. As oxidative stress may be involved in the pathogenesis of Alzheimer's, tocopherols have been tested as both a means of prevention and treatment. The results of these studies have been mixed, with some research suggesting that high levels of vitamin E in the diet may reduce the risk of Alzheimer's, while other studies found no such link. Studies on progression have also been contradictory, with the Alzheimer’s Disease Cooperative Study suggesting that vitamin E supplementation might be beneficial, but a later trial finding no clinical benefit. Due to this contradictory and confusing evidence, vitamin E or tocopherol supplements are not currently recommended for treating or preventing Alzheimer's disease.
As of 2009[update], human trials and surveys that have investigated potential association of vitamin E intake with incidence of cancer remain generally inconclusive. Antioxidants such as vitamin E help protect against the damaging effects of free radicals, which may contribute to the development of chronic diseases such as cancer. Vitamin E also may block the formation of nitrosamines, which are carcinogens formed in the stomach from nitrites consumed in the diet. It also may protect against the development of cancers by enhancing immune function.
Some evidence associates higher intake of vitamin E with a decreased incidence of prostate cancer (see ATBC study) and breast cancer. Some studies correlate additional cofactors, such as specific vitamin E isomers, e.g. gamma-tocopherol, and other nutrients, e.g. selenium, with dramatic risk reductions in prostate cancer. However, an examination of the effect of dietary factors, including vitamin E, on incidence of postmenopausal breast cancer in over 18,000 women from New York State did not associate a greater vitamin E intake with a reduced risk of developing breast cancer. A study of the effect on lung cancer in smokers also showed no benefit.
Recent studies have found that increased intake of vitamin E, especially among smokers may be responsible for an increase in the incidence of lung cancer, with one study finding an increase in the incidence of lung cancer by 7% for each 100 IU of vitamin E taken daily.
A potential confounding factor is the form of Vitamin E used in these studies. As explained earlier, synthetic, racemic mixtures of Vitamin E isomers are not bioequivalent to natural, non-racemic mixtures, yet are widely used academically and commercially. The SELECT study for prostate cancer used racemic alpha-tocopherol, for instance, and has shown no benefit. The study, cited above, showing a modest increase in cancer risk with Vitamin E supplementation, reported that over 90% of its respondents used a racemic form of Vitamin E (d,l-alpha-tocopherol). A meta-analysis of studies using Vitamin E, sorting results by the form (racemic vs non-racemic) used, is necessary.
Antioxidants are being studied to determine whether they can help prevent or delay age-related growth of cataracts, a clouding of the tissue of the lens of the eye. A controlled trial of high doses of vitamins C and E and beta carotene found no effect on the risk of developing cataracts. Similarly, a trial using vitamin E alone found that vitamin E supplementation produced no change in the risk of developing cataracts or the rate of progression of existing cataracts.
A 2007 study published in the European Journal of Ophthalmology found that, along with other treatments for glaucoma, adding alpha-tocopherol appeared to help protect the retina from glaucomatous damage. Groups receiving 300 mg and 600 mg per day of alpha-tocopherol, delivered orally, showed statistically significant decreases in the resistivity index in the posterior ciliary arteries and in the pulsatility index in the ophthalmic arteries, after six and twelve months of therapy. Alpha-tocopherol-treated patients also had significantly lower differences in mean visual field deviations."
Heart disease 
Preliminary research has led to a widely held belief that vitamin E may help prevent or delay coronary heart disease, but larger controlled studies have not shown any benefit. Many researchers advance the belief that oxidative modification of LDL-cholesterol (sometimes called "bad" cholesterol) promotes blockages in coronary arteries that may lead to atherosclerosis and heart attacks. Vitamin E may help prevent or delay coronary heart disease by limiting the oxidation of LDL-cholesterol. Vitamin E also may help prevent the formation of blood clots, which could lead to a heart attack. Observational studies have associated lower rates of heart disease with higher vitamin E intake. A study of approximately 90,000 nurses suggested that the incidence of heart disease was 30% to 40% lower among nurses with the highest intake of vitamin E from diet and supplements. The range of intakes from both diet and supplements in this group was 21.6 to 1,000 IU (32 to 1,500 mg), with the median intake being 208 IU (139 mg). A 1994 review of 5,133 Finnish men and women aged 30 – 69 years suggested that increased dietary intake of vitamin E was associated with decreased mortality (death) from heart disease.
Despite these promising observations, randomized clinical trials have consistently shown lack of benefit to the role of vitamin E supplements in heart disease. The Heart Outcomes Prevention Evaluation (HOPE) Study followed almost 10,000 patients for 4.5 years who were at high risk for heart attack or stroke. In this intervention study the subjects who received 265 mg (400) IU of vitamin E daily did not experience significantly fewer cardiovascular events or hospitalizations for heart failure or chest pain when compared to those who received a sugar pill. The researchers suggested that it is unlikely that the vitamin E supplement provided any protection against cardiovascular disease in the HOPE study. This study is continuing, to determine whether a longer duration of intervention with vitamin E supplements will provide any protection against cardiovascular disease.
Furthermore, meta analysis of several trials of antioxidants, including vitamin E, have not shown any benefit to vitamin E supplementation for preventing coronary heart disease. One study suggested that Vitamin E (as alpha-tocopherol only) supplementation may increase the risk for heart failure. Supplementing alpha-tocopherol without gamma-tocopherol is known to lead to reduced serum gamma- and delta-tocopherol concentrations.
A large-scale 10-year study published in 2007 examined the rates of venous thromboembolism (VTE) and pulmonary embolism in women taking 600 IU of vitamin E on alternate days. The study found a significant reduction in VTE especially in women who had a history of thrombtic events or a genetic predispostion.
Parkinson's disease 
In May 2005, The Lancet Neurology published a study suggesting that vitamin E may help protect against Parkinson's disease. Individuals with moderate to high intakes of dietary vitamin E were found to have a lower risk of Parkinson's. No conclusion could be made whether supplemental vitamin E has the same effect. Other trials have tested whether giving vitamin E supplements reduces the risk of Parkinson's disease, or if they can slow the progression of the disease. In a 1998 study, vitamin E supplements had no effect on the rate of progression.
Recent studies into the use of both vitamin C and the single isomer vitamin E esters as possible aids in preventing oxidative stress leading to pre-eclampsia has failed to show significant benefits, but did increase the rate of babies born with a low birthweight in one study.
Topical use 
Vitamin E is widely used as an inexpensive antioxidant in cosmetics and foods. Vitamin E containing products are commonly used in the belief that vitamin E is good for the skin; many cosmetics include it, often labeled as tocopherol acetate, tocopheryl linoleate or tocopheryl nicotinate. Some individuals experience allergic reactions to some tocopheryl esters or develop a rash and hives that may spread over the entire body from the use of topical products with alpha tocopheryl esters.
Vitamin E is often claimed by manufacturers of skin creams and lotions to play a role in encouraging skin healing and reducing scarring after injuries such as burns on the basis of limited research, but the weak evidence of a benefit of silicon gel sheeting with or without added Vitamin E is limited by the poor quality of the research. One study found that it did not improve or worsen the cosmetic appearance in 90% of patients, with a third developing contact dermatitis.
See also 
- Wagner, Karl-Heinz; Afaf Kamal-Eldin, Ibrahim Elmadfa (2004). "Gamma-tocopherol--an underestimated vitamin?". Annals of nutrition and metabolism 48 (3): 169–88. doi:10.1159/000079555. PMID 15256801. "In North America, the intake of γ-tocopherol has been estimated to exceed that of α-tocopherol by a factor of 2–4 ... due to the fact that soybean oil is the predominant vegetable oil in the American diet (76.4%) followed by corn oil and canola oil (both 7%) ... The supply of dietary fats ... is much more diverse in Europe ... The oils mainly consumed in Europe, i.e. sunflower, olive and canola oil, provide less γ-tocopherol but more α-tocopherol ... [T]he ratio of α-:γ-tocopherol is at least 1:2. Therefore, the average γ-tocopherol intake can be estimated as 4–6 mg/day, which is about 25–35% of the USA intake. In accordance with the lower estimated European intake of γ-tocopherol, the serum levels of γ-tocopherol in European populations are 4–20 times lower than that of α-tocopherol"
- Jiang, Q; Christen, S; Shigenaga, MK; Ames, BN (2001). "gamma-tocopherol, the major form of vitamin E in the US diet, deserves more attention". The American journal of clinical nutrition 74 (6): 714–22. PMID 11722951.
- http://www.fao.org/docrep/004/Y2809E/y2809e0f.htm Summary of the role of vitamin E in human metabolic processes
- Burton, G. W.; Ingold, K. U. (1981). "Autoxidation of biological molecules. 1. Antioxidant activity of vitamin E and related chain-breaking phenolic antioxidants in vitro". J. Am. Chem. Soc. 103: 6472–6477. doi:10.1021/ja00411a035.
- US Food and Drug Administration: "Listing of Food Additives Status Part II". Retrieved 2011-10-27.
- UK Food Standards Agency: "Current EU approved additives and their E Numbers". Retrieved 2011-10-27.
- Australia New Zealand Food Standards Code"Standard 1.2.4 - Labelling of ingredients". Retrieved 2011-10-27.
- Rigotti, A (2007). "Absorption, transport, and tissue delivery of vitamin E". Molecular Aspects of Medicine 28 (5–6): 423–36. doi:10.1016/j.mam.2007.01.002. PMID 17320165.
- Jensen, S; Lauridsen, C (2007). "α‐Tocopherol Stereoisomers". Vitamins & Hormones 76: 281–308. doi:10.1016/S0083-6729(07)76010-7. PMID 17628178.
- Brigelius-Flohé R, Traber MG (1 July 1999). "Vitamin E: function and metabolism". FASEB J. 13 (10): 1145–55. PMID 10385606.
- Composition of Foods Raw, Processed, Prepared USDA National Nutrient Database for Standard Reference, Release 20 USDA, February 2008
- Sen, C; Khanna, S; Roy, S (2006). "Tocotrienols: Vitamin E beyond tocopherols". Life Sciences 78 (18): 2088–98. doi:10.1016/j.lfs.2005.12.001. PMC 1790869. PMID 16458936.
- Evans, H. M.; Bishop, K. S. (1922). "On the Existence of a Hitherto Unrecognized Dietary Factor Essential for Reproduction". Science 56 (1458): 650–651. doi:10.1126/science.56.1458.650. PMID 17838496.
- Evans H. M., Emerson O. H., Emerson G. A. (1 February 1936). "The isolation from wheat germ oil of an alcohol, a-tocopherol, having the properties of vitamin E". Journal of Biological Chemistry 113 (1): 319–332.
- Fernholz, E. (1938). Journal of the American Chemical Society 60 (3): 700–705. doi:10.1021/ja01270a057.
- Iuliano, L.; Micheletta, F.; Maranghi, M.; Frati, G.; Diczfalusy, U.; Violi, F. (2001). "Bioavailability of Vitamin E as Function of Food Intake in Healthy Subjects: Effects on Plasma Peroxide-Scavenging Activity and Cholesterol-Oxidation Products". Arteriosclerosis, Thrombosis, and Vascular Biology 21 (10): e34–e37. doi:10.1161/hq1001.098465.
- Vitamin E Fact sheet
- http://www.efsa.europa.eu/de/efsajournal/pub/640.htm Opinion on mixed tocopherols, tocotrienol tocopherol and tocotrienols as sources for vitamin E added as a nutritional substance in food supplements (The EFSA Journal (2008) 640,1,34)
- http://www.ncc.umn.edu/products/databaseNUTvitamins.html University of Minnesota Nutrition Coordinating Center on Vitamins
- Packer L, Weber SU, Rimbach G (February 2001). "Molecular aspects of alpha-tocotrienol antioxidant action and cell signalling". J. Nutr. 131 (2): 369S–73S. PMID 11160563.
- J. Bauernfeind in: L. J. Machlin (ed.): Vitamin E – A Comprehensive Treatise, Marcel Dekker, New York 1980, p. 99
- "USDA National Nutrient Database for Standard Reference". USDA Agricultural Research Service. Retrieved 2009-11-26.
- Weiser H, Riss G, Kormann AW (1 October 1996). "Biodiscrimination of the eight alpha-tocopherol stereoisomers results in preferential accumulation of the four 2R forms in tissues and plasma of rats". J. Nutr. 126 (10): 2539–49. PMID 8857515.
- "Taken together, these data indicate that of the eight stereoisomers (RRR, RSR, RRS, RSS, SRR, SSR, SRS, SSS) in all-rac-α-tocopherol, only the four 2R-forms (RRR, RSR, RSS, RRS) are recognized by α-TTP and maintained in the plasma. Indeed, the Food and Nutrition Board (Food and Nutrition Board and Institute of Medicine, 2000) has defined that only α-tocopherol, specifically the 2R-forms of α-tocopherol, can fulfill the human requirement for vitamin E. Thus, all-rac-α-tocopherol has only half the activity of RRR-α-tocopherol." Taken from the discussion in Lauridsen, C.; Engel, H.; Craig, AM.; Traber, MG. (Mar 2002). "Relative bioactivity of dietary RRR- and all-rac-alpha-tocopheryl acetates in swine assessed with deuterium-labeled vitamin E" (PDF). J Anim Sci 80 (3): 702–7. PMID 11890405.
- Mathias PM, Harries JT, Peters TJ, Muller DP (July 1981). "Studies on the in vivo absorption of micellar solutions of tocopherol and tocopheryl acetate in the rat: demonstration and partial characterization of a mucosal esterase localized to the endoplasmic reticulum of the enterocyte". J. Lipid Res. 22 (5): 829–37. PMID 7288289.
- Ajandouz el H, Castan S, Jakob S, Puigserver A (2006). "A fast, sensitive HPLC method for the determination of esterase activity on alpha-tocopheryl acetate". J Chromatogr Sci 44 (10): 631–3. PMID 17254374.
- Horwitt M, Elliott W, Kanjananggulpan P, Fitch C (1984). "Serum concentrations of alpha-tocopherol after ingestion of various vitamin E preparations". Am J Clin Nutr 40 (2): 240–5. PMID 6465056. link
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