Vitamin E

Author: Enrico Garelli
Date: 18/11/2009



Vitamin E is a name for eight antioxidants, of which the only one active in the human body is referred to as α-tocopherol. The name derives from the greek Tocos tocopherol, which means birth, and that means pursuing pherein.
Vitamin E is a fat-soluble antioxidant that stops the production of reactive oxygen species formed when fat undergoes oxidation. Of these, α-tocopherol (also written as alpha-tocopherol) has been most studied as it has the highest bioavailability, is an essential nutrient the human body needs to function normally. The term vitamin E actually represents a group of substances, the most important (to the human body) being alpha-tocopherol. The deficiency is rare and occurs almost exclusively in people with an inherited or acquired condition that impairs their ability to absorb this vitamin. Symptoms of vitamin E deficiency include muscle weakness, visual problems (especially at night), and a poor sense of balance. Over a long period, vitamin E deficiency may progress to blindness, heart disease, and impaired thinking. Supplements are usually only necessary or recommended for people with vitamin E deficiency or a condition that puts them at risk for this deficiency.


Vitamin E can prolong the prothrombin time (PT) in animal models by inhibiting vitamin K – dependent carboxylase. Administration of vitamin K corrects this. High doses increase the vitamin K requirement and, therefore, cause coagulopathy only in patients who are deficient in vitamin K.3,4 Vitamin E at dosages of 1600 IU/d also reduces platelet thromboxane production. Vitamin E supplementation may impair the hematologic response to iron in children with iron-deficiency anemia.
Lipoprotein effects - In the Heart Protection Study, a combination of vitamin E (600 IU), vitamin C , and beta-carotene did not affect mortality. However, it did cause a significant, albeit small, increase in total cholesterol, low-density lipoprotein (LDL) cholesterol , and triglycerides, as well as a decrease in high-density lipoprotein (HDL). In 2 randomized trials, an antioxidant cocktail that included vitamin E blunted the beneficial increase in HDL2 levels associated with niacin and simvastatin therapy.5,6
Immunologic - Vitamin E can depress leukocyte oxidative bactericidal activity and mitogen-induced lymphocyte transformation.


Clinical trials with vitamin E have yielded contrasting results. In these trials, the amount of vitamin E given was different, and the compliance was not assessed in all studies. In addition, the modality of intake, ie, in relation to food, was not specified in any trial. Vitamin E is lipophilic, and its absorption is expected to be increased by food. We studied the bioavailability of vitamin E in relation to food intake and the effect on the lipid peroxide–scavenging activity of plasma and on 7ß-hydroxycholesterol and 7-ketocholesterol (oxysterols) as markers of oxidant stress. Twenty healthy Italian subjects were randomly assigned to take vitamin E at 300 mg/d on an empty stomach (group A) or during dinner (group B) for 15 days. Plasma vitamin E markedly increased in group B (84%) compared with group A (29%). The lipid peroxide–scavenging activity of plasma increased significantly in group B (14%, P=0.005) but did not change in group A. All subjects showed very low levels of plasma oxysterols, which were not affected by vitamin E supplementation in either group. This study shows that plasma concentration of vitamin E and plasma antioxidant activity in response to oral supplementation are markedly affected by food intake. Healthy Italian subjects show very low levels of cholesterol oxidation products; these low levels are possibly related to the Mediterranean diet. To obtain maximal absorption, vitamin E must be given at meals. These data should be taken into account in clinical trials with vitamin E.

Bioavailability of Vitamin E as Function of Food Intake in Healthy Subjects

Effects of vitamin E on thyroid

The thyroid hormones metabolism is considerably altered in many pathological processes including fever. The study confirmed our previous observations in vitro that lipid peroxidation (free radical formation) influences the 5'-monodeiodinase activity in tissues and alters the thyroid hormones metabolism.


In examine the relationship between selenium (Se)- and vitamin E(VE)-deficiency and thyroid hormone (TH) metabolic disturbance, especially type I iodothyronine 5'-deiodinase (ID-I) activity. GSH-Px activity is influenced mainly by Se level, but ID-I activity is influenced by VE concentration in addition to Se level. VE seemed to play a protective role on ID-I and its mechanism might be related to the fact that VE protects the stability of microsomal membrane in which ID-I exists, avoiding from free radical damage as well as the coordinated action and mutual sparing effect of Se and VE.


Necrosis and apoptosis coexist in the thyroid during goitre development and involution, but little is known about their respective causes. To test the possible role of free radicals, we analysed separately necrosis and apoptosis in male Wistar rats with depressed or normal antioxidant protection. Vitamin E-deficient and -sufficient rats were made goitrous with perchlorate in drinking water; involution was induced by repeated injection of NaI, without or with methimazole. Increase of thyroid malondialdehyde concentration and decrease of glutathione peroxidase activity confirmed the depressed antioxidant protection in vitamin E-deficient rats. Plasma thyroxine and TSH levels were not modified. Necrosis (swollen cells) and apoptosis (pyknotic cells) were quantified on histological sections. In vitamin E-sufficient rats, dead cells were very rare in control thyroids, increased 3-fold in goitre and still further during involution. Necrotic epithelial cells predominated in the goitre and their number declined after iodide supplementation, without or with methimazole. In contrast, the number of apoptotic cells and the caspase-3 activity were increased in goitre and further increased after involution, with two-thirds of pyknotic cells being observed in the interstitium. Apoptosis was prevented by methimazole. Vitamin E deficiency significantly increased total cell death and epithelial cell necrosis and induced the occurrence of much cell debris in the follicular lumen during involution, with no modification of the apoptotic reaction. These results show that the type of cell death is differentially regulated during goitre development and involution: necrosis is related to the oxidative status of the cells, while apoptosis comes with iodine-induced involution.


Peroxidase inhibition

Protective effect of quercetin and alpha-tocopherol on experimental reflux oesophagitis in rats was investigated. Rats received quercetin, (100 mg/kg), alpha-tocopherol (16 mg/kg), omeprazole (30 mg/kg) given at 1 h prior to surgery. Quercetin and alpha-tocopherol significantly inhibited the oesophagitis index to 1.33+/-0.12 (P<0.001) and 1.83+/-0.14 (P<0.001) respectively, as compare to control group 3.5+/-0.21. Further, acid and pepsin out put of gastric contents were significantly decreased in treated groups. Indeed, quercetin significantly inhibited the lipid peroxidation (from 0.69+/-0.05 to 0.43+/-0.04 nmol of malonyldialdehyde (MDA)/mg protein) (P<0.001) and increased in levels of catalase to 29.5+/-2.7 units of catalase activity/mg protein and superoxide dismutase (SOD) to 92.4+/-10.5 units/mg protein (P<0.001). The alpha-tocopherol and omperazole showed significant inhibition in lipid peroxidation (0.34+/-0.02 and 0.38+/-0.01) (P<0.01) and enhanced the activities of catalase (34.3+/-3.6 and 31.5+/-3.4) (P<0.01) and SOD (87.3+/-9.2 and 76.60+/-6.9) activity. Quercetin and alpha-tocopherol treated group significantly increased the glutathione level to 36.5+/-2.78 (P<0.01) and 32.1+/-2.34 (P<0.05) respectively. However, it altered the elevated levels of sialic acid and hexose contents in oesophageal tissue. Indeed, quercetin significantly decreased the elevated plasma histamine content (P<0.05). Quercetin and alpha-tocopherol significantly attenuated the elevated level of collagen in oesophageal tissue as of the omeprazole. The results suggest that antioxidants could attenuate the severity of reflux oesophagitis and prevent the oesophageal mucosal damage and validate its therapeutic use in gastroesophageal reflux disease.

Peroxidase inhibition


The natural form of the vitamin is synthesized only by plants and is found predominantly in plant oils. Vitamin E (tocopherol) is also present in high amounts within the chloroplast and therefore the leaves of most plants. In contrast, the tocotrienols are synthesized and found in the germ and bran sections of the plant. The fat-soluble property of vitamin E allows it to be stored within fatty tissue of animals, relatively rich animal sources are egg yolk, liver and flour of some fish. Therefore a diet that includes meat supplies additional vitamin E. However, the amount of vitamin E obtained in a meat inclusive diet is less than the amount supplied by plant sources.
The main sources of vitamin E in the diet are vegetable oils (especially safflower oil, sunflower oil, and cottonseed oil), green leafy vegetables, nuts, cereals, meats, egg yolks, wheat germ, and whole wheat products.. The lack of dietary vitamin E is rare.

In Plants

A major barrier to the commercialization of somatic embryogenesis technology in loblolly pine (Pinus taeda L.) is recalcitrance of some high-value crosses to initiate embryogenic tissue and continue early-stage somatic embryo growth. Developing initiation and multiplication media that resemble the seed environment may decrease this recalcitrance. Organic acid analyses were performed weekly throughout the sequence of seed development for female gametophyte and zygotic embryo tissues to determine physiological concentrations present that may be beneficial if added to somatic embryogenesis media. Major differences in stage-specific organic acids were observed. A simple bioassay was used to evaluate potential growth promotion of individual organic acids added to initiation or multiplication media at physiological concentrations. Nine vitamins and 25 organic acids were screened. Compounds showing statistically significant increases in early-stage embryo growth were then tested for initiation of loblolly pine. Two vitamins and five organic acids including Vitamins B12 and E, α-ketoglutaric, pyruvic, succinic, oxalic, quinic, and ascorbic acids produced statistically significant increases in early-stage embryo growth. When tested for improved initiation, Vitamins B12 and E, α-ketoglutaric, pyruvic, and succinic acids increased initiation when alone and when combined. Analyses of organic acids in the seed environment coupled with a bioassay to screen potential media supplements for protocol improvement resulted in statistically significant increases in the loblolly pine embryogenic tissue initiation protocol and saved much time and expense.


Deficiencies / Excess

Genuine Vitamin E deficiency is unusual in adult men. It is indicated by problems with the nervous system.
In most cases, a deficiency is the result of serious and prolonged difficulty with lipid metabolism and absorption.
Epidemiological studies indicate that about 5% of the French population consumes very little Vitamin E. Nonetheless, values below the threshold indicating a biological deficiency are not found in the general population.
Excess Vitamin E does not appear to be toxic. However, there is currently no absolute certainty that prolonged moderate or significant intake of Vitamin E is harmless.

Studies on the effect of vitamin deficiency and excess

Frank vitamin E deficiency is rare and overt deficiency symptoms have not been found in healthy people who obtain little vitamin E from their diets. Premature babies of very low birth weight (<1,500 grams) might be deficient in vitamin E. Vitamin E supplementation in these infants might reduce the risk of some complications, such as those affecting the retina, but they can also increase the risk of infections.

Because the digestive tract requires fat to absorb vitamin E, people with fat-malabsorption disorders are more likely to become deficient than people without such disorders. Deficiency symptoms include peripheral neuropathy, ataxia, skeletal myopathy, retinopathy, and impairment of the immune response. People with Crohn’s disease, cystic fibrosis, or an inability to secrete bile from the liver into the digestive tract, for example, often pass greasy stools or have chronic diarrhea; as a result, they sometimes require water-soluble forms of vitamin E, such as tocopheryl polyethylene glycol-1000 succinate.

A primary barrier to characterizing the roles of vitamin E in health is the lack of validated biomarkers for vitamin E intake and status to help relate intakes to valid predictors of clinical outcomes. This section focuses on four diseases and disorders in which vitamin E might be involved: heart disease, cancer, eye disorders, and cognitive decline.

Research has not found any adverse effects from consuming vitamin E in food. However, high doses of alpha-tocopherol supplements can cause hemorrhage and interrupt blood coagulation in animals, and in vitro data suggest that high doses inhibit platelet aggregation. Two clinical trials have found an increased risk of hemorrhagic stroke in participants taking alpha-tocopherol; one trial included Finnish male smokers who consumed 50 mg/day for an average of 6 years and the other trial involved a large group of male physicians in the United States who consumed 400 IU every other day for 8 years. Because the majority of physicians in the latter study were also taking aspirin, this finding could indicate that vitamin E has a tendency to cause bleeding.
The effects in sport were tested in eight trained male cyclists, MDA concentrations were significantly increased after EAC supplementation at rest before exercise and after moderate exercise (p < .05). MDA concentrations showed no differences between treatments after strenuous exercise (p > .1). Pl-GPx concentrations decreased at all time points of measurement after EAC treatment (p < .05). CONCLUSIONS: The EAC induced an increase of LIPOX as indicated by MDA and decreased pl-GPx concentrations pre- and postexercise.

Increased lipid peroxidation in trained men after 2 weeks of antioxidant supplementation.

Vitamin E effects

High-dosage (≥400 IU/d) vitamin E supplements may increase all-cause mortality and should be avoided.


Potential fields of application

· Alzheimer: Oxidative stress is a fundamental process contributing to the neuronal degeneration and death observed in Alzheimer disease, and many studies using markers of oxidative damage have provided evidence supporting this hypothesis. Consequently, antioxidants that prevent the detrimental consequences of oxidative stress are considered to be a promising approach to neuroprotection. While the clinical value of antioxidants for the prevention of AD is currently ambiguous, they still appear to be the most promising weapons that can be developed against disease progression.

· Autistic Speech: daily supplements of omega-3 and vitamin E were associated with improvements in speech, imitation, eye contact, and behaviour


· Fertility: The name derives from the greek Tocos tocopherol, which means birth, and that means pursuing pherein. This name was conferred to highlight its essential role in reproduction. The supplements most important in enhancing fertility in men are vitamin C, E, zinc and L-arginine. Vitamin C helps prevent sperm from clumping or sticking together, Thus improving the chances for fertility. Vitamin E is the fertility vitamin because it corrects the functioning of the endocrine glands. Vitamin E plays a key role in inhibiting free-radical damage to the unsaturated fatty acids of the sperm membrane. Low levels of this nutrient have been linked to a low fertility in men. In addition, vitamin E has been shown to increase the ability of sperm to fertilize an egg in test tubes.
to examine whether disturbances in fatty acid profile as a result of increased oxidative stress could be one of the causes of female infertility. Likewise, levels of MDA, a peroxidative product of essential fatty acids, were increased (p < 0.05) and vitamin E concentrations were decreased (p < 0.05) in infertile women[...] In infertile women, suggesting that increased oxidative stress and consequent altered essential polyunsaturated fatty acids are associated with infertility. The cause and effect relationship between oxidative stress and membrane essential polyunsaturated fatty acids in infertile women. These data have important implications for the supplementation of a combination of omega-3 fatty acids and antioxidants in the successful management of female infertility.


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