Toxno Substance Profile
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Substance Name

Alpha-Tocopherol
Identification Number: CASRN | 59-02-9

  Substance Attributes


  • Metabolic Interference or Disruption

    Interferes with human metabolism. This can be a very serious thing. Some of these interference mechanics are well established. However, often long term effects and health consequences remain largely unknown. Additionally an emerging area of concern and one that is not currently studied, is the combined synergistic effects these metabolically disrupting chemicals have on human health.


    Metabolic interference happens when the substance produces highly reactive and often damaging intermediates during detoxification or when the substance binds to specific enzymes, important structural groups on molecules, receptors and membranes or targets DNA or mimics key nutrients.

  • Has known Side Effects

    This is often the result of long or short term medication use. The same medication can have a range of side effects ranging from none at all to totally debilitating symptoms within different individuals. Reasons for this include individual genetics, individual detoxification capacity, nutrition status, duration of use and total number of medications being taken.


    It becomes very difficult to establish clear causes of symptoms when multiple medications are being taken at once.


    See SIDE EFFECTS LINKOUT at end of this profile.

These attributes are ONLY based on peer-reviewed evidence. See link to Data Sources below. Everyone benefits from knowing this stuff. Please Share.



  • CATEGORIES: Medication or Drug | Household Toxin | Food Toxin | Natural Toxin | Inert Pesticide Ingredient USA - Non Food Use Only | Inert Pesticide Ingredient USA - FRAGRANCE ( Generally Not used on Food)
  • SUBSTANCE LINEAGE: Organic Compounds | Lipids and Lipid-Like Molecules | Prenol Lipids | Quinone and Hydroquinone Lipids | Tocopherols
  • SYNONYMS: (+)-a-Tocopherol | (+)-alpha-Tocopherol | (+)-α-tocopherol | (2R)-3,4-Dihydro-2,5,7,8-tetramethyl-2-[(4R,8R)-4,8,12-trimethyltridecyl]-2H-1-benzopyran-6-ol | (2R,4'R,8'R)-a-Tocopherol | (2R,4'R,8'R)-alpha-Tocopherol | (R,R,R)-a-Tocopherol | (R,R,R)-alpha-Tocopherol | (R,R,R)-α-tocopherol | 5,7,8-Trimethyltocol | a-D-Tocopherol | a-Tocopherol | alpha-delta-Tocopherol | alpha-Tocopherol | Amino-Opti-E | Aquasol E | D-alpha-Tocopherol | d-α-tocopherol | delta-alpha-Tocopherol | Denamone | Eprolin | Phytogermin | Phytogermine | RRR-alpha-tocopherol | RRR-alpha-tocopheryl | Vitamin E | Vitamin Ea | α-Tocopherol
  • DESCRIPTION: A generic descriptor for all tocopherols and tocotrienols that exhibit alpha-tocopherol activity. By virtue of the phenolic hydrogen on the 2H-1-benzopyran-6-ol nucleus, these compounds exhibit varying degree of antioxidant activity, depending on the site and number of methyl groups and the type of isoprenoids.
  • COMMENTS:
  • toxin chemical structure pubchem
  • FORMULA: C29H50O2
  • DATA SOURCES: DATA SOURCES: ARTICLE 4 | T3DB | PubChem | EPA USA - Pesticide Inerts | Drugbank
  • LAST UPDATE: 28/04/2018

  Health Associations

Mostly focused on Health Implications of Long Term Exposure to this substance

  • SYMPTOMS:
  • POSSIBLE HEALTH CONSEQUENCES: | Hepatic.
  • ACTION OF TOXIN: Although all forms of Vitamin E exhibit antioxidant activity, it is known that the antioxidant activity of vitamin E is not sufficient to explain the vitamin's biological activity.
    Vitamin E's anti-atherogenic activity involves the inhibition of the oxidation of LDL and the accumulation of oxLDL in the arterial wall. It also appears to reduce oxLDL-induced apoptosis in human endothelial cells. Oxidation of LDL is a key early step in atherogenesis as it triggers a number of events which lead to the formation of atherosclerotic plaque. In addition, vitamin E inhibits protein kinase C (PKC) activity. PKC plays a role in smooth muscle cell proliferation, and, thus, the inhibition of PKC results in inhibition of smooth muscle cell proliferation, which is involved in atherogenesis.
    Vitamin E's antithrombotic and anticoagulant activities involves the downregulation of the expression of intracellular cell adhesion molecule(ICAM)-1 and vascular cell adhesion molecule(VCAM)-1 which lowers the adhesion of blood components to the endothelium. In addition, vitamin E upregulates the expression of cytosolic phospholipase A2 and cyclooxygenase (COX)-1 which in turn enhances the release of prostacyclin. Prostacyclin is a vasodilating factor and inhibitor of platelet aggregation and platelet release. It is also known that platelet aggregation is mediated by a mechanism involving the binding of fibrinogen to the glycoprotein IIb/IIIa (GPIIb/IIIa) complex of platelets. GPIIb/IIIa is the major membrane receptor protein that is key to the role of the platelet aggregation response. GPIIb is the alpha-subunit of this platelet membrane protein. Alpha-tocopherol downregulates GPIIb promoter activity which results in reduction of GPIIb protein expression and decreased platelet aggregation. Vitamin E has also been found in culture to decrease plasma production of thrombin, a protein which binds to platelets and induces aggregation. A metabolite of vitamin E called vitamin E quinone or alpha-tocopheryl quinone (TQ) is a potent anticoagulant. This metabolite inhibits vitamin K-dependent carboxylase, which is a major enzyme in the coagulation cascade.
    The neuroprotective effects of vitamin E are explained by its antioxidant effects. Many disorders of the nervous system are caused by oxidative stress. Vitamin E protects against this stress, thereby protecting the nervouse system.
    The immunomodulatory effects of Vitamin E have been demonstrated in vitro, where alpha-tocopherol increases mitogenic response of T lymphocytes from aged mice. The mechanism of this response by vitamin E is not well understood, however it has been suggested that vitamin E itself may have mitogenic activity independent of its antioxidant activity.
    Lastly, the mechanism of action of vitamin E's antiviral effects (primarily against HIV-1) involves its antioxidant activity. Vitamin E reduces oxidative stress, which is thought to contribute to HIV-1 pathogenesis, as well as to the pathogenesis of other viral infections. Vitamin E also affects membrane integrity and fluidity and, since HIV-1 is a membraned virus, altering membrane fluidity of HIV-1 may interfere with its ability to bind to cell-receptor sites, thus decreasing its infectivity. | Although all forms of Vitamin E exhibit antioxidant activity, it is known that the antioxidant activity of vitamin E is not sufficient to explain the vitamin's biological activity.
    Vitamin E's anti-atherogenic activity involves the inhibition of the oxidation of LDL and the accumulation of oxLDL in the arterial wall. It also appears to reduce oxLDL-induced apoptosis in human endothelial cells. Oxidation of LDL is a key early step in atherogenesis as it triggers a number of events which lead to the formation of atherosclerotic plaque. In addition, vitamin E inhibits protein kinase C (PKC) activity. PKC plays a role in smooth muscle cell proliferation, and, thus, the inhibition of PKC results in inhibition of smooth muscle cell proliferation, which is involved in atherogenesis.
    Vitamin E's antithrombotic and anticoagulant activities involves the downregulation of the expression of intracellular cell adhesion molecule(ICAM)-1 and vascular cell adhesion molecule(VCAM)-1 which lowers the adhesion of blood components to the endothelium. In addition, vitamin E upregulates the expression of cytosolic phospholipase A2 and cyclooxygenase (COX)-1 which in turn enhances the release of prostacyclin. Prostacyclin is a vasodilating factor and inhibitor of platelet aggregation and platelet release. It is also known that platelet aggregation is mediated by a mechanism involving the binding of fibrinogen to the glycoprotein IIb/IIIa (GPIIb/IIIa) complex of platelets. GPIIb/IIIa is the major membrane receptor protein that is key to the role of the platelet aggregation response. GPIIb is the alpha-subunit of this platelet membrane protein. Alpha-tocopherol downregulates GPIIb promoter activity which results in reduction of GPIIb protein expression and decreased platelet aggregation. Vitamin E has also been found in culture to decrease plasma production of thrombin, a protein which binds to platelets and induces aggregation. A metabolite of vitamin E called vitamin E quinone or alpha-tocopheryl quinone (TQ) is a potent anticoagulant. This metabolite inhibits vitamin K-dependent carboxylase, which is a major enzyme in the coagulation cascade.
    The neuroprotective effects of vitamin E are explained by its antioxidant effects. Many disorders of the nervous system are caused by oxidative stress. Vitamin E protects against this stress, thereby protecting the nervouse system.
    The immunomodulatory effects of Vitamin E have been demonstrated in vitro, where alpha-tocopherol increases mitogenic response of T lymphocytes from aged mice. The mechanism of this response by vitamin E is not well understood, however it has been suggested that vitamin E itself may have mitogenic activity independent of its antioxidant activity.
    Lastly, the mechanism of action of vitamin E's antiviral effects (primarily against HIV-1) involves its antioxidant activity. Vitamin E reduces oxidative stress, which is thought to contribute to HIV-1 pathogenesis, as well as to the pathogenesis of other viral infections. Vitamin E also affects membrane integrity and fluidity and, since HIV-1 is a membraned virus, altering membrane fluidity of HIV-1 may interfere with its ability to bind to cell-receptor sites, thus decreasing its infectivity.
  • TOXIN SITES OF ACTION IN CELL: "Cytoplasm", "Extracellular", "Membrane"
  • Additional Exposure Routes: Vitamin E, known for its antioxidant activities, is protective against cardiovascular disease and some forms of cancer and has also demonstrated immune-enhancing effects. It may be of limited benefit in some with asthma and rheumatoid arthritis. It may be helpful in some neurological diseases including Alzheimer's, some eye disorders including cataracts, and diabetes and premenstrual syndrome. It may also help protect skin from ultraviolet irradiation although claims that it reverses skin aging, enhances male fertility and exercise performance are poorly supported. It may help relieve some muscle cramps.
  • SEE MEDICATION SIDE EFFECTS

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