Tocotrienols: Vitamin E beyond tocopherols.
Life Sci. 2006 Mar 27;78 ( 18 ) :2088-98. Epub 2006 Feb 3.
Sen CK, Khanna S, Roy S.
Department of Surgery, Davis Heart and Lung Research Institute, The Ohio State University Medical Center, Columbus, Ohio 43210, USA. email@example.com
In nature, eight substances have been found to have vitamin E activity: alpha-, beta-, gamma- and delta-tocopherol; and alpha-, beta-, gamma- and delta-tocotrienol. Yet, of all papers on vitamin E listed in PubMed less than 1% relate to tocotrienols.
The abundance of alpha-tocopherol in the human body and the comparable efficiency of all vitamin E molecules as antioxidants, led biologists to neglect the non-tocopherol vitamin E molecules as topics for basic and clinical research. Recent developments warrant a serious reconsideration of this conventional wisdom.
Tocotrienols possess powerful neuroprotective, anti-cancer and cholesterol lowering properties that are often not exhibited by tocopherols. Current developments in vitamin E research clearly indicate that members of the vitamin E family are not redundant with respect to their biological functions. alpha-Tocotrienol, gamma-tocopherol, and delta-tocotrienol have emerged as vitamin E molecules with functions in health and disease that are clearly distinct from that of alpha-tocopherol. At nanomolar concentration, alpha-tocotrienol, not alpha-tocopherol, prevents neurodegeneration. On a concentration basis, this finding represents the most potent of all biological functions exhibited by any natural vitamin E molecule.
An expanding body of evidence support that members of the vitamin E family are functionally unique. In recognition of this fact, title claims in manuscripts should be limited to the specific form of vitamin E studied. For example, evidence for toxicity of a specific form of tocopherol in excess may not be used to conclude that high-dosage "vitamin E" supplementation may increase all-cause mortality. Such conclusion incorrectly implies that tocotrienols are toxic as well under conditions where tocotrienols were not even considered. The current state of knowledge warrants strategic investment into the lesser known forms of vitamin E. This will enable prudent selection of the appropriate vitamin E molecule for studies addressing a specific need.
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Thanks for the link to the abstract of that interesting review. If anyone's interested, they can access a free paper by the same group of authors which discusses how alpha-tocotrienol may inhibit 12-lipoxygenase to mediate neuroprotection.
- Molecular Basis of Vitamin E Action: Tocotrienol Modulates 12-Lipoxygenase, a Key Mediator of Glutamate-Induced Neurodegeneration.
The Journal of Biological Chemistry, 278(44): 3508–43515, 2003
Vitamin E is a generic term for tocopherols and tocotrienols. This work is based on our striking evidence that, in neuronal cells, nanomolar concentrations of alpha-tocotrienol, but not alpha-tocopherol, block glutamate-induced death by suppressing early activation of c-Src kinase (Sen, C. K., Khanna, S., Roy, S., and Packer, L. (2000) J. Biol. Chem. 275, 13049–13055). This study on HT4 and immature primary cortical neurons suggests a central role of 12-lipoxygenase (12-LOX) in executing glutamate-induced neurodegeneration. BL15, an inhibitor of 12-LOX, prevented glutamate-induced neurotoxicity. Moreover, neurons isolated from 12-LOX-deficient mice were observed to be resistant to glutamate-induced death. In the presence of nanomolar alpha-tococotrienol, neurons were resistant to glutamate-, homocysteine-, and L-buthionine sulfoximine-induced toxicity. Long-term time-lapse imaging studies revealed that neurons and their axo-dendritic network are fairly motile under standard culture conditions. Such motility was arrested in response to glutamate challenge. Tocotrienol-treated primary neurons maintained healthy growth and motility even in the presence of excess glutamate. The study of 12-LOX activity and metabolism revealed that this key mediator of glutamate-induced neurodegeneration is subject to control by the nutrient alpha-tocotrienol. In silico docking studies indicated that alpha-tocotrienol may hinder the access of arachidonic acid to the catalytic site of 12-LOX by binding to the opening of a solvent cavity close to the active site. These findings lend further support to alpha-tocotrienol as a potent neuroprotective form of vitamin E.
per serving Percent
Wheat germ oil, 1 tablespoon 20.3 100
Almonds, dry roasted, 1 ounce 7.4 40
Sunflower seed kernels, dry roasted, 1 ounce 6.0 30
Sunflower oil, over 60% linoleic, 1 tablespoon 5.6 30
Safflower oil, over 70% oleic, 1 tablespoon 4.6 25
Hazelnuts, dry roasted, 1 ounce 4.3 20
Peanut butter, smooth style, vitamin and mineral fortified, 2 Tablespoons 4.2 20
Peanuts, dry roasted, 1 oz 2.2 10
Corn oil (salad or vegetable oil), 1 tablespoon 1.9 10
Spinach, frozen, chopped, boiled, ½ cup 1.6 6
Broccoli, frozen, chopped, boiled, ½ cup 1.2 6
Soybean oil, 1 tablespoon 1.3 6
Kiwi, 1 medium fruit without skin 1.1 6
Mango, raw, without refuse, ½ cup sliced 0.9 6
Spinach, raw, 1 cup 0.6 4
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The 309th Hospital of Chinese People's Liberation Army, Beijing, China
Vitamin E administration erases an enhanced oxidation in multiple sclerosis
Systemic peroxidation status has been reported as a pathogenic factor for multiple sclerosis (MS). Systemically elevated oxidation levels are associated with serum lipid peroxidation and somatic telomere length (TL) shortening. We investigated whether vitamin E (VE) administration suppresses peroxidation and improves clinical symptoms in 34 MS patients. We analyzed serum lipid peroxidation and degree of TL in circulating leukocytes of MS patients before and after VE treatment. The oxidation level was enhanced and TL was shortened in MS. The MS population treated with VE 400 mg/day for 3 months showed significantly reduced serum lipid oxidation level with maintenance of TL. These findings showed that systemic peroxidation is associated with the development of MS. Antioxidants such as vitamin E can be candidates for supplementary therapeutic agents for MS
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