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something you should know about vitamin E

TRADE NAMES

Alph-E (The Key Company), Vitamin E-d-Alpha (Mason Vitamins), Vitamin E-dl Alpha (Health Products Corp., Mason Vitamins), E Mixed (Rexall Consumer), Vitamin E Dry (Swanson Health Products), Total E (Westlake Labs), Vitamin E MTC (National Vitamin), Nutr-E-Sol (Advanced Nutritional), Aquasol E (Astra Zeneca), Aquavit-E (Cypress Pharmaceutical), Liquid E (Freeda Vitamins), E-Pherol (Vitaline Corp.), Dry E (Nature's Life).

DESCRIPTION

Vitamin E is the collective term for a family of chemical substances that are structurally and, in some cases, biologically related to the best known member of this family, alpha-tocopherol. Vitamin E is a fat-soluble vitamin and an essential nutrient for humans. However, in contrast with the other vitamins present in human nutrition, its exact biochemical role remains unknown.

Vitamin E does not appear to play roles in reproduction and lactation in humans as it does in such animals as rats, and overt deficiency states of this vitamin are rare. Deficiency states of vitamin E, however, do exist in humans, and sub-optimal nutriture of the vitamin may increase the risk of certain degenerative disorders, such as coronary heart disease, Alzheimer's disease and cancer.

Vitamin E deficiency occurs as a result of rare genetic abnormalities affecting the alpha-tocopherol transfer protein (alpha-TTP), as a result of various malabsorption syndromes and as a result of protein-energy malnutrition. Alpha-TTP is a protein found in the liver, heart, cerebellum and retina. Alpha-TTP selectively recognizes alpha-tocopherol and is believed to mediate the secretion of alpha-tocopherol taken up by the liver cells into the circulation. It may also function in delivering alpha-tocopherol to the cerebellum and retina.

Genetic defects in alpha-TTP are associated with a characteristic syndrome, ataxia with vitamin E deficiency or AVED, previously called familial isolated vitamin E (FIVE) deficiency. AVED patients suffer from neurologic symptoms that are characterized by progressive peripheral neuropathy.

Vitamin E deficiency can also be caused by genetic defects in lipoprotein synthesis. Lipoproteins containing apolipoprotein (apo-B) are necessary for absorption and transport of vitamin E. Those with homozygous hypobetalipoproteinemia have a defect in the apo-B gene and those with abetalipoproteinemia have genetic defects in the microsomal triglyceride-transfer protein. Homozygous hypobetalipoproteinemics and abetalipoproteinemics become vitamin E-deficient and develop the progressive peripheral neuropathy characteristic of vitamin E deficiency.


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