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Physiological Effects of Vitamin E

Peter T. Pugliese, MD

In the September 2009 issue of Skin Inc. magazine, Peter T. Pugliese, MD, discusses how vitamin E affects the skin in the article "Vitamin E: A Skin Care Ally." Following is more information from Dr. Pugliese regarding how the vitamin works in other bodily functions, as well.

Sometimes in life you have great and exciting experiences, one of which is discovering new things. It’s like opening a door to a new house and walking down a hallway only to find many more doors that open to wondrous rooms filled with beautiful things of all types. Vitamin E is such a discovery, and after 80 years, only parts of its function are beginning to be understood.

The absorption of vitamin E occurs in the small intestine with other lipids where it is acted on by enzymes called esterases and bile acid. Vitamin E is then absorbed into the intestinal wall, called the mucosa and, along with other lipids, are formed in little lipid spheres called micelles, in which form it enters cells known as enterocytes. In the enterocytes, the lipids, including vitamin E, are formed into structures called chylomicrons, which are then transferred from the enterocyte into the lymphatic system. The lymphatic system carries the chylomicrons into the blood stream, which delivers their contents to individual cells. After reaching the liver, the vitamin E combined with the chylomicrons is released and then bound to a protein known as alpha tocopherol transfer protein that is in the cell cytoplasm. From here, it is carried to the endoplasmic reticulum and packaged in lipoproteins of the low density type, or VLDL. The largest amount of vitamin is found in the fatty tissue, though no particular tissue is selected as a storage area, for it can be found in the adrenals, lungs, muscles and heart. The adipose tissue releases the vitamin E slowly, while the liver turns it over rapidly. As a result, the amount of vitamin E in the liver can be used as a measure of vitamin E dietary intake. The reader should note that any disorder of the pancreas or the bowel can markedly decrease the vitamin E absorption. Vitamin E is excreted mainly via the bowel of the kidneys.

Free radicals and antioxidants

The principal function of vitamin E is to protect cell membranes from oxidative damage to the unsaturated fatty acids within the phospholipid bilayer of the cell. Free radical chemistry occurs in three stages: initiation, propagation and termination. Because the cell lives in a watery environment, it will be subjected to highly reactive hydroxyl radicals, OH, which arise from water ions. The double bond structure of polyunsaturated fatty acids (PUFAs) within the lipid bilayer are quick to react with OH radicals. The OH radical reacts with the PUFA to form a compound known as a carbon-centered radical (Lc.) and water, which is called the initiation stage. The carbon-centered radical will react with molecular oxygen (O2) to form the peroxyl radical (L00.) two oxygen atoms), starting a chain reaction (the propagation stage) because the peroxyl radical extracts hydrogen for other organic compounds, such as PUFAs next door, leaving a carbon-centered radical. The propagation stage must be terminated in order to stop cellular damage. Vitamin E is one line of defense against cellular damage. Vitamin E is located within the lipid bilayer and is more reactive with OH and L00. than are PUFAs. It is able both to prevent lipid peroxidation at the initiation stage, or terminate the reaction at the propagation state. The termination by vitamin E produces the tocopherol radical, or oxidized vitamin E, which is reduced back to vitamin E by vitamin C and lipoic acid.

Antioxidant and anti-atherosclerosis

The major function of vitamin E is to protect the integrity of the cell membrane. Vitamin E is located in the cell membrane between the phospholipids. View it as a large hat pin with one end sticking in the cell membrane and the other near the surface of the membrane. In this capacity, it acts as an antioxidant, particularly in preventing arterial disease known as arteriosclerosis. Vitamin E is regenerated by vitamin C and other compounds. See Figure 5 for an illustration of these mechanisms. The anti-atherogenic activity of vitamin E is due to the inhibition of the oxidation of LDL in the arterial wall. These oxidized LDL are able to induce apoptosis, also known as cell death, in human endothelial cells. This is an early but key step in atherogenesis, because it is the start of a number of events leading to the formation of atherosclerotic plaque. Further, vitamin E inhibits protein kinase C (PKC), which is an enzyme that causes proliferative activity in cells. In blood vessels, PKC causes smooth muscle cell proliferation, therefore by inhibition of PKC, vitamin E inhibits smooth muscle cell proliferation, thus helping to prevent atherosclerosis.

Antithrombotic and anticoagulant activity

An additional major role of vitamin E is to control the coagulation of blood, which occurs stepwise. Vitamin E’s antithromboticc and anticoagulant activities are quite complex because they involve the regulation of cellular activities. One function to control clotting is the down regulationd of the factor responsible for intracellular cell adhesion, and the molecule that causes vascular cell adhesion. When these molecules are lower, the adhesion of blood components to the endothelium, or lining of the blood vessels, is reduced. A second function in preventing clotting is the up regulation of cytosolic phospholipase A2 and cyclooxygenase, which are two substances that release of prostacyclin, a vasodilating factor and inhibitor of platelet aggregation. Platelets are needed in blood coagulation (aspirin also reduces platelet aggregation), and, along with this function, vitamin E decreases plasma production of thrombin, a protein that binds to platelets and induces aggregation.

Immunomodulatory and antiviral effects

The neuroprotective effects of vitamin E are most likely due to its antioxidant effects. Nervous tissue, being a lipid-covered structure and subjected to lipid peroxidation, can easily be a victim of oxidative stress. Vitamin E, being lipid-soluble, can protect against oxidative stress in the nervous system. Vitamin E has been observed to be an antioxidant in tissue-cultured cells. Using the T lymphocyte as a model cell and the increase in mitosis as a response, alpha tocopherol produced an increase in the number of T lymphocytes in aged mice. The T lymphocyte is an important component of the immune system. The mechanism of this mitotic activity makes it apparent that it is produced by vitamin E. It is possible that the antiviral effects of vitamin E against HIV-1 are related to an antioxidant activity since Vitamin E is known to counteract the biological stress from oxidation, and oxidation is known to contribute to the pathogenesis of HIV-1 viral infections. One theory is that since vitamin E helps to control the integrity and fluidity of the cell membrane, it is possible that by altering membrane fluidity of HIV-1, virus 1 is not able to bind to cell-receptor sites. Cell infection in most viruses requires that they bind to some part of the cell, and then enter the cell to place their DNA, or RNA, in the cell nucleus. If they cannot do this, the infectivity of the virus is markedly reduced.

Vitamin E and NF kappa B

Much of the body’s inflammation is mediated by a cellular compound known as nuclear factor kappa B. These proteins are a family of eukaryotic transcription factors that are involved in the control of a large number of normal cellular processes, such as immune and inflammatory responses, developmental processes, cellular growth and apoptosis. These transcription factors are very active in a number of disease states, such as cancer, arthritis, chronic inflammation, asthma, neurodegenerative diseases and heart disease.

You should be aware of this process because it involves the tocotrienols and a major pathway to tumorogenesis. Very little is known about tocotrienols, but a recent research article investigated the role a-tocotrienol had on the NF-kB pathway. Their results showed that ?-tocotrienol completely abolished NF-kB activation, while a similar dose of a tocopherol was noted to have no effect. Their results show that ?-tocotrienol suppressed the NF-kB activated by a variety of stimuli, suggesting that it acts at a step common to all these activators, but equally important, they found that atocotrienol blocked the activation of NF-kB without directly interfering with the DNA binding of NF-kB. This is very important since NF-kB is critical to many normal body defense functions.

In summary, vitamin E functions depend on its antioxidant ability, which means vitamin E stops free radicals propagations. It helps to protect the nervous system, the musculoskeletal system and the retinas. It is believed to reduce lipid peroxidation in cells and proteins, to protect DNA, and to help prevent cancer and arteriosclerosis.

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