Physiology Sponsored by
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.
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.
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.