vitamin E....Properties and Uses

vitamin E....Properties and Uses

In recent years, consumers have been advised to use polyunsaturated fats instead of saturated fats in order to reduce the risk of heart disease. Some preliminary data suggest that this advice is having a favorable impact in reducing the risk of heart disease. It has been reported that in animals, the dietary need for vitamin E increases when the intake of polyunsaturated fatty acids becomes greater. Nutrition scientists have established that cellular membranes containing polyunsaturated fats are more easily damaged by free radicals than those which contain saturated fats. In order to protect membranes which contain high levels of polyunsaturated fats, the increased consumption of vitamin E is not only justified but essential.

In chickens, selenium deficiency causes poor absorption of vitamin E from the digestive tract. Vitamin E enhances the cancer preventive effect of selenium on chemical-induced breast cancer in rats. The relevance of this observation in humans has not been evaluated as yet.

Both vitamin E and zinc act as a stabilizer of cellular membranes. Red blood cells from zinc - or vitamin E-deficient animals are easily broken by free radicals. Supplementation of diets with either vitamin E or zinc makes these membranes more resistant to free radical attack. Zinc-deficient diets cause skin and joint damage in the chicken. Dietary supplementation with high vitamin E doses prevents the above harmful effects of zinc deficiency. These studies suggest that some effects of vitamin E and zinc on cells are similar.

The exposure of vitamin E to iron and copper enhances the destruction of vitamin E. It has been reported that in low birth weight infants, administration of iron may cause the development of vitamin E deficiency anemia, particularly in those infants who were fed formula containing higher levels of polyunsaturated fatty acids.

Vitamin C protects vitamin E from the harmful effects of iron and copper as well as helps to regenerate vitamin E immediately after it has been destroyed by free radicals. During vitamin E deficiency, the levels of vitamin A (retinol and retinyl esters) in liver and retinol in plasma decrease. These levels are increased during alpha tocopherol supplementation. The consumption of higher levels of dietary vitamin A increase the need for vitamin E in the body. Most human studies suggest that the consumption of vitamin E is essential for efficient vitamin A utilization and liver storage. Vitamin E deficiency may also cause deficiency of vitamin B-12. Thus the alterations in the level of vitamin E may effect the levels of other vitamins such as vitamins A, C and B-12.

Vitamin E has been shown to interact with some pollutants which are present in the environment and diet. The primary atmospheric pollutants are ozone and nitric oxide which are capable of generating free radicals in the body. Vitamin E has been shown to protect against the harmful effect of ozone and nitric oxide. The major food pollutants are nitrites which are present in fresh fruits and vegetables as well as in bacon, sausage and cured meat. Nitrites by themselves are not harmful to adults, but they can combine with amines in the stomach to form nitrosamine. Nitrosamines are among the most potent cancer causing agents for both animals and human beings. The presence of vitamin C or vitamin E in the stomach may prevent the formation of or reduce the levels of nitrosamines. Taking vitamin C or E before eating fresh fruits and vegetables that contain high levels of nitrites is not needed, because they contain another group of chemicals called phenolics, which, like vitamin E, act as an antioxidant and can prevent the formation of nitrosamines. However, it is important to take vitamin E just before eating bacon, sausage, or cured meat in order to prevent the formation of nitrosamines.

In addition to nitrosamines, many other mutagenic substances (agents which cause genetic changes) are formed in the digestive tract. All mutations do not cause cancer, but all cancers are preceded by mutations. It has been shown that the levels of mutagenic substances in the feces are higher for persons who are meat eaters than for those who are vegetarians. The presence of higher levels of fecal mutagenic substances may increase the risk of some cancers. It has been reported that taking vitamin E or vitamin C reduces the mutagenic substances in the feces. Furthermore, reports indicate that taking both vitamin E and C is more effective than taking either individually.

Many chemicals are not carcinogenic until they are converted to an active form in the body. In some cases vitamin E can prevent the conversion of inactive forms of such cancer causing substances to active forms. Vitamin E also prevents the action of tumor promoting and tumor initiating agents which are present in the environment and diet.

Vitamin E influences the effectiveness of many drugs which are currently used in cancer treatment. The above concept has been demonstrated on cancer cells in vitro. For example, vitamin E acetate in combination with vincristine, 5-fluorouracil, adriamycin, or cholorozotocin produced a synergistic effect, whereas vitamin E in combination with bleomycin, 1-2-cholrethyl)-3-cyclohexyl-1-triazeno-imidazole-4-carboxamide (DIIC), mutamycin or cis-diamine) dichloro-platiumn 11 (cis-platiumn 11) produces an additive effect on the inhibition of growth of neuroblastoma cells in vitro. In glioma cell cultures, vitamin E acetate in combination with vincristine or CCNU produced a synergistic effect whereas vitamin E in combination with bleomycin, 5-fluoracil, adriamycin, DTIC, mutamycin and cis-platinum produced an additive effect on the inhibition of growth. These studies suggest that the effectiveness of the interaction of vitamin E with cancer chemotherapeutic drugs depends upon tumor form and type of drug. Vitamin E succinate also enhances the effect of some naturally occurring substance such as prostaglandins and sodium butyrate on neuroblastoma cells in vitro. The relevance of the above results in humans is not known at this time.

Several experimental studies have been reported that vitamin E protects normal tissue against radiation damage; however, higher doses of vitamin E succinate enhance the effect of radiation on cancer cells in vitro. In addition, vitamin E succinate markedly reduces the occurrence of radiation induced cancer in vitro. High doses of vitamin E succinate also enhance the effect of heat on cancer cells in vitro. The above effects of vitamins have not been tested on humans as yet.

Vitamin E protects cells from the toxicity of certain heavy metals. For example, organic mercury is known to cause neurological diseases because of damage to the brain cells. The administration of vitamin E immediately before treatment of animals with organic mercury markedly reduces the symptoms of brain damage in rats, mice and quail. Vitamin E succinate also protects glia cells, one of the cell types present in brain, in vitro against organic mercury-induced toxicity.

Only selenium appears to enhance the effect of vitamin E on the prevention of chemical-induced cancer in vitro.

Vitamin E administration has been useful in the treatment of those disease in humans which are due to vitamin E deficiency. Vitamin E acetate (400 IU) has been shown to be useful in the treatment of cystic mastitis, the most common cancerous growth of the breast in females. Vitamin E acetate (1600 IU/day) before the administration of adriamycin reduces its toxic effect in patients with cancer. This is consistent with the animal studies in which vitamin E has been shown to reduce the toxic effects of adriamycin on heart and skin. Vitamin E also protects against lung damage in animals produced by bleomycin, a commonly used drug in the treatment of cancer. One study reports that vitamin E therapy reduces some of the symptoms of premenstrual syndrome.

Several animal and a few human studies have suggested that vitamin E may be useful in the prevention of some human cancer. Currently, the effect of oral intake of vitamin E (400 to 800 IU/day) in the form of alpha tocopherol, alpha tocopheryl acetate or alpha tocopheryl succinate on the risk of developing some forms of cancer among the high risk human populations is being studies.

Vitamin E may reduce lung damage produced by cigarette smoke. There is increasing evidence that free radicals are generated in the lung by the substances which are present in the cigarette smoke. These free radicals are responsible for increasing the risk of lung cancer well as of emphysema (a chronic lung disease in which breathing becomes difficult). The level of vitamin E in the fluid surrounding lung tissue is six times less among smokers in comparison to those who do not smoke. The presence of higher levels of vitamin E in these fluids or in lung tissue may protect lungs from the attack of free radicals.

Vitamin E may have a role in the management of some neurological diseases. A group of neurologists are initiating a new clinical study using vitamin E in combination with deprenyl in order to slow down the progression of disease in patients with Parkinsonism. It is believed that free radicals are generated by degradation products of dopamine (a chemical which is essential for brain function) and by drugs used in the treatment of Parkinson's Disease.

There are very limited animal studies regarding the use of vitamin E in the management of cancer. One clinical study has utilized high intravenous doses (up to 2 grams per day) of alpha tocopherol in the treatment of 1V Stage metastic neuroblastomas. The objective regression was observed in 50% of treated patients. Preliminary data suggest that vitamin E can help in the management of cancer in more than one way. It can kill tumor cells, enhance the effect of tumor therapeutic agents (drug, radiation and heat), reduce their toxic effect and enhance the immune functions. Numerous animal and one human study suggest that high doses of vitamin may enhance the body's immune defense system. More human studies are needed to evaluate the rate of vitamin E in the treatment of cancer.

Free radicals have been implicated in accelerating the aging processes of organisms as well as individual organs in the body. Therefore, the supplemental use of vitamins on a regular basis should slow down aging processes. This hypothesis has not been adequately tested in humans or animals. In vitro data show that the addition of vitamin E increases the survival of nerve cells.