Vitamin E has shown promise as a possible cardioprotective agent. In particular, D-alpha tocopherol, the most biologically active isomer in the vitamin E family, has been shown to decrease the risk of myocardial infarction, particularly in those with existing cardiovascular disease. The role of vitamin E in cardioprotection is thought to be one of an antioxidant, and this makes logical sense because the primary role of vitamin E in human physiology is one of a lipid soluble reducing agent. Vitamin E accumulates in cell membranes where it protects the lipids from peroxidation thus decreasing damage to cell membrane. Vitamin E is known to accumulate in the cell membranes of those cells in the cardiovascular system including the blood cells and endothelial cells of the arteries. Here it could potentially decrease oxidative stress and thus protect the cells of the cardiovascular system from damage. Molecular experiments using rats and other rodents have provided most of the mechanistic data for such a hypothesis.
For example, in one study1, the ability of rabbit aortas to synthesis the eicosanoid prostacyclin PGI2 was investigated. Prostacyclin PGI2 is synthesised in tissues of the cardiovascular system where it causes a decrease in platelet aggregation and also causes vasodilation. Rabbits were fed differing intakes of vitamin E in order to change the concentrations of alpha-tocopherol in the cells of their cardiovascular system. In this regard one group of rabbits were fed a normal control diet containing adequate vitamin E, another group were fed a vitamin E depletion diet, while a third group were fed a vitamin E depletion diet, followed by a repletion diet to restore vitamin E intake to control levels. The presence of PGI2 was confirmed through detection of a stable metabolite, 6-keto PGF1α. The results showed that rabbits deficient in vitamin E synthesised significantly less PGI2 than control animals, and repletion of vitamin E for 48 hours returned PGF1α to normal levels, indicating that PGI2 activity had been restored.
Therefore the PGI2 synthesis in the aorta of rabbits may be influenced by the presence of vitamin E. Human studies investigating the effects of vitamin E have shown positive effects for alpha tocopherol. However, controversy does still surround this issue, and the inconsistent findings may relate to methodological inconsistencies between studies. In this regard many studies have used high levels of synthetic vitamin E, chemically designated the DL-alpha tocopherol form. This can be problematic for a number of reasons, most notably the fact that high levels of alpha tocopherol can decrease plasma levels of other important cardioprotective vitamin E isomers, particularly the tocotrienols and gamma-tocopherol. The synthetic version of vitamin E, as used in this study, does not have the same biological activity as the natural D-alpha form. Therefore it is not clear if the isolated effects of the synthetic vitamin E in this study would have overall benefits because other aspects of cardiovascular health may have been detrimentally affected.
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