Antioxidant effect
Alpha-tocopherol is found in all biological membranes of animal cells. As a lipid-soluble antioxidant, its major biological function is to prevent the destruction of polyunsaturated fatty acids-omega-3 fatty acids (such as alpha-linolenic acid, EPA, and DHA) and omega-6 fatty acids (such as linoleic acid, gamma-linolenic acid, and arachidonic acid)-in tissues, cells, cell organelles, and artificial systems by lipid peroxidation, thus protecting membrane lipids, lipoproteins, and depot lipids. Vitamin E, as an electron acceptor, has the ability to bind lipid peroxyl radicals and thus interrupt the chain reaction in the peroxidation of polyunsaturated fatty acids. In a chain reaction, as a result of a radical attack, membrane lipids become lipid radicals by splitting off a hydrogen atom. The latter react with oxygen and are converted to peroxyl radicals. Subsequently, the peroxyl radicals remove a hydrogen atom from further fatty acids, which in turn radicalize them. The end products of lipid peroxidation include malondialdehyde or 4-hydroxynonenal, which exhibit strong cytotoxic effects and can alter DNA. Vitamin E inhibits the radical chain reaction by donating a hydrogen atom and becoming a radical itself. The vitamin E radical is exceedingly inert due to resonance stabilization and cannot continue lipid peroxidation due to its location in the cell membrane. Vitamin E – in the lipid phase of biological systems – and antioxidants, such as vitamin C, coenzyme Q10 and glutathione – in the aqueous phase of biological systems – act synergistically in protecting membranes against lipid peroxidation. Accordingly, tocopherols and antioxidants exhibit a joint effect and promote each other. Vitamin C, coenzyme Q10, and glutathione possess the ability to regenerate vitamin E. For this purpose, they take over the radical of tocopherol and inactivate it via peroxidases, catalases and superoxide dismutases. Vitamin C present in the aqueous medium of the cytosol converts vitamin E radicals, previously “tipped” from the lipid phase into the aqueous phase, into vitamin E with the formation of dehydroascorbic acid or by glutathione. Subsequently, vitamin E “flips” back to the lipophilic phase to be effective again as an antioxidant.
Influence on both cellular signaling and interactions between blood components and the endothelial cell membrane:
- Vitamin E inhibits protein kinase C activity and thus the new formation or proliferation of smooth muscle cells, platelets (thrombocytes), and monocytes (white blood cells).
- By enrichment of vitamin E in the endothelial cells, the cholesterol is protected from oxidation (provided there is sufficient vitamin C for the regeneration of vitamin E available) – as a result, there is a reduction in the synthesis of adhesion molecules (ICAM, VCAM), which prevents both the adhesion of blood cells and their accumulation or accumulation to minimal intimal lesions of the arteries
Protection against autoimmune processes of the musculoskeletal system:
- Vitamin E in sufficient amounts prevents the oxidation of phospholipids in the cell membrane and thus the oxidation of arachidonic acid – this prevents arachidonic acid altered by oxidation from promoting the formation of reactive eicosanoids, such as leukotrienes, thromboxanes, and prostaglandins, which promote, among other things, vasoconstriction, blood clotting disorders, inflammation, and the rapid progression of rheumatoid diseases
- Immunomodulatory effect – vitamin E increases the production of cellular and humoral defenses.
Effects of vitamin E under discussion:
- Protective influence on the nervous system, retina (retinal), protein biosynthesis (new protein formation), and neuromuscular system.
- Anti-inflammatory effect (attributed to the antioxidant effect of vitamin E – especially the suppression of the formation of unfavorable eicosanoids).
- Antithrombotic effect (e.g., inhibition of protein kinase C activity prevents proliferation of both platelets (blood clots) and monocytes, thus preventing blood clotting disorders and thrombosis (blood vessel occlusion)).
