CAS 4345-03-3

Molecular Weight	530.8 g/mol
Molecular Formula	C₃₃H₅₄O₅
XLogP3	10.2
Hydrogen Bond Donor Count	1
Hydrogen Bond Acceptor Count	5
Rotatable Bond Count	17
Exact Mass	530.39712482 g/mol
Monoisotopic Mass	530.39712482 g/mol
Topological Polar Surface Area	72.8 Å²
Heavy Atom Count	38
Formal Charge	0
Complexity	720
Isotope Atom Count	0
Defined Atom Stereocenter Count	3
Undefined Atom Stereocenter Count	0
Defined Bond Stereocenter Count	0
Undefined Bond Stereocenter Count	0
Covalently Bonded Unit Count	1

Molecular Weight

530.8 g/mol

Molecular Formula

C₃₃H₅₄O₅

XLogP3

10.2

Hydrogen Bond Donor Count

Hydrogen Bond Acceptor Count

Rotatable Bond Count

Exact Mass

530.39712482 g/mol

Monoisotopic Mass

530.39712482 g/mol

Topological Polar Surface Area

72.8 Å²

Heavy Atom Count

Formal Charge

Complexity

720

Isotope Atom Count

Defined Atom Stereocenter Count

Undefined Atom Stereocenter Count

Defined Bond Stereocenter Count

Undefined Bond Stereocenter Count

Covalently Bonded Unit Count

Without further evidence to suggest otherwise, alpha-tocpherol succinate is generally believed to undergo a logical de-esterification in the gastrointestinal tract before being subsequently absorbed as free tocopherol. The free alpha-tocopherol is therefore available and capable of the following activities. Vitamin E's antioxidant capabilities are perhaps the primary biological action associated with alpha-tocopherol. In general, antioxidants protect cells from the damaging effects of free radicals, which are molecules that consist of an unshared electron. These unshared electrons are highly energetic and react rapidly with oxygen to form reactive oxygen species (ROS). In doing so, free radicals are capable of damaging cells, which may facilitate their contribution to the development of various diseases. Moreover, the human body naturally forms ROS when it converts food into energy and is also exposed to environmental free radicals contained in cigarette smoke, air pollution, or ultraviolet radiation from the sun. It is believed that perhaps vitamin E antioxidants might be able to protect body cells from the damaging effects of such frequent free radical and ROS exposure. Specifically, vitamin E is a chain-breaking antioxidant that prevents the propagation of free radical reactions. The vitamin E molecule is specifically a peroxyl radical scavenger and especially protects polyunsaturated fatty acids within endogenous cell membrane phospholipids and plasma lipoproteins. Peroxyl free radicals react with vitamin E a thousand times more rapidly than they do with the aforementioned polyunsaturated fatty acids. Furthermore, the phenolic hydroxyl group of tocopherol reacts with an organic peroxyl radical to form an organic hydroperoxide and tocopheroxyl radical. This tocopheroxyl radical can then undergo various possible reactions: it could (a) be reduced by other antioxidants to tocopherol, (b) react with another tocopheroxyl radical to form non-reactive products like tocopherol dimers, (c) undergo further oxidation to tocopheryl quinone, or (d) even act as a prooxidant and oxidize other lipids. In addition to the antioxidant actions of vitamin E, there have been a number of studies that report various other specific molecular functions associated with vitamin E. For example, alpha-tocopherol is capable of inhibiting protein kinase C activity, which is involved in cell proliferation and differentiation in smooth muscle cells, human platelets, and monocytes. In particular, protein kinase C inhibition by alpha-tocopherol is partially attributable to its attenuating effect on the generation of membrane-derived dialglycerol, a lipid that facilitates protein kinase C translocation, thereby increasing its activity. In addition, vitamin E enrichment of endothelial cells downregulates the expression of intercellular cell adhesion molecule (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), thereby decreasing the adhesion of blood cell components to the endothelium. Vitamin E also upregulates the expression of cytosolic phospholipase A2 and cyclooxygenase-1. The increased expression of these two rate-limiting enzymes in the arachidonic acid cascade explains the observation that vitamin E, in a dose-dependent fashion, enhanced the release of prostacyclin, a potent vasodilator and inhibitor of platelet aggregation in humans. Furthermore, vitamin E can inhibit platelet adhesion, aggregation, and platelet release reactions. The vitamin can also evidently inhibit the plasma generation of thrombin, a potent endogenous hormone that binds to platelet receptors and induces aggregation of platelets. Moreover, vitamin E may also be able to decrease monocyte adhesion to the endothellium by downregulating expression of adhesion molecules and decreasing monocyte superoxide production. Given these proposed biological activities of vitamin E, the substance continues to generate ongoing interest and studies in whether or not vitamin E can assist in delaying or preventing various diseases with any one or more of its biologic actions. For instance, studies continue to see whether vitamin E's ability to inhibit low-density lipoprotein oxidation can aid in preventing the development of cardiovascular disease or atherogenesis. Similarly, it is also believed that if vitamin E can decrease the chance of cardiovascular disease then it can also decrease the chance of related diabetic disease and complications. In much the same way, it is also believed that perhaps the antioxidant abilities of vitamin E can neutralize free radicals that are constantly reacting and damaging cellular DNA. Furthermore, it is also believed that free radical damage does contribute to protein damage in the ocular lens - another free radical-mediated condition that may potentially be prevented by vitamin E use. Where it is also suggested that various central nervous system disorders like Parkinson's disease, Alzheimer's disease, Down's syndrome, and Tardive Dyskinesia possess some form of oxidative stress component, it is also proposed that perhaps vitamin E use could assist with its antioxidant action. There have also been studies that report the possibility of vitamin E supplementation can improve or reverse the natural decline in cellular immune function in healthy, elderly individuals. As of this time, however, there is either only insufficient data or even contradicting data (where certain doses of vitamin E supplementation could even potentially increase all-cause mortality) on which to suggest the use of vitamin E could formally benefit in any of these proposed indications. Furthermore, there are ongoing studies that demonstrate alpha-tocopherol succinate's unique possession of capabilities that allow it to induce differentiation, inhibit proliferation and apoptosis in cancer cells, enhance the growth-inhibitory effect of ionizing radiation, hyperthermia, and some chemotherapeutic agents and biological response modifiers on tumor cells, all the while protecting normal cells against any adverse effects. Despite being able to demonstrate such effects on animal and human cells in culture, the value of these effects has not drawn significant attention from researchers and clinicians and nor has the specific mechanisms of action been elucidated. Additionally, other studies have also shown that alpha-tocopherol succinate seemingly possesses an ability exclusive from other tocopherol esters to inhibit and minimize prostaglandin E2 production in human lung epithelial cells. Considering increased prostaglandin E2 production has been observed frequently in lung cancer patients, there may be another avenue in which alpha-tocopherol succinate may be able to treat lung cancer. Nevertheless, the possibility of such activity requires further elucidation.

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