Tocopherol quinones

Lipid radicals and other radicals may be removed by a number of endogenous compounds as well as GSH. One is vitamin E, (which includes a-tocopherol) a lipophilic substance. It can react with and neutralize lipid radicals and hydroperoxides, in the process becoming a free radical itself. This a-tocopheryl radical is relatively stable and can then be converted back into the a-tocopherol by vitamin C (ascorbate) or react with more radicals and become a-tocopherol quinone ... 

Antagonists of vitamin K substances include dicoumarol, sulfonamides, antibiotics, a-tocopherol quinone, dihydroxysteanc acid glycide, salicylates, iodinin, warfarin. Synergists include ascorbic acid, somatotropinn (growth hormone), and vitamins A and E. 

In human subjects, however, 8 weeks of vitamin E supplementation (800 IU/day) to the diet produced a lowered plasma PGI2 level, as measured by 6-keto-PGF1(X, compared with that in non-supplemented controls [129]. Addition of vitamin E to human platelets in concentrations which resemble normal plasma levels produced a moderately potent but consistent reduction in cyclo-oxygenase activity, with a dose-dependent response up to 1 mM. a-Tocopherol quinone was equally effective in this test [ 130]. 

Infante JP (1999) A function for the vitaminE metabolite alpha-tocopherol quinone as an essential enzyme cofactor for the mitochondrial fatty acid desaturases. FEES letters 446, 1-5. 

Figure 4.3. Reaction of tocopherol with hpid peroxides the tocopheroxyl radical can he reduced to tocopherol or undergo irreversihle onward oxidation to tocopherol quinone.

Lipid radicals and other radicals may be removed by a number of endogenous compounds as well as glutathione. One is vitamin E (a-tocopherol), which reacts with lipid hydroperoxide radicals to yield the hydroperoxide and a-tocopherol quinone ... 

Tocopherols behave as chain breaking antioxidants by competing with the substrate (RH) for the chain peroxyl radicals (ROO ) that are normally present in the highest concentration in the system. Tocopherols donate hydrogen to a peroxyl radical resulting in an a-tocopherol semiquinone radical (reaction 1). This may further donate hydrogen to produce methyl tocopherol quinone or react with another a-tocopheryl semiquinone radical (reactions 2 and 3) to produce an a-tocopherol dimer which also possesses antioxidant activity. ... 

Studies of the metabolism of vitamin E were triggered by the observations of Alaupovic and coworkers [126, 127]. When " [Cj-D-a-tocopherol-5-methyl was administered to rats or pigs and attempts were made to detect metabolic derivatives, two compounds were separated by chromatography. One of the compounds is " [C]-D-a-tocopherol quinone the other is either a dimer or a trimer of a-tocopherol. The dimer and trimer are terminal oxidation products of a-tocopherol and are excreted in the bile. a-Tocopherol quinone can be converted to a-hydroquinone. a-Tocopherol hydroquinone may be esterified in liver and eliminated in the feces after concentration in the bile and excretion in the intestine, or it may be oxidized in the kidney to a-tocopheronic acid, which may be converted into an a-tocopheronolactone conjugate, which is excreted in the urine. In conclusion, vitamin E is excreted as such in the urine or the bile after conversion to a dimer or a trimer, in the form of a conjugated hydroxy-quinone or tocopheronic acid (see Fig. 4-43). 

Among the metabolites identified, a-tocopherol quinone seems to be the active compound. That compound is known to participate in photosynthetic electron transport in chloroplasts, but there is no evidence that it functions on an active vitamin E. In fact, no available evidence indicates that a metabolite of the vitamin constitutes the active form. 

Standards a-, P-, y-, and 8-Tocopherols, tocopherol quinones, tocopherol hydroquinones TMS derivatives GC-MS Rtx-5MS column, temperature 220-290°C 0-15 ng tocopherols 40 pg/pL for all tocopherols Melchert et al. (2002)... 

Interest in the role of vitamin E in disease prevention has encouraged the search for reliable indices of vitamin E status. Most studies in human subjects make use of static biomarkers of status, usually a-tocopherol concentrations in plasma, serum, erythrocytes, lymphocytes, platelets, lipoproteins, adipose tissues, buccal mucosal cells, and LDL, and the a-tocopherol 7-toco-pherol ratio in serum or plasma. Other markers of vitamin E status include susceptibility of erythrocyte or plasma LDL to oxidation, breath hydrocarbon exhalation, and the concentration of a-tocopherol quinone in cerebrospinal fluid. There is no consensus as to the threshold concentration of plasma or sermn a-tocopherol at which a person can be defined as having inadequate tocopherol status, but values of <11.6, 11.6-16.2, and >16.2 pmol are normally regarded as indicating a deficient, low, and acceptable vitamin E status, respectively. It is recommended that... 

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