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At least 19 recordsLinked to original sources
PubMed1997

Bioavailability of alpha-tocopherol fed with retinol and relative bioavailability of D-alpha-tocopherol or DL-alpha-tocopherol acetate.

Two experiments were conducted to examine the effects of the form of alpha-tocopherol or interactions of alpha-tocopherol with vitamin A on its bioavailability. In Experiment 1, Holstein steers were fed a diet that was low in vitamins A and E for 1 mo; then, steers were blocked by body weight (X = 97.5 kg) and assigned randomly to one of four oral treatments: 1) no added vitamins, 2) 442 mg of retinyl acetate, 3) 1342 mg of D-alpha-tocopherol, or 4) 442 mg of retinyl acetate and 1342 mg of D-alpha-tocopherol. Each treatment was given as a pulse dose. Blood was sampled over a 36-h period. Concentrations of plasma retinyl palmitate peaked at 2 to 6 h postsupplementation for all calves and then peaked again at 22 to 28 h for calves receiving vitamin supplements. Concentrations of plasma alpha-tocopherol peaked earliest with D-alpha-tocopherol supplementation alone at 12 to 20 h after supplementation, but simultaneous supplementation with retinyl acetate resulted in lower plasma alpha-tocopherol concentrations. Plasma retinyl palmitate decreased during peak alpha-tocopherol concentrations. In Experiment 2, blood and tissue were analyzed after a single gastric tube administration of a powder (DL-alpha-tocopheryl acetate) or a liquid (D-alpha-tocopherol) form of vitamin E to Holstein calves. Plasma and kidney concentrations of alpha-tocopherol were higher when calves were fed D-alpha-tocopherol than when calves were fed the DL-alpha-tocopherol acetate form. Concentrations in the liver, spleen, adipose tissue, heart, muscle, cellular blood fraction, and gut did not differ between the two forms.

Animals↗
PubMed1994

Human adipose alpha-tocopherol and gamma-tocopherol kinetics during and after 1 y of alpha-tocopherol supplementation.

Alpha-tocopherol and gamma-tocopherol were monitored in human adipose by using needle biopsies in four subjects during a 1-y supplementation trial with 800 mg all-rac-alpha-tocopherol/d, and for 1 additional year after cessation of supplement. Some increase in adipose alpha-tocopherol (per milligram adipose cholesterol) and a more consistent decrease in gamma-tocopherol were observed during the supplementation period. The alpha-tocopherol/gamma-tocopherol ratio rose consistently during supplementation and fell only gradually after the supplement was stopped. We estimate that > or = 2 y are required for the alpha-tocopherol/gamma-tocopherol ratio to reach a new steady state after a change in alpha-tocopherol intake. In a cross-sectional measurement in five subjects who reported long-term use of alpha-tocopherol supplements (> or = 250 mg/d), and in five other subjects who reported no supplement use, the adipose alpha-tocopherol/gamma-tocopherol ratio clearly discriminated between the two groups (P < 0.002). This ratio may be of value in ranking individuals according to long-term alpha-tocopherol intake.

Adipose Tissue↗
PubMed1990

Comparative evaluation of the antioxidant activity of alpha-tocopherol, alpha-tocopherol polyethylene glycol 1000 succinate and alpha-tocopherol succinate in isolated hepatocytes and liver microsomal suspensions.

The antioxidant activity of alpha-tocopherol polyethylene glycol 1000 succinate (TPGS) and of alpha-tocopherol succinate (TS) has been examined in isolated hepatocytes and microsomal fractions from rat liver. Both TPGS and TS require esterase activity to yield free alpha-tocopherol and, hence, antioxidant activity. TPGS and TS consistently exerted a more effective antioxidant protection than an equivalent amount of directly-added free alpha-tocopherol. The low antioxidant efficiency of directly added free alpha-tocopherol in such water-based experimental systems as used here seems to be due to its extreme hydrophobicity. TPGS, on the other hand, is an extremely hydrophilic compound that is being examined as a useful source of alpha-tocopherol in certain clinical situations and is here shown to be a convenient and effective source for experimental studies into lipid peroxidation and antioxidant mechanisms.

Animals↗
PubMed1985

Red blood cell tocopherol and liver tocopherol in hyperlipemic rats as compared with plasma tocopherol.

In rats with hyperlipemia induced by Triton WR-1339, changes in tocopherol concentrations in plasma and RBC were compared with those in the liver and its subcellular fractions, microsomes and mitochondria. After daily injection with Triton, plasma total lipids at 3 days and 7 days, respectively, showed elevations 6.5 times and 15 times as high as those in the control rats, and triglycerides showed the most predominant elevation. With the hyperlipemia, the concentrations of tocopherol in RBC and the subcellular fractions decreased, as plasma lipids and plasma tocopherol increased, while no change occurred in tocopherol concentrations in liver homogenates. The changes in the ratio of tocopherol to total lipids in plasma coincided with changes in tocopherol concentrations in the RBC and subcellular fractions.

Animals↗
PubMed1988

Stopped-flow investigation of antioxidant activity of tocopherols. Finding of new tocopherol derivatives having higher antioxidant activity than alpha-tocopherol.

Second-order rate constants, kappa s, for H-atom abstraction by phenoxyl radicals from five tocopherol (vitamin E) derivatives have been measured spectrophotometrically at 25.0 degrees C by the stopped-flow method, as a model reaction of tocopherols with unstable free radicals (LOO., LO., and HO.) in biological systems. Three new tocopherol derivatives with a five-membered heterocyclic ring were found to be 1.9-2.1 times more active than the alpha-tocopherol which has the highest antioxidant activity among natural tocopherols. The proton hyperfine splittings for the five tocopheroxyl radicals derived from these tocopherols by the reaction with phenoxyl were also determined by ESR measurements.

Antioxidants↗
PubMed1991

Comparison of plasma alpha- and gamma-tocopherols after oral and intramuscular administration of RRR-alpha-tocopherol or RRR-gamma-tocopherol to weanling pigs.

Equimolar amounts of either RRR-alpha-tocopherol (alpha-TOH) or RRR-gamma-tocopherol (gamma-TOH) were given as single doses orally and, as water-based emulsions, by intramuscular (i.m.) injection to weanling pigs. Venous blood was sampled at regular intervals and plasma was analyzed for comparison of alpha-TOH and gamma-TOH kinetics. Irrespective of the method of application no significant differences were found between alpha-TOH and gamma-TOH in (a) the maximum increase above initial concentration (delta C), (b) the time of peak concentration (tmax), and (c) the time from half-maximum concentrations on the ascending and the descending parts of the plasma curve. However, alpha-TOH was retained longer in plasma than gamma-TOH, and the areas-under-curve from Oh to 24 h and from Oh to 48 h (AUC0-24 and AUC0-48) were significantly greater for alpha-TOH. In diarrheic pigs given oral gamma-TOH, tmax was prolonged, delta C was lower and AUC0-24 and AUC0-48 were reduced compared with healthy pigs (p less than 0.05). The results indicate that pigs absorb both vitamers to a similar extent but that gamma-TOH is eliminated from plasma more rapidly.

Absorption↗
PubMed1997

Graded dietary levels of RRR-gamma-tocopherol induce a marked increase in the concentrations of alpha- and gamma-tocopherol in nervous tissues, heart, liver and muscle of vitamin-E-deficient rats.

The effect of dietary RRR-gamma-tocopherol supplementation on serum and tissue alpha- and gamma-tocopherol concentrations was studied in vitamin-E-deficient rats fed diets containing adequate levels of RRR-alpha-tocopherol and graded levels of RRR-gamma-tocopherol over a 60 day period. Feeding rats with a RRR-alpha-tocopherol-supplemented diet induced in forebrain, sciatic endoneurium, skeletal muscle, heart and liver a marked increase in alpha-tocopherol concentration. In contrast, feeding rats with a diet containing the same level of RRR-gamma-tocopherol induced a small increase in gamma-tocopherol concentrations in brain, sciatic endoneurium, skeletal, muscle, heart and liver and a slight but significant decrease in alpha-tocopherol concentration in all tissues examined. In rats fed diets containing a constant level of RRR-alpha-tocopherol and graded levels of RRR-gamma-tocopherol, the concentrations of alpha-tocopherol in all tissues were much higher than those in rats fed a control diet containing RRR-alpha-tocopherol alone. The higher the gamma/alpha ratio, the more the alpha-tocopherol concentrations increased. Significant positive linear regressions were found between the gamma/alpha ratio and the alpha- and gamma-tocopherol concentrations in most of the tissues examined. These results indicate that when gamma-tocopherol was supplied continuously in the diet gamma-tocopherol accumulated significantly in the tissues but to a much smaller extent than when rats were fed with RRR-alpha-tocopherol. These experiments also indicate that gamma-tocopherol did not depress the serum and tissue alpha-tocopherol concentrations. On the contrary, gamma-tocopherol supplements induced a marked increase in alpha-tocopherol concentrations in the serum and tissues. These results suggest that there is a relationship between alpha- and gamma-tocopherol levels in vivo and that the biopotency of alpha-tocopherol should be reevaluated especially when high levels of gamma-tocopherol were present in the diet.

Animals↗
PubMed1987

Mechanisms of absorption, transport and tissue uptake of RRR-alpha-tocopherol and d-gamma-tocopherol in the white rat.

The metabolism of alpha- and gamma-tocopherol was studied in three groups of rats that were fed a modified AIN-76 diet containing normal (NE, 0.2 g alpha-tocopherol/kg), high (HE, 1.0 g alpha-tocopherol/kg) or low (LE, less than 0.02 alpha-tocopherol/kg) vitamin E for 3 mo. After 1, 2 and 3 d of an oral dose of 20 mg of alpha-tocopherol, gamma-tocopherol or both, the levels of the two vitamers were measured in plasma and tissues and in some cases in isolated microsomal and mitochondrial fractions from liver. Twenty-four hours after an oral dose of 20 mg gamma-tocopherol the levels of alpha-tocopherol in plasma and tissues remained constant and higher levels of gamma-tocopherol were found in tissues in which low alpha-tocopherol levels could be found such as in the LE group. In spite of this, it was enabled to remain there, after 2 and 3 d gamma-tocopherol had decreased levels in all tissues. When given in combination with alpha-tocopherol, the levels of gamma-tocopherol were lower than when gamma-tocopherol was given alone. Microsomes and mitochondria from livers of LE group bound five and nine times more alpha-tocopherol than gamma-tocopherol in rats dosed with equal amount of alpha- or gamma-tocopherol, respectively. These data indicate that the mechanisms that regulate the metabolism of vitamin E are highly specific for alpha-tocopherol. Moreover, the relative amount of alpha-tocopherol determined the levels of gamma-tocopherol in tissues. However, the retention of gamma-tocopherol in tissues did not depend on the presence of alpha-tocopherol.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorption↗
PubMed1996

[Vitamin E: comparison of efficiency of incorporation of alpha-tocopherol in the organs in comparison to gamma-tocopherol].

Refeeding rats deficient in vitamin E with alpha-tocopherol induces increased amount of this compound in brain, cerebellum, sciatic nerve and muscle. This increase is regular with time. The optimum level (corresponding to non-deficient animals) is not reached within 8 weeks after refeeding. Thus recovery is very slow for the nervous tissue (as it has been demonstrated for polyunsaturated fatty acids). In contrast, the optimum level is reached within 2 weeks for liver and serum. Refeeding rat deficient in vitamin E with gamma-tocopherol induces an increase of this compound in the liver, the plateau is reached within 2 weeks, but is clearly lower than the one obtained with alpha-tocopherol : approximately 4 times lower. In the muscle, the uptake is linear with time, the plateau is not reached within 8 weeks, its level is 4 times lower than with alpha-tocopherol. Important point : feeding animals deficient in vitamin E with gamma-tocopherol induces in the nervous system a level of gamma-tocopherol which is not the one of the residual alpha-tocopherol; the plateau is not reached within 8 weeks. In sciatic nerve and cerebellum (but not in the brain) increased amount of gamma-tocopherol as a function of time is parallel with a slight but significant reduction of the residual alpha-tocopherol. In another experiment, rats were fed a diet deficient with vitamin E until 60 days of age. From this age, they received a non deficient diet until 120 days. In all organs, increasing the ratio gamma/alpha tocopherol (with a constant amount of alpha-tocopherol) induces an increase of alpha-tocopherol. This result is unexpected, as it was possible to propose that gamma-tocopherol could reduce alpha-tocopherol utilisation by competition. Conversely, the presence of alpha-tocopherol seems to increase incorporation of gamma-tocopherol, except in brain and sciatic nerve. The presence of gamma-tocopherol seems to induce increased need of alpha-tocopherol. This specificity for alpha-tocopherol is very important in terms of nutrition and pharmacology. In fact, at least to preserve biological membranes, it is important to provide only alpha-tocopherol, and not other molecules.

Animals↗
PubMed1983

Biological activity of all-rac-a-tocopherol and RRR-a-tocopherol determined by three different rat bioassays.

The biological activity of 2 R, 4' R, 8' R-(RRR)-a-tocopherol and all-rac-a-tocopherol has been determined by 3 different bioassays: Resorption-gestation test, red blood cell hemolysis test and rat liver storage test. Expressed in relation to all-rac-a-tocopheryl acetate is found by the resorption-gestation test with the doses given in vegetable oil potency ratios of 0.79 for all-rac-a-tocopherol and 1.06 for RRR-a-tocopherol, by the red blood cell hemolysis test ratios of 0.85 for all-rac-a-tocopherol and 1.13 for RRR-a-tocopherol and by the rat liver storage test ratios of 1.03 for all-rac-a-tocopherol and 1.32 for RRR-a-tocopherol. Furthermore is by the resorption-gestation test found a potency ratio of 0.90 between RRR-a-tocopheryl succinate and all-rac-a-tocopheryl acetate. By the evaluation of these figures, most weight must be added to the results from the resorption-gestation test, as it involves the most complex biological mechanism of the 3 methods. The potency ratios found in this investigation are significantly lower than the currently accepted potency ratios of 1.10 between all-rac-a-tocopherol and all-rac-a-tocopheryl acetate, 1.49 between RRR-a-tocopherol and all-rac-a-tocopheryl acetate and 1.21 between RRR-a-tocopheryl succinate and all-rac-a-tocopheryl acetate (all values calculated from their corresponding acetate by multiplication with the ratio of the molecular weight), but the potency ratio between RRR-a-tocopherol and all-rac-a-tocopherol calculated from the 3 different bioassays does not deviate significantly from the currently accepted value of 1.36. It seems necessary to reconsider the biological activity of all-rac-a-tocopherol and RRR-a-tocopherol, and it is suggested to use a potency ratio of 0.80 between all-rac-a-tocopherol and all-rac-a-tocopheryl acetate and 1.0 between RRR-a-tocopherol and all-rac-a-tocopheryl acetate.

Animals↗
PubMed1997

The effect of alpha-tocopherol and beta-tocopherol on proliferation, protein kinase C activity and gene expression in different cell lines.

alpha-Tocopherol, but not beta-tocopherol, negatively regulates proliferation of A7r5 vascular smooth muscle cells at physiological concentration. The HeLa cell line was not affected whereas the Chinese hamster ovary cell line (CHO) was slightly inhibited by both alpha-tocopherol and beta-tocopherol. In A7r5 cells alpha-tocopherol inhibited protein kinase C activity, and this correlated with inhibition of proliferation. beta-Tocopherol did not inhibit either protein kinase C or proliferation. In HeLa cells no inhibition by alpha-tocopherol or beta-tocopherol of protein kinase C activity and cell proliferation was observed. In Chinese hamster ovary cells both tocopherols inhibited protein kinase C activity but not proliferation. Thus in the latter cells proliferation was not protein kinase C-dependent. In A7r5 cells alpha-tocopherol but not beta-tocopherol activated AP-1-mediated gene expression. In HeLa cells no change in gene expression was observed in agreement with the finding that also protein kinase C was not affected. In CHO cells gene-expression was activated by both alpha-tocopherol and beta-tocopherol. In this case also a positive correlation was found with similar inhibition of protein kinase C activity. In these cells, however, the changes at the level of protein kinase C activity and gene expression did not result in proliferation changes. The effect of alpha-tocopherol and beta-tocopherol on protein kinase C activity and gene expression suggest a cause-to-effect relationship. Inhibition of proliferation, however, correlates in the case of A7r5 and HeLa cells but not in the case of CHO suggesting a different proliferation pathway for these cells.

Animals↗
PubMed1989

[The transformation of gamma-tocopherol to alpha-tocopherol in the animal organism; a generational study in rats].

The biosynthesis of alpha-tocopherol, the most effective vitamer among the vitamin E-group, is found only in higher plants and microorganisms. Due to the lack of the shikimate pathway, animals are not able to synthesize alpha-tocopherol. Also not found is a whole enteral synthesis; only the conversion of dimethyletocol to trimethyletocol seems to be possible. Using four generations of rats, we sought to determine: Is a transformation of gamma-tocopherol to alpha-tocopherol in the animal body possible? Are there any differences in the transformation rates in organs, tissues, or in the entire body along the generations? Does gut flora play any role in the conversion of gamma-tocopherol? Is it possible to increase the efficiency of the transformation by supplying additional CH3-groups? Wistar rats were fed a semisynthetic basal diet, supplemented with 78.8 mg DL-gamma-tocopherol/kg in the first three generations (F1-F3). In the fourth generation (F4), some of the animals were fed a vitamin E-free diet and gamma-tocopherol (approx. 1.5 mg on alternate days) was injected s.c. Two other groups of animals received the basal diet containing additional methionine (0.25%) or choline (0.45%), as well as gamma-tocopherol (as in F1-F3). alpha- and gamma-tocopherol were analyzed by HPTLC in the whole body and in serum, liver, heart, lung, gut, gonads, and feces. The ratio of alpha-/gamma-tocopherol (micrograms/micrograms) as transformation rate and vitamin E-biopotency (microgram alpha-tocopherol equivalents/g) were calculated. Growth and fertility were normal until the fourth generation; no abnormal developments could be recognized. alpha-tocopherol was found in the whole-body as well as in all tissues and organs. In the whole-body, vitamin E-biopotency decreased 25-70% in F2 and F3. On the other hand, the increase of the transformation rate of gamma- to alpha-tocopherol amounted to 23% (F2) and 168% (F3). Highest conversion rates were found in F2 and F3 for feces, followed by gonads and lungs; the lowest rates were found for serum and liver. Due to the s.c. injection of gamma-tocopherol, feces showed a four-times lower transformation rate in F4 than in F3. There was an increase in heart, gut, lung and serum for both transformation rate and vitamin E-biopotency. These parameters could be improved also by the additional supplements of methionine and choline. Both methyl-group-donators revealed nearly the same positive effect. The results show that the animal organism can adapt to gamma-tocopherol supply over generations.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Nascent VLDL from liver perfusions of cynomolgus monkeys are preferentially enriched in RRR- compared with SRR-alpha-tocopherol: studies using deuterated tocopherols.

The transport and secretion of vitamin E in lipoproteins have been studied in cynomolgus monkeys fed tocopherols labeled with different amounts of deuterium. The animals were fed a single dose of vitamin E containing 60 mumol of each 2R,4'R,8'R-alpha-(5,7-(C2H3)2)tocopheryl acetate (d6-RRR-alpha-tocopheryl acetate; alpha-tocopherol with natural stereochemistry), 2S,4'R,8'R-alpha-5-(C2H3)tocopheryl acetate (d3-SRR-alpha-tocopheryl acetate; alpha-tocopherol with unnatural stereochemistry), and 2R,4'R,8'R-gamma-(3,4-2H)tocopherol (d2-RRR-gamma-tocopherol; gamma-tocopherol with natural stereochemistry). Chylomicrons, as well as the other plasma lipoproteins, contained equal concentrations of all three tocopherols at the earliest time points after feeding suggesting that all three tocopherols were absorbed equally. At later times plasma lipoproteins became preferentially enriched in d6-RRR-alpha-tocopherol. This is likely to be due to hepatic secretion of VLDL (very low density lipoproteins) and other lipoproteins, which were enriched in d6-RRR-alpha-tocopherol, as demonstrated in the lipoproteins isolated from perfused livers that had been obtained 24 h following the administration of the deuterated tocopherols. Taken together these data demonstrate that the liver, not the intestine, is the likely site of discrimination between tocopherol isomers and that the liver secretes nascent lipoproteins preferentially enriched in d6-RRR-alpha-tocopherol.

Animals↗
PubMed1993

Gamma-tocopherol detoxification of nitrogen dioxide: superiority to alpha-tocopherol.

In the vitamin E group, alpha-tocopherol is generally considered to be the most potent antioxidant with the highest vitamin bioactivity, yet gamma-tocopherol is produced in greater amounts by many plants and is the principal tocopherol in the United States diet. This report describes a fundamental difference in the chemical reactivities of alpha-tocopherol and gamma-tocopherol with nitrogen dioxide (NO2), which leads to the formation of a nitrosating agent from alpha-tocopherol, but not from gamma-tocopherol. Nitric oxide (NO) is a major product of the reaction of gamma-tocopherol with NO2, while alpha-tocopherol reacts with NO2 to form an intermediate tocopheroxide analogue. The biological significance of gamma-tocopherol is suggested by limited epidemiological data as well as the observation that it is a more potent inhibitor than alpha-tocopherol of neoplastic transformation during the postinitiation phase in 3-methylcholanthrene-treated C3H/10T1/2 murine fibroblasts. This latter property suggests the superiority of gamma-tocopherol in a mammalian biological assay and a role for endogenous NO production in promotion of neoplastic transformation.

Animals↗
PubMed1985

Oral alpha-tocopherol supplements decrease plasma gamma-tocopherol levels in humans.

In a cross-sectional survey of 86 elderly persons, it was observed that subjects with elevated plasma alpha-tocopherol levels had depressed plasma gamma-tocopherol. Tocopherols were measured by both reverse-phase and normal-phase high performance liquid chromatography (HPLC). When eight human volunteers (age range 30-60) were given 1200 IU of all-rac-alpha-tocopherol daily for 8 wk, plasma gamma-tocopherol and beta-tocopherol decreased in all subjects. After supplementation, gamma-tocopherol values were typically 30-50% of initial values, and alpha-tocopherol values were typically 200-400% of initial values. These results suggest that intestinal uptake and/or plasma transport make more efficient use of alpha-tocopherol than of gamma- or beta-tocopherol. Moreover, the results indicate that the ratio of gamma- to alpha-tocopherol in plasma would be a more satisfactory index to measure compliance in trials involving supplementation with alpha-tocopherol.

Administration, Oral↗
PubMed1992

Suppression of hepatic prostaglandin F2 alpha in rats by dietary alpha-tocopherol acetate is independent of total hepatic alpha-tocopherol.

Groups of eight weanling female F344/N rats were fed semipurified diets that supplied 0, 50, 500, 5000, or 15,000 mg alpha-tocopherol acetate/kg diet, with and without 0.05% phenobarbital (PB) for 9 weeks. Both plasma and hepatic alpha-tocopherol levels, measured by HPLC, strongly correlated with alpha-tocopherol intake (r greater than 0.73, p less than 0.0001). Phenobarbital both depleted hepatic alpha-tocopherol and increased plasma alpha-tocopherol significantly. Although treatment with PB for 9 weeks significantly increased GST activity, PB did not affect hepatic prostaglandin (PG)F2 alpha status, as determined by radioimmunoassay. PGF2 alpha was significantly greater (by 52%) in rats fed no alpha-tocopherol than in rats fed 15,000 mg alpha-tocopherol acetate/kg diet. Hepatic PGF2 alpha status was correlated inversely but weakly with dietary alpha-tocopherol (r = -0.24, p less than 0.05). Hepatic PGF2 alpha status was not correlated with hepatic or plasma alpha-tocopherol status. This finding suggests either that there is a small depletion-resistant subcellular alpha-tocopherol pool which regulates PGF2 alpha production or that alpha-tocopherol alters PGF2 alpha production in vivo by an indirect mechanism.

Animals↗
PubMed1989

Preferential incorporation of alpha-tocopherol vs gamma-tocopherol in human lipoproteins.

Approximately 12 h after the ingestion of a single dose containing 1000 mg each of all-rac-alpha-tocopherol and RRR-gamma-tocopherol, the plasma and lipoproteins of normal subjects contained equal increases of both tocopherols; by 24 h the concentration of gamma-tocopherol, but not the alpha-tocopherol, decreased sharply. Similar studies in hyperlipidemic subjects demonstrated that the plasma and the chylomicron fraction from lipoprotein lipase-deficient patients (with elevated chylomicrons) contained both tocopherols up to 24 h, whereas plasma from a patient with dysbetalipoproteinemia (with elevated beta very-low-density lipoproteins) displayed the decrease in gamma-tocopherol at 24 h. These studies demonstrate that both alpha- and gamma-tocopherols are absorbed and secreted by the intestine in chylomicrons, and suggest that alpha-tocopherol is preferentially secreted by the liver in nascent lipoproteins. Furthermore, studies in post-gall bladder surgery patients suggest a preferential secretion of gamma-tocopherol in bile. Thus, the liver rather than the intestine appears to discriminate between alpha- and gamma-tocopherols.

Adult↗
PubMed1983

Relative antioxidant effectiveness of alpha-tocopherol and gamma-tocopherol in iron-loaded rats.

The relative antioxidant effectiveness of RRR-alpha-tocopherol and d-gamma-tocopherol against in vivo lipid peroxidation in vitamin E-depleted, iron-loaded rats was assessed by measurement of expired pentane. Rats fed a vitamin E-deficient diet were each administered 103 +/- 2 mg of iron as iron dextran over a 4-week period. After 3 weeks, their erythrocytes were 96.9 +/- 0.6% hemolyzed by dialuric acid. After 6 weeks, the rats exhaled 22.4 +/- 3.4 pmol pentane/(100 g body weight . minute). Groups of 4 rats each were then fed varying levels of RRR-alpha- and d-gamma-tocopherol for 2 weeks, after which the pentane levels were directly related to the dietary tocopherol content. Covariance analysis of the log of pentane production versus the log of dietary tocopherol showed the relative antioxidant effectiveness of 1:0.31 for alpha-tocopherol:gamma-tocopherol. In an independent estimation of relative antioxidant effectiveness, covariance analysis of the log of lipid soluble fluorophores in the spleens of the rats versus the log of dietary tocopherol showed a ratio of 1:0.37 for alpha-tocopherol:gamma-tocopherol. Regression analysis showed the fluorophores also to be correlated with the integrated amount of pentane produced over the 7-week experiment (r = 0.84, P less than 0.001). gamma-Tocopherol was more effective as an in vivo antioxidant than has been reported for its inhibition of vitamin E-deficiency syndromes.

Animals↗