Search PubMed⌕ Search

Biomedical subjects

Maret G Traber

Publications and source records attributed to Maret G Traber.

At least 19 recordsLinked to original sources
PubMed2007

Genome wide responses of murine lungs to dietary alpha-tocopherol.

Alpha-tocopherol (alpha-T) may affect biological processes by modulating mRNA concentrations. This study screened the responses of approximately 15,000 lung mRNAs to dietary alpha-T in mice. The lung was chosen as the target organ because it is subjected to cyclical variations in oxidant and inflammatory stressors and alpha-T has been implicated in their modulations. The analysis identified approximately 400 mRNAs sensitive to alpha-T status of lungs determined by dietary alpha-T. The female lung transcriptome appears to be more sensitive to the alpha-T status than that of the male lungs. Here, we focus on the induction of 13 cytoskeleton genes by dietary alpha-T because they were similarly induced in the male and the female lungs. Their inductions were confirmed by quantitative-real-time-polymerase chain reaction (qRT-PCR). Immunohistochemical analyses of three of the encoded proteins suggest that they are expressed in lung vasculature and alveolar regions. The data suggest that the lung alpha-T status may modulate cytoarchitecture of lungs.

Animals↗
PubMed2007

Heart disease and single-vitamin supplementation.

Heart disease is the number one cause of death in the United States and has long been recognized to be multifactorial. A growing body of evidence suggests that not only free radical-mediated reactions but also inflammatory responses play major roles in atherogenesis. Vitamin E has both antioxidant and antiinflammatory properties and is the most widely studied vitamin in clinical trials and thus will be the primary example used in this review. Clinical trials of vitamin E efficacy, in hindsight, have been overly optimistic in their expectation that a vitamin could reverse poor dietary habits and a sedentary lifestyle as well as provide benefit beyond that of pharmaceutical agents in treating heart disease. However, it is also apparent that most Americans do not consume dietary amounts adequate to meet established vitamin E requirements. In response to oxidative stressors, vitamin E can decrease biomarkers of lipid peroxidation, is itself killed, and requires optimal vitamin C status to function most effectively. Thus, adequate vitamin E intakes are clearly needed, but what is adequate for what function has yet to be defined. It is noteworthy that in most trials, biomarkers were not used nor were oxidative stress and lipid peroxidation markers used or plasma vitamin E concentrations measured.

Antioxidants↗
PubMed2006

Dietary zinc restriction in rats alters antioxidant status and increases plasma F2 isoprostanes.

Approximately 12% of Americans do not consume the estimated average requirement for zinc and could be at risk for zinc deficiency. Since zinc has proposed antioxidant function, inadequate zinc consumption may lead to an enhanced susceptibility to oxidative stress through several mechanisms, including altered antioxidant defenses. In this study, we hypothesized that dietary zinc restriction would result in lower antioxidant status and increased oxidative damage. We fed weanling Sprague-Dawley rats (n=12 per group) a zinc-adequate (50 mg/kg of zinc) diet, a zinc-deficient (<0.05 mg/kg of zinc) diet or a pair-fed diet for 3 weeks and then assessed their antioxidant status and oxidative stress parameters. Rats were zinc deficient as indicated by a significant (P<.05) reduction in body weight (49%) and 19% lower (P<.05) hepatic zinc (20.6+/-2.1 mg/kg) as compared with zinc-adequate rats (24.6+/-2.2 mg/kg). Zinc deficiency resulted in elevated (P<.05) plasma F(2) isoprostanes. Zinc deficiency-mediated oxidative stress was accompanied by a 20% decrease (P<.05) in the ferritin-reducing ability of plasma assay and a 50% reduction in plasma uric acid (P<.05). No significant change in plasma ascorbic acid or in plasma alpha-tocopherol and gamma-tocopherol was observed. However, hepatic alpha-tocopherol and gamma-tocopherol concentrations were decreased by 38% and 27% (P<.05), respectively, as compared with those in zinc-adequate rats. Hepatic alpha-tocopherol transfer protein levels were unaltered (P>.05) by zinc deficiency, but cytochrome P450 (CYP) 4F2 protein levels were elevated (P<.05) as compared with those in zinc-adequate rats. Collectively, zinc deficiency increased oxidative stress, which may be partially explained by increased CYP activity and reductions in hepatic alpha-tocopherol and gamma-tocopherol and in plasma uric acid.

Animals↗
PubMed2006

Three non-allelic epistatically interacting methyltransferase mutations produce novel tocopherol (vitamin E) profiles in sunflower.

Wildtype sunflower (Helianthus annuus L.) seeds are a rich source of alpha-tocopherol (vitamin E). The g = Tph(2) mutation disrupts the synthesis of alpha-tocopherol, enhances the synthesis of gamma-tocopherol, and was predicted to knock out a gamma-tocopherol methyltransferase (gamma-TMT) necessary for the synthesis of alpha-tocopherol in sunflower seeds--wildtype (g(+) g(+)) lines accumulated > 90% alpha-tocopherol, whereas mutant (g g) lines accumulated > 90% gamma-tocopherol. We identified and isolated two gamma-TMT paralogs (gamma-TMT-1 and gamma-TMT-2). Both mapped to linkage group 8, cosegregated with the g locus, and were transcribed in developing seeds of wildtype lines. The g mutation greatly decreased gamma-TMT-1 transcription, caused alternative splicing of gamma-TMT-1, disrupted gamma-TMT-2 transcription, and knocked out one of two transcription initiation sites identified in the wildtype; gamma-TMT transcription was 36 to 51-fold greater in developing seeds of wildtype (g(+) g(+)) than mutant (g g) lines. F(2) populations (B109 x LG24 and R112 x LG24) developed for mapping the g locus segregated for a previously unidentified locus (d). B109, R112, and LG24 were homozygous for a null mutation (m = Tph(1)) in MT-1, one of two 2-methyl-6-phytyl-1,4-benzoquinone/2-methyl-6-solanyl-1,4-benzoquinone methyltransferase (MPBQ/MSBQ-MT) paralogs identified in sunflower. The d mutations segregating in B109 x LG24 and R112 x LG24 were allelic to a cryptic mutation identified in the other MPBQ/MSBQ-MT paralog (MT-2) and disrupted the synthesis of alpha- and gamma-tocopherol in F(2) progeny carrying m or g mutations--m m g(+) g(+) d d homozygotes accumulated 41.5% alpha- and 58.5% beta-T, whereas m m g g d d homozygotes accumulated 58.1% gamma- and 41.9% delta-T. MT-2 cosegregated with d and mapped to linkage group 4. Hence, novel tocopherol profiles are produced in sunflower seed oil by three non-allelic epistatically interacting methyltransferase mutations.

Alleles↗
PubMed2006

Alpha-tocopherol regulation of hepatic cytochrome P450s and ABC transporters in rats.

To test the hypothesis that supra-elevated hepatic alpha-tocopherol concentrations would up-regulate mechanisms that result in increased hepatic alpha-tocopherol metabolism and excretion, rats received daily subcutaneous alpha-tocopherol injections (10 mg/100 g body wt) and then were sacrificed on Day 0 or 12 h following their previous injection on Days 3, 6, 9, 12, 15, and 18. Liver alpha-tocopherol concentrations increased from 12 +/- 1 nmol/g (mean +/- SE) to 819 +/- 74 (Day 3), decreased at Day 9 (486 +/- 67), and continued to decrease through Day 18 (338 +/- 37). alpha-Tocopherol metabolites and their intermediates increased and decreased similarly to alpha-tocopherol albeit at lower concentrations. There were no changes in known vitamin E regulatory proteins, i.e., hepatic alpha-tocopherol transfer protein or cytochrome P450 (CYP) 4F. In contrast, both CYP3A and CYP2B, key xenobiotic metabolizing enzymes, doubled by Day 6 and remained elevated, while P450 reductase increased more slowly. Consistent with the decrease in liver alpha-tocopherol concentrations, a protein involved in biliary xenobiotic excretion, p-glycoprotein, increased at Day 9, doubling by Day 15. Thus hepatic alpha-tocopherol concentrations altered hepatic proteins involved in metabolism and disposition of xenobiotic agents.

ATP-Binding Cassette Transporters↗
PubMed2006

Vitamin E biokinetics, oxidative stress and cigarette smoking.

Vitamin E is comprised of four tocopherols and four tocotrienols, and functions as a lipophilic chain-breaking antioxidant that prevents lipid peroxidation. Although it is well recognized that cigarette smoke is source of oxidative stress, relatively little is known regarding how oxidative stress alters vitamin E utilization in humans. Therefore, this review will highlight the recent knowledge regarding how cigarette smoking alters vitamin E (as alpha- and gamma-tocopherols) utilization in humans. Specifically, we will discuss the mechanisms by which cigarette smoking increases the turnover of plasma vitamin E, decreases the P450-mediated metabolism of vitamin E, and increases the nitration of gamma-tocopherol to result in the formation of 5-nitro-gamma-tocopherol. In addition, the interrelationship between oxidative stress and vitamin C will also be emphasized as it relates to vitamin E utilization.

Journal Article↗
PubMed2006

Absence of VLDL secretion does not affect alpha-tocopherol content in peripheral tissues.

alpha-Tocopherol is a lipid-soluble antioxidant that helps to prevent oxidative damage to cellular lipids. alpha-Tocopherol is absorbed by the intestine and is taken up and retained by the liver; it is widely presumed that alpha-tocopherol is then delivered to peripheral tissues by the secretion of VLDL. To determine whether VLDL secretion is truly important for the delivery of alpha-tocopherol to peripheral tissues, we examined alpha-tocopherol metabolism in mice that lack microsomal triglyceride transfer protein (Mttp) expression in the liver and therefore cannot secrete VLDL (Mttp(Delta/Delta) mice). Mttp(Delta/Delta) mice have low plasma lipid levels and increased stores of lipids in the liver. Similarly, alpha-tocopherol levels in the plasma were lower in Mttp(Delta/Delta) mice than in controls, whereas hepatic alpha-tocopherol stores were higher. However, alpha-tocopherol levels in the peripheral tissues of Mttp(Delta/Delta) mice were nearly identical to those of control mice, suggesting that VLDL secretion is not critical for the delivery of alpha-tocopherol to peripheral tissues. When fed a diet containing deuterated alpha-tocopherol, Mttp(Delta/Delta) and control mice had similar incorporation of deuterated alpha-tocopherol into plasma and various peripheral tissues. We conclude that the absence of VLDL secretion has little effect on the stores of alpha-tocopherol in peripheral tissues, at least in the mouse.

Animals↗
PubMed2006

Benefits of prolonged gradient separation for high-performance liquid chromatography-tandem mass spectrometry quantitation of plasma total 15-series F-isoprostanes.

The F(2)-isoprostanes are products of free-radical-induced oxidation of arachidonic acid (AA) that are stereoisomers of prostaglandin F(2alpha) (PGF(2alpha)). We describe a method for quantitation of several 15-series PGF isomers (15-PGFs) and AA by high-performance liquid chromatography-tandem mass spectrometry (HPLC-MS-MS). Plasma samples were subjected to alkaline hydrolysis and acidified, and total (free + esterified) 15-PGFs and AA were extracted with organic solvents. The analytes were separated by gradient reverse-phase HPLC and detected by multiple reaction monitoring on a triple-quadrupole mass spectrometer, using deuterated internal standards for quantitation. The assay had a linear range of 1-40 pg of 8-iso-PGF(2alpha) on column and can quantify as little as 40 pg/mL (0.11 nM) in plasma. Outcomes significantly correlated (p < 0.0001) with data obtained by gas chromatography-mass spectrometry GC-MS or enzyme-linked immunosorbent assay. All plasma 15-PGF isomers increased over time with in vitro cigarette smoke exposure and correlated (p < 0.0001) with each other. The same strong inter-15-PGF correlations were observed in plasma from healthy young adult subjects. The coefficients of variation of HPLC-MS-MS measurements (24-32%) were smaller than those obtained by GC-MS (53%). Thus, HPLC-MS-MS potentially offers greater precision and allows quantitation of more compounds with simpler sample preparation than existing methods. Ours is the first validated quantitative assay using HPLC-tandem MS applied to plasma total 15-PGFs.

Adolescent↗
PubMed2006

Relationship of vitamin E metabolism and oxidation in exercising human subjects.

During endurance exercise, oxygen consumption by the skeletal muscle can increase 100-200 times. We previously found that during an ultramarathon race (50 km, forest trail through hilly terrain) compared with a day of rest, vitamin E disappeared faster (as measured using 2H-labelled alpha-tocopherol) and lipid peroxidation increased. Therefore, we hypothesized that prior supplementation with antioxidants (vitamins E and C) would decrease oxidative stress during distance running and, therefore, decrease lipid peroxidation and inflammation, decrease DNA damage, decrease muscle damage and/or improve recovery. To test these hypotheses, we carried out a randomized, double-blind study in runners (n 11 females, 11 males) who were participants in an annual ultramarathon race. We found that supplementation with both vitamins E and C only prevented increases in lipid peroxidation, but had no apparent effect on DNA damage, inflammation or muscle damage. These results suggest that the mechanism of oxidative damage is operating independently of the inflammatory and muscle damage responses.

Ascorbic Acid↗
PubMed2006

Does gamma-tocopherol play a role in the primary prevention of heart disease and cancer? A review.

Vitamin E consists of a group of eight isomers, four tocopherols (alpha-, beta-, gamma-, delta-tocopherol) and four tocotrienols (alpha-, beta-, gamma-, delta-tocotrienol). While extensive literature has been published on the potential health benefits of alpha-tocopherol, little is known about gamma-tocopherol, the major form of vitamin E in food in the U.S. gamma-tocopherol has recently received more research attention based on findings from in vitro and animal studies indicating that it has potent anti-inflammatory and antioxidant properties. Based on these recent studies, it is important to investigate the possible health benefits of gamma-tocopherol in humans. In this article, we review publications on dietary gamma-tocopherol intake, plasma gamma-tocopherol levels, cardiovascular disease and cancer risk in humans.

Diet↗
PubMed2006

Human vitamin E requirements assessed with the use of apples fortified with deuterium-labeled alpha-tocopheryl acetate.

BACKGROUND: Little is known about factors that modulate dietary alpha-tocopherol bioavailability. OBJECTIVES: The study aimed to assess the efficacy of vitamin E-fortified apples as a low-fat vitamin E delivery system, the influence of fat on vitamin E absorption, and human vitamin E requirements by using plasma alpha-tocopherol kinetics at a dosage of alpha-tocopherol found in food. DESIGN: Apples fortified with deuterium-labeled alpha-tocopheryl acetate were consumed by 5 participants at a breakfast containing 0%, 6%, or 21% kcal from fat in 3 sequential trials. The trials were separated by a 2-wk washout period. Blood samples were obtained up to 72 h, and plasma was analyzed for labeled and unlabeled alpha-tocopherol. RESULTS: Compared with observations in the 0% fat trial, the maximum observed plasma d6-alpha-tocopherol concentrations (Cmax) and the areas under the curve increased 2- and 3-fold during the 6% and 21% fat trials, respectively. The mean (+/-SD) estimated percentage d6-alpha-tocopherol absorbed increased from 10 +/- 4% during the 0% fat trial to 20 +/- 3% and 33 +/- 5% during the 6% and 21% fat trials, respectively. The mean time to Cmax (9 +/- 2 h), fractional disappearance rates (0.022 +/- 0.003 pools/d), and half-lives (32 +/- 4 h) did not differ significantly between the trials. With the use of fractional disappearance rates and baseline plasma alpha-tocopherol concentrations, the estimated daily plasma alpha-tocopherol efflux was 13-14 mg. The estimated rate of alpha-tocopherol delivery to tissues was 5 mg/d. CONCLUSIONS: Given an estimated 33% absorption, the amount of dietary vitamin E needed daily to replace irreversible losses is </=15 mg. These estimates support the current human vitamin E requirements despite the claims that the median amount of vitamin E that Americans consume is 7 mg/d.

Adolescent↗
PubMed2006

Aerosolized alpha-tocopherol ameliorates acute lung injury following combined burn and smoke inhalation injury in sheep.

Victims of fire accidents who sustain both thermal injury to the skin and smoke inhalation have gross evidence of oxidant injury. Therefore, we hypothesized that delivery of vitamin E, an oxygen superoxide scavenger, directly into the airway would attenuate acute lung injury postburn and smoke inhalation. Sheep (N = 17 female, 35 +/- 5 kg) were divided into 3 groups: (1) injured, then nebulized with vitamin E (B&S, Vitamin E, n = 6); (2) injured, nebulized with saline (B&S, Saline, n = 6); and (3) not injured, not treated (Sham, n = 5). While under deep anesthesia with isoflurane, the sheep were subjected to a flame burn (40% total body surface area, 3rd degree) and inhalation injury (48 breaths of cotton smoke, <40 degrees C). All groups were resuscitated with Ringer lactate solution (4 mL/kg/%burn/24 h) and placed on a ventilator [positive end-expiratory pressure (PEEP) = 5 cm H2O, tidal volume = 15 mL/kg] for 48 h. B&S injury halved the lung alpha-tocopherol concentrations (0.9 +/- 0.1 nmol/g) compared with sham-injured animals (1.5 +/- 0.3), whereas vitamin E treatment elevated the lung alpha-tocopherol concentrations (7.40 +/- 2.61) in the injured animals. B&S injury decreased pulmonary gas exchange (PaO2/FiO2 ratios) from 517 +/- 15 at baseline to 329 +/- 49 at 24 h and to 149 +/- 32 at 48 h compared with sham ratios of 477 +/- 14, 536 +/- 48, and 609 +/- 49, respectively. Vitamin E treatment resulted in a significant improvement of pulmonary gas exchange; ratios were 415 +/- 34 and 283 +/- 42 at 24 and 48 h, respectively. Vitamin E nebulization therapy improved the clinical responses to burn and smoke inhalation-induced acute lung injury.

Acute Disease↗
PubMed2006

Vitamin E attenuates acute lung injury in sheep with burn and smoke inhalation injury.

INTRODUCTION: A decrease in alpha-tocopherol (vitamin E) plasma levels in burn patients is typically associated with increased mortality. We hypothesized that vitamin E supplementation (alpha-tocopherol) would attenuate acute lung injury induced by burn and smoke inhalation injury. MATERIALS AND METHODS: Under deep anesthesia, sheep (33 +/- 5 kg) were subjected to a flame burn (40% total body surface area, third degree) and inhalation injury (48 breaths of cotton smoke, < 40 degrees C). Half of the injured group received alpha-tocopherol (1000 IU vitamin E) orally, 24 h prior to injury. The sham group was neither injured nor given vitamin E. All three groups (n = 5 per group) were resuscitated with Ringer's lactate solution (4 ml/kg/%burn/24 h), and placed on a ventilator (PEEP = 5 cmH2O; tidal volume = 15 ml/kg) for 48 h. RESULTS: Plasma alpha-tocopherol per lipids doubled in the vitamin E treated sheep. Vitamin E treatment prior to injury largely prevented the increase in pulmonary permeability index and moderated the increase in lung lymph flow (52.6 +/- 6.2 ml/min, compared with 27.3 +/- 6.0 ml/min, respectively), increased the PaO2/FiO2 ratio, ameliorated both peak and pause airway pressure increases, and decreased plasma conjugated dienes and nitrotyrosine. CONCLUSIONS: Pretreatment with vitamin E ameliorated the acute lung injury caused by burn and smoke inhalation exposure.

Acute Disease↗
PubMed2006

Antioxidants did not prevent muscle damage in response to an ultramarathon run.

PURPOSE: This study was conducted to determine if 6 wk of supplementation with vitamins E and C could alleviate exercise-induced muscle damage. We studied 22 runners during a 50-km ultramarathon. METHODS: Subjects were randomly assigned to one of two groups: (a) placebos (PL) or (b) antioxidants (AO) (1000 mg vitamin C and 300 mg RRR-alpha-tocopheryl acetate). Blood samples were obtained before supplementation (baseline), 24 h pre-, 12 h pre-, and 1 h prerace; midrace, postrace, 2 h postrace, and for 6 d postrace. Plasma alpha-tocopherol (alpha-TOH), ascorbic acid (AA), and muscle damage markers (creatine kinase (CK) and lactate dehydrogenase (LDH)), as well as maximal voluntary contraction (MVC) of the hamstring and quadriceps were assessed. RESULTS: With supplementation, plasma alpha-TOH and AA increased in the AO but not the PL group. LDH and CK increased in response to the race; LDH peaked at postrace and CK reached maximal values 2 h and 1 d postrace; neither was affected by treatment. Adjusting for between-subject differences in baseline CK values revealed that men had higher levels of CK than did women throughout the study. Correcting CK values for lean body mass (kg) eliminated sex differences, but not changes over time. CK was significantly correlated (R = 0.52, P < 0.0001) with C-reactive protein, an acute phase response marker. MVC decreased 14-26% in all groups in response to the run. Eccentric hamstring (EH) torque and concentric quadriceps (CQ) power exhibited the largest deficits, 26 and 24%, respectively, with no effect of treatment. CQ recovered at a faster rate in women than in men. CONCLUSION: Antioxidants appeared to have no effect on exercise-induced increases in muscle damage or recovery, but important sex differences were observed.

Adolescent↗
PubMed2005

Faster plasma vitamin E disappearance in smokers is normalized by vitamin C supplementation.

Vitamin E disappearance is accelerated in cigarette smokers due to their increased oxidative stress and is inversely correlated with plasma vitamin C concentrations. Therefore, we hypothesized that ascorbic acid supplementation (500 mg, twice daily; 2 weeks) would normalize smokers' plasma alpha- and gamma-tocopherol disappearance rates and conducted a double-blind, placebo-controlled, randomized crossover investigation in smokers (n=11) and nonsmokers (n=13) given a single dose of deuterium-labeled alpha- and gamma-tocopherols (50 mg each d6-RRR-alpha and d2-RRR-gamma-tocopheryl acetate). During the placebo trial, smokers, compared with nonsmokers, had significantly (P<0.05) greater alpha- and gamma-tocopherol fractional disappearance rates and shorter half-lives. Ascorbic acid supplementation doubled (P<0.0001) plasma ascorbic acid concentrations in both groups and attenuated smokers', but not nonsmokers', plasma alpha- and gamma-tocopherol (P<0.05) fractional disappearance rates by 25% and 45%, respectively. Likewise, smokers' plasma deuterium-labeled alpha- and gamma-tocopherol concentrations were significantly higher (P<0.05) at 72 h during ascorbic acid supplementation compared with placebo. Ascorbic acid supplementation did not significantly change (P>0.05) time of maximal or maximal-labeled alpha- and gamma-tocopherol concentrations. Smokers' plasma F2alpha-isoprostanes were approximately 26% higher than nonsmokers (P>0.05) and were not affected by ascorbic acid supplementation in either group (P>0.05). In summary, cigarette smoking increased plasma alpha- and gamma-tocopherol fractional disappearance rates, suggesting that the oxidative stress from smoking oxidizes tocopherols and that plasma ascorbic acid reduces alpha- and gamma-tocopheroxyl radicals to nonoxidized forms, thereby decreasing vitamin E disappearance in humans.

Administration, Oral↗
PubMed2005

Ascorbylated 4-hydroxy-2-nonenal as a potential biomarker of oxidative stress response.

Oxidative stress, resulting from the generation of reactive oxygen species, contributes to the development of a multitude of age-related diseases. Current methods of assessing oxidative stress levels range from the detection of lipid peroxidation products, such as F(2)-isoprostanes and malondialdehyde, to monitoring the redox status of glutathione. While useful, traditional biomarkers of oxidative stress are not without their drawbacks, including low in vitro concentrations and possible artifact formation. In the present study, we utilize liquid chromatography coupled with tandem mass spectrometry for investigation into the use of a novel compound, ascorbylated 4-hydroxy-2-nonenal, as a potential biomarker of oxidative stress.

Adolescent↗
PubMed2005

Studies in humans using deuterium-labeled alpha- and gamma-tocopherols demonstrate faster plasma gamma-tocopherol disappearance and greater gamma-metabolite production.

We hypothesized that human plasma alpha- and gamma-tocopherol concentrations reflect differences in their kinetics, especially influenced by gamma-tocopherol metabolism. Vitamin E kinetics were evaluated in humans (n=14) using approximately 50 mg each of an equimolar ratio of d6-alpha- and d2-gamma-tocopheryl acetates administered orally. Mass spectrometry was used to measure deuterated plasma tocopherols, as well as plasma and urinary vitamin E metabolites, alpha- and gamma-carboxyethylhydroxychromans (CEHCs). Plasma d2-gamma-tocopherol fractional disappearance rates (FDR; 1.39+/-0.44 pools/day, mean+/-SD) were more than three times greater than those of d6-alpha-tocopherol (0.33+/-0.11, p<0.001). The d2-gamma-tocopherol half-life was 13+/-4 h compared with 57+/-19 for d6-alpha-tocopherol. Whereas neither plasma nor urinary d6-alpha-CEHC was detectable (limit of detection 1 nmol/L), gamma-CEHC (labeled plus unlabeled) increased from 129+/-20 to 258+/-40 nmol/L by 12 h and returned to baseline by 48 h; at 12 h d2-gamma-CEHC represented 54+/-4% of plasma gamma-CEHC. Women compared with men had a greater d2-gamma-tocopherol FDR (p<0.004) and a greater maximal plasma d2-gamma-CEHC concentration (p<0.02) and CEHC FDR (p<0.007), as well as excreting four times as much d2-gamma-CEHC (p<0.04) in urine. Thus, gamma-tocopherol is rapidly metabolized to gamma-CEHC, and to a greater degree in women than in men, whereas alpha-tocopherol is maintained in the plasma and little is metabolized to alpha-CEHC.

Adult↗