Tissue Α-tocopherol Concentrations Research Articles

Effects of dietary vitamin E on hematology, tissue α-tocopherol concentration and non-specific immune responses of Japanese eel, Anguilla japonica

In a 16-week feeding trial, the effects of dietary vitamin E (α-tocopherol, α-Toc) levels on tissue α-Toc concentration, hematology and non-specific immune responses of Japanese eel were examined. Totally five diets were used in this experiment, consisting a basal commercial diet (control) and supplementing 100, 150, 200 or 400mgα-Tockg−1 diet in the form of dl-α-tocopherol acetate. The analyzed α-Toc concentrations of the diets were 32, 112, 158, 212 and 428mgkg−1 diet, respectively. For each experimental diet, triplicate groups of fish (initial body weight, 360g) were fed at a ratio of 2% body weight. At the end of the feeding trial, α-Toc concentration in liver, kidney, muscle and gonad were increased significantly in a dose dependent manner (P<0.05). Significantly higher hemoglobin and white blood cells count were found in fish fed 212mgα-Tockg−1 diet compared to control. Plasma glucose concentration was decreased significantly in all α-Toc supplemented groups, also significantly higher aspartate aminotransferase and alanine aminotransferase values were obtained at 32 and ≤158mgα-Tockg−1 diet compared to the other groups. Significantly higher lysozyme and SOD activities were recorded in fish fed 428mgα-Tockg−1 diet compared to the other groups. The optimal dietary α-Toc requirement was estimated at 212.9mgα-Tockg−1 diet by broken-line regression model based on liver α-Toc concentration.

Cluster-determinant 36 (CD36) impacts on vitamin E postprandial response.

A single nucleotide polymorphism in the cluster determinant 36 (CD36) gene has recently been associated with plasma α-tocopherol concentration, suggesting a possible role of this protein in vitamin E intestinal absorption or tissue uptake. To investigate the involvement of CD36 in vitamin E transport, we first evaluated the effect of CD36 on α- and γ-tocopherol transmembrane uptake and efflux using transfected HEK cells. γ-Tocopherol postprandial response was then assessed in CD36-deficient mice compared with wild-type mice, after the mice had been fully characterized for their α-tocopherol, vitamin A and lipid plasma, and tissue contents. Both α- and γ-tocopherol uptake was significantly increased in cells overexpressing CD36 compared with control cells. Compared with wild-type mice, CD36-deficient mice displayed a significantly decreased cholesterol hepatic concentration, and males exhibited significantly higher triacylglycerol contents in liver, brain, heart, and muscle. Although tissue α-tocopherol concentration after adjustment for lipid content was not modified, γ-tocopherol postprandial response was significantly increased in CD36-deficient mice compared with controls, likely reflecting the postprandial hypertriglyceridemia observed in these mice. Our findings show for the first time that CD36 participates-directly or indirectly-in vitamin E uptake, and that CD36 effect on postprandial lipid metabolism in turn modifies vitamin E postprandial response.

α-Tocopherol adipose tissue stores are depleted after burn injury in pediatric patients

We previously showed that thermal injury depletes plasma vitamin E in pediatric burn patients; however, plasma changes may reflect immediate alterations in vitamin E nutriture. Adipose tissue α-tocopherol concentrations are generally accepted to reflect long-term vitamin E status. To test the hypothesis that thermal injury depletes body stores of vitamin E, α-tocopherol concentrations were measured in adipose tissue samples. Pediatric patients (n = 8) were followed up to 1 y after burn injury. Surgically obtained samples were collected at various intervals and stored at -80°C in a biorepository. α- and γ-Tocopherols, cholesterol, and triglycerides were measured in the same tissue aliquot. During the first week after injury, adipose tissue α-tocopherol concentrations were within the expected normal range of 199 ± 40 nmol/g adipose tissue but were substantially lower at weeks 2 and 3 (133 ± 13 and 109 ± 8 nmol/g adipose tissue, respectively). Individual rates of decrease, estimated by linear regression, showed that adipose tissue α-tocopherol decreased by an average of 6.1 ± 0.6 nmol/g daily. During the first month after injury, adipose tissue triglyceride concentrations also decreased, whereas no changes in cholesterol concentrations occurred. These data emphasize that the burn injury experienced by these pediatric patients altered their metabolism such that vitamin E status diminished during the month after injury. Further studies are needed to evaluate the mechanism and consequences of the observed vitamin E depletion. This trial was registered at clinicaltrials.gov as NCT00675714.

Meta-analysis of effects of dietary vitamin E and post slaughter storage conditions on changes of redness (a*) of pork

Abstract. A meta-analysis was carried out to quantify the effects of dietary vitamin E and storage conditions on colour changes of pork from M. longissimus dorsi. After standardisation procedures, redness of pork (CIE colour specification a*), one of the most important objective colour attributes, was used as an indicator for colour changes in this analysis. The analysis was based on results from five experiments, which met selection criteria. Analysis of changes of other objective colour attributes, lightness (L*) and yellowness (b*) was not possible due to lack of published data. The statistical analysis (using mixed models) found significant effects of tissue α-tocopherol concentration in M. longissimus dorsi, simplified supplemented vitamin E levels as well as storage time and storage light on redness of pork and its changes over time. The relationship between redness and α-tocopherol concentration was found to be linear, and between redness and storage time was non-linear (third degree polynomial) in one model. This model suggested that an increase of 1 μg of α-tocopherol in the muscle led to an expected increase a* value of 0.11. Another model identified significant interactions about 0.28 between α-tocopherol concentration and storage time in late storage periods. A third model found a significant difference of −0.48 between predicted a* values at lower (≤50 IU/kg feed) and higher supplemented vitamin E levels (≥100 IU/kg feed). The models predicted an initial increase for 3 days, a stable period for 5 days and then a decrease for a* values over storage time. The a* values were significantly lower by about 1.4 when samples were exposed to light in the models, the effect of light found to be constant over time. Further studies, carried out with standardized methods, are needed to increase the predictive power of the derived models and to validate the models for other muscles.

Effect of vitamin E source, natural versus synthetic, and quantity on serum and tissue α-tocopherol concentrations in finishing swine

Relative vitamin E status of pigs fed natural or synthetic vitamin E was evaluated based on serum and tissue alpha-tocopherol concentrations. Individually fed finishing gilts at a BW of 70.5 kg (n = 24) were allotted to dietary treatments based on initial BW. The 5 dietary treatments consisted of a positive control diet using synthetic vitamin E acetate (Syn E Ac) supplemented at 22 mg/kg, and 4 dietary levels of natural vitamin E acetate (Nat E Ac) supplemented at 6.71, 8.33, 11.00, and 16.18 mg/kg of diet. Before initiation of the 32-d experiment, pigs were fed a non-vitamin E-fortified diet for 30 d. Diets were formulated to contain true ileal digestible lysine of 0.9 and 0.8% for the pretest and test diets. Serum samples were collected on d 15 and 32, whereas tissue samples were collected on d 32 for alpha-tocopherol analysis. Serum alpha-tocopherol concentrations on d 15 and 32 were greater (P < 0.05) in pigs fed 8.33, 11.00, or 16.18 mg/kg of Nat E Ac than in pigs fed 22 mg/kg of Syn E Ac. When compared with pigs fed 22 mg/kg of Syn E Ac, alpha-tocopherol concentrations were greater (P < 0.05) in 6 tissues (heart, kidney, spleen, liver, lung, and adipose) in pigs fed 16.18 mg/kg of Nat E Ac; greater (P < 0.05) in heart, kidney, spleen, liver, and adipose tissue in pigs fed 11.00 mg/kg of Nat E Ac; and greater (P < 0.05) in spleen, loin, and adipose tissue in pigs fed 8.33 mg/kg of Nat E Ac. As dietary Nat E Ac increased from 6.71 to 16.18 mg/kg, serum alpha-tocopherol increased linearly (P < 0.01) on d 15 and 32 of the experiment. Increasing dietary Nat E Ac linearly increased (P < 0.05) alpha-tocopherol concentrations for lung, heart, kidney, spleen, and liver. These results indicate that Nat E Ac was an effective vitamin E source and its relative bioavailability was substantially greater than 1.36 for finishing swine when compared with Syn E Ac.

High dietary vitamin A interferes with tissue α-tocopherol concentrations in fattening pigs: a study that examines administration and withdrawal times

This study aimed to assess the interaction between different dietary vitamin A (dVitA) levels and the same concentration of vitamin E (100 IU all-rac-α-tocopheryl acetate/kg feed) in growing-finishing pigs. In the first experiment, two fat sources × two dVitA levels (0 v. 100 000 IU) were used. The supplementation of 100 000 IU dVitA induced a range of 5.13 to 30.03 μg retinol/g liver, 62.78 to 426.88 μg retinol palmitate/g liver, and 0.60 to 1.96 μg retinol/g fat. Dietary fat did not affect retinol or retinyl palmitate deposition in pigs. The high concentration of dVitA produced lower fat and liver α-tocopherol concentrations, and increased susceptibility of muscle tissue to oxidation. A second experiment was carried out to study the retinol and α-tocopherol retention at different withdrawal times prior to slaughter (two dVitA levels; 0 v. 100 000 IU). A high dose of 100 000 IU vitamin A during a short 2-week period was enough to induce α-tocopherol depletion in liver and fat to a similar extent as when 100 000 IU were administered during the whole fattening. Muscle, fat and liver α-tocopherol concentrations were not affected by dVitA in the 1300–13 000 IU/kg range, but liver α-tocopherol concentration was higher when vitamin A was removed from the vitamin mix 5 weeks prior to slaughter (experiment 3).

Prolonged α-Tocopherol Deficiency Decreases Oxidative Stress and Unmasks α-Tocopherol-dependent Regulation of Mitochondrial Function in the Brain

Vitamin E is the major lipid-soluble chain-breaking antioxidant in mammals and plays an important role in normal development and physiology. Deficiency (whether dietary or genetic) results in primarily nervous system pathology, including cerebellar neurodegeneration and progressive ataxia (abnormal gait). However, despite the widely acknowledged antioxidant properties of vitamin E, only a few studies have directly correlated levels of reactive oxygen species with vitamin E availability in animal models. We explored the relationship between vitamin E and reactive oxygen species in two mouse models of vitamin E deficiency: dietary deficiency and a genetic model (tocopherol transfer protein, Ttp-/- mice). Both groups of mice developed nearly complete depletion of alpha-tocopherol (the major tocopherol in vitamin E) in most organs, but not in the brain, which was relatively resistant to loss of alpha-tocopherol. F4-neuroprostanes, an index of lipid peroxidation, were unexpectedly lower in brains of deficient mice compared with controls. In vivo oxidation of dihydroethidium by superoxide radical was also significantly lower in brains of deficient animals. Superoxide production by brain mitochondria isolated from vitamin E-deficient and Ttp-/- mice, measured by electron paramagnetic resonance spectroscopy, demonstrated a biphasic dependence on exogenously added alpha-tocopherol. At low concentrations, alpha-tocopherol enhanced superoxide flux from mitochondria, a response that was reversed at higher concentrations. Here we propose a mechanism, supported by molecular modeling, to explain decreased superoxide production during alpha-tocopherol deficiency and speculate that this could be a beneficial response under conditions of alpha-tocopherol deficiency.

Vitamin E Regulatory Mechanisms

Dietary and supplemental vitamin E is absorbed and delivered to the liver, but of the various antioxidants with vitamin E activity, only alpha-tocopherol is preferentially recognized by the alpha-tocopherol transfer protein (alpha-TTP) and is transferred to plasma, while the other vitamin E forms (e.g., gamma-tocopherol or tocotrienols) are removed from the circulation. Hepatic alpha-TTP is required to maintain plasma and tissue alpha-tocopherol concentrations. The liver is the master regulator of the body's vitamin E levels in that it not only controls alpha-tocopherol concentrations, but also appears to be the major site of vitamin E metabolism and excretion. Vitamin Es are metabolized similarly to xenobiotics; they are initially omega-oxidized by cytochrome P450s, undergo several rounds of beta-oxidation, and then are conjugated and excreted. As a result of these various mechanisms, liver alpha-tocopherol and other vitamin E concentrations are closely regulated; thus, any potential adverse vitamin E effects are limited.

Plasma and tissue α-tocopherol concentrations and meat colour stability in sheep grazing saltbush (Atriplex spp.)

Dry senesced pastures available during the summer and autumn period in Western Australia and other areas with a Mediterranean climate are low in vitamin E. The use of expensive and labour-intensive supplements to prevent nutritional myopathy induced by vitamin E deficiency in weaner sheep is common. Low vitamin E concentrations in the muscle preslaughter can also reduce the shelf life of meat. There is growing interest in incorporating saltbush into farming systems in Western Australia. The potential for saltbush to boost the vitamin E status of sheep and improve the shelf life of meat was investigated. Fifty (2 × 25) 18-month-old Merino hogget wethers (average liveweight 48 kg) were grazed on either a saltbush-dominant saline pasture or on a ‘control’ dry pasture, stubble plot for 14 weeks. At the start of the experiment, all animals were orally supplemented with 2500 IU of dl-α-tocopherol acetate in 6.25 mL solution. The α-tocopherol content in saltbush was 139 and 116 mg/kg dry matter for old man and river saltbush, respectively. Concentrations of α-tocopherol were measured in plasma at Weeks 0, 4, 8, and 12 and in muscle and liver samples taken at slaughter. Grazing on saltbush significantly elevated α-tocopherol concentrations in the liver and muscle compared with grazing on dry pasture, well above the threshold for vitamin E inadequacy (P &lt; 0.001). Plasma α-tocopherol concentrations in sheep fed saltbush increased up to Week 8 and then decreased until the end of the experiment as availability of saltbush declined (P &lt; 0.05). Plasma α-tocopherol in sheep fed dry pasture increased in the first 4 weeks due to the initial vitamin E treatment but declined thereafter, indicating that the pasture was low in vitamin E. The high muscle concentrations of α-tocopherol in sheep fed saltbush also improved colour stability and may have had an influence on drip and cooking loss. The meat from the saltbush-grazed sheep was moister but drip and cooking loss was the same as from the drier meat of the control sheep. In conclusion, this study demonstrates that saltbush is a potential vitamin E source for sheep.

Enhanced inflammatory responses in α-tocopherol transfer protein null mice

The liver preferentially secretes α-tocopherol into plasma under the control of the hepatic α-tocopherol transfer protein (α-TTP). α-TTP-null mice ( Ttpa −/− mice) are vitamin E deficient, therefore were used for investigations of in vivo responses to sub-normal tissue α-tocopherol concentrations during inflammation. Increased basal oxidative stress in Ttpa −/− mice was documented by increased plasma lipid peroxidation, and superoxide production by bone marrow-derived neutrophils stimulated in vitro with phorbol 12-myristate 13-acetate. Lipopolysaccharide (LPS) injected intraperitoneally induced increases in lung and liver HO-1 and iNOS, as well as plasma NO x in Ttpa +/+ mice. LPS induced more modest increases in these markers in Ttpa −/− mice, while more marked increases in plasma IL-10 and lung lavage TNFα were observed. Taken together, these results demonstrate that α-tocopherol is important for proper modulation of inflammatory responses and that sub-optimal α-tocopherol concentrations may derange inflammatory–immune responses.

Effect of dietary levels of vitamin E (all-rac-tocopheryl acetate) with or without added fat on weanling pig performance and tissue α-tocopherol concentration

Two experiments involving 496 cross-bred pigs evaluated the efficacy of various dietary levels of vitamin E, with or without supplemental fat, on postweaning pig performance and weekly serum and terminal tissue alpha-tocopherol concentrations. The first trial involved 248 pigs weaned at an average of 15 d of age and 4.8 kg BW. The experiment was a randomized complete block design conducted in seven replicates. Vitamin E was added as dl-alpha-tocopheryl acetate at 0, 20, 40, 60, 80, 100, 150, or 200 IU/kg diet. Pigs were bled initially and at 7-d intervals for a 42-d period. Liver and s.c. adipose tissue samples were collected from six pigs per treatment group at 42 d. In Exp. 2, a 2 x 4 factorial arrangement of treatments in a randomized complete block design was conducted in seven replicates. The experiment used a total of 248 pigs weaned at 19 d of age and averaged 6.4 kg BW. Four vitamin E levels (0, 20, 40, and 60 IU/kg diet) and two added fat levels of 0 or 5% were fed for 35 d. Four pigs per treatment pen were bled weekly, and at 35 d a total of four pigs per treatment group were killed and liver, heart, and s.c. adipose tissues were collected and analyzed for alpha-tocopherol. The basal diet in both experiments contained an average 7.9 IU for period 1, and later diets averaged 11.0 IU vitamin E/kg. In both experiments serum alpha-tocopherol concentrations declined from weaning to 7 d after weaning and continued to decline each week after weaning when the basal diets were fed. Serum alpha-tocopherol concentrations increased (P < 0.01) each week as the dietary vitamin E level increased in both experiments. In Exp. 2, when fat was added to the diet serum alpha-tocopherol concentrations were higher (P < 0.01) than in diets without added fat. Liver, heart muscle, and adipose tissue alpha-tocopherol concentrations increased (P < 0.01) as vitamin E level increased, but at the higher dietary vitamin E level the liver surpassed the adipose tissue in its alpha-tocopherol concentration. Liver and adipose alpha-tocopherol concentrations were higher (P < 0.01) when fat was added to the diet. These results indicate that supplementation of 40 to 60 IU/kg diet with added fat resulted in a relatively constant balance of serum and tissue concentration of alpha-tocopherol during the nursery period, but when fat was not supplemented a dietary vitamin E level of 80 to 100 IU/kg diet may be needed. The current NRC recommendations for vitamin E for the pig from 5 to 20 kg BW may need to be reevaluated.

Reply: Vitamin E Supplementation in Cystic Fibrosis

To the Editor: We are grateful for the opportunity to respond to Dr. Winklhofer-Roob's detailed critique of our article, which was, as described in our introduction, a study around normal clinical practice in the setting of a children's cystic fibrosis (CF) clinic. In our study, conducted between 1989 and 1991, we were able to exploit the fact that measurement of erythrocyte α-tocopherol levels was being undertaken before the implementation throughout our clinic population of current supplementation guidelines, affording an invaluable opportunity to study steady-state α-tocopherol concentrations at various levels of supplementation, as opposed to Dr. Winklhofer-Roob's study of short-term changes in erythrocyte α-tocopherol response to a single dose of the vitamin (1). As we state, many patients were, at the beginning of the study, receiving no supplementation, or daily Ketovite, which contains 15 mg of vitamin E, hence data for this dosage. In our experience, RRR-α-tocopherol alone is used in the United Kingdom, so the racemic form of the vitamin is not an issue in this study. Recent work has shown that the free phenol and esterified forms of α-tocopherol (α-tocopherol and α-tocopherol acetate, respectively) have similar bioavailabilities (2). As Dr. Winklhofer-Roob points out, the association between erythrocyte and tissue α-tocopherol concentrations have not been measured in patients with CF. In light of this, and as the α-tocopherol is bound in the membrane with polyunsaturated fatty acids, we believe that erythrocyte levels are more representative of tissue levels than the more commonly used plasma levels. In our article, some measurements are shown in graphic form only because, for clarity, we chose to tabulate only the most common supplementation regimens. Dr. Winklhofer-Roob attempts to comment on the numbers of subjects in each group when, unfortunately, tight clustering of α-tocopherol concentrations makes counting of subjects on the graphs impossible, particularly at 100 mg/day. As shown in Table 1, there were in fact 46 measurements at this dosage, and only 8 of these were below the reference range. Likewise, the distribution of data cannot be inferred from this graph. We appreciate Dr. Winklhofer-Roob's concerns regarding statistical validity where data from the same patient are used twice; this study gathered all available data on α-tocopherol concentrations within a population of patients receiving a variety of supplements, prescribed independently of α-tocopherol level, during a 2-year period. In no case were data for the same patient entered twice less than 1 year apart. The results of our study confirm and complement those carried out by Dr. Winklhofer-Roob in indicating that relatively large α-tocopherol supplements (100 mg/day) are required by most CF patients to normalise plasma levels (at this time we do not know about tissue levels directly). There are a number of variables that may have an impact on the response of a CF patient to a particular α-tocopherol supplement, and studies on the magnitude of these responses are currently under way in our group. Given the lack of understanding of the positive role that reactive oxygen species may play in cell metabolism, caution should be exercised before prescribing very large α-tocopherol supplements to all CF patients. Until we have this information, we recommend normalisation only. S. A. Peters; F. J. Kelly Children's Unit; St. Mary's Hospital; Portsmouth, England

Modulation of tissue α-tocopherol in African catfish, Clarias gariepinus (Burchell), fed oxidized oils, and the compensatory effect of supplemental dietary vitamin E

Juvenile African catfish, Clarias gariepinus (Burchell), of mean initial weight 15 g, were fed practical diets containing fresh or rancid oil (1:1 cod liver:corn oil) supplemented with either 20 or 100 mg all-rac-α-tocopheryl acetate per kg dry diet, at 0.03 × body weight per day for 8 weeks. After this time, catfish had grown by at least four times in body weight. Significant (P < 0.05) inter-treatment differences in final body weight were noted. Clarias fed low-tocopherol: oxidized-oil diets performed least well with regard to growth, though elevated dietary vitamin E partially abrogated this effect. Growth of fish fed fresh-oil diets did not benefit from increased dietary α-tocopherol content. Muscle, liver, plasma, heart and spleen all responded significantly (P < 0.05) to dietary vitamin E dose. Inclusion of oxidized oil in catfish diets decreased tissue α-tocopherol concentration. Hepatic α-tocopherol concentration (μg α-tocopherol per g liver) was observed to be lowered by 90% by the rancid oil diets. When fish previously fed fresh-oil diets were switched to oxidized: low-tocopherol diets, hepatic α-tocopherol concentration was significantly (P < 0.05) lowered within 2 weeks. The results highlight the importance of dietary oil quality in modulating tissue α-tocopherol concentrations in African catfish.

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

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

The adverse effects of an in vivo inflammatory challenge on the vitamin E status of rats is accentuated by fish oil feeding 1–3

To investigate the impact of dietary fish oil on tissue α-tocopherol concentration following an acute inflammatory challenge, weanling Sprague-Dawley female rats were fed diets containing 20% lard or menhaden fish oil, Dietary α-tocopherol was equalized across treatment groups (60 mg/kg). After 5 weeks, rats were injected intraperitoneally with one of two sterile inflammatory agents (i.e., glycogen or thioglycollate broth) or received no injection (control). Vitamin E (i.e., α-tocopherol) concentration was measured by reverse-phase HPLC for plasma, liver and immune cells isolated from the blood, lungs, spleen, and peritoneum. Aliquots of peripheral blood and peritoneal immune cells were analyzed for H 2O 2 production by flow cytometry. We found that fish oil-fed rats had lower baseline plasma (P < 0.0001) and liver (P < 0.005) α-tocopherol concentrations than lard-fed rats. The differences in plasma and hepatic α-tocopherol concentration between rats fed fish oil and those fed lard were increased following inflammatory challenge. In general, fish oil did not reduce immune cell α-tocopherol, with one notable exception. Peripheral blood immune cells from glycogen-challenged fish oil-fed rats had 45% less α-tocopherol than lard-fed counterparts (P < 0.05). The effect of diet on in vitro immune cell H 2O 2 production was modest, with the only significant difference occurring in peritoneal cells isolated from thioglycollate-challenged rats. In those animals, fish oil feeding led to an increased capacity to produce H 2O 2 in response to PMA stimulation. In summary, dietary fish oil adversely affects vitamin E status of rats and an in vivo inflammatory challenge accentuated this effect.

Plasma and tissue concentrations of vitamin E following supplementation of two forms of vitamin E in sheep

Twenty-five lambs were used to determine the plasma and tissue concentrations of vitamin E after oral supplementation of two forms and in two doses. Five lambs were assigned to each of the following treatments: (1) control, no supplemental vitamin E, (2) 500 IU of DL-α-tocopherol, (3) 500 IU of D-α-tocopherol, (4) 1000 IU of DL-α-tocopherol, and (5) 1000 IU of D-α-tocopherol. Animals were supplemented daily with either 500 or 1000 IU of their respective vitamin E sources for 28 consecutive days. Blood samples were collected twice a week until Day 28. Animals were subsequently slaughtered at Day 28 and ten different tissues were collected for α-tocopherol analysis. All supplemented groups were higher in plasma α-tocopherol concentration than the control. When sheep were dosed with 500 IU there was a tendency for higher plasma concentration following D-α-tocopherol than DL-α-tocopherol administration and this difference became significant after 1000 IU dosing ( P < 0.05). Tissue α-tocopherol concentrations for all treatment groups were higher than those of control. Across all treatments, the highest α-tocopherol concentrations were noted in liver and pancreas and the lowest in neck and hip muscle. Results of this study suggested that in lambs blood and liver concentrations of vitamin E were higher following supplementation of D-α-tocopherol than with DL-α-tocopherol. Supplementation of vitamin E resulted in accumulation of different levels of α-tocopherol in different organs.

Tissue vitamin E concentrations after single injection of α-tocopherol in pigs

Forty pigs were randomly assigned to one of the four treatment groups: control, 500 IU, 1500 IU, and 2500 IU of vitamin E given as a single intramuscular injection. Out of 40 pigs, 20 were slaughtered at day 3 and the remaining 20 at day 7 after injection. Effect of treatment was significant (P &lt; 0.05) for vitamin E concentrations in all tissues. The effect of time of slaughter after the injection was significant (P &lt; 0.05) for spleen, liver, kidney, lung, hip muscle and adrenal, while the interaction of treatment with time was significant (P &lt; 0.05) for most of the tissues except adipose tissue and neck muscle. Concentration of α-tocopherol in all tissues increased with increased dose of injection. In most tissues, α-tocopherol concentration was higher at 3 d than at 7 d after injection. By 7 d, levels had dropped significantly but were still much higher than control levels. Intramuscular injection of vitamin E in pigs resulted in significant differences in tissue α-tocopherol concentrations. Key words: Vitamin E, tissues, pigs

Tissue Vitamin E Status Is Compromised by Dietary Protein Insufficiency in Young Growing Rats ,

Abstract In vitro erythrocyte hemolysis previously has been found to be significantly elevated in rats fed a low protein diet. To investigate the effects of dietary protein insufficiency on tissue vitamin E status, four groups of male weanling Long-Evans rats were given free access to either an 8% (wt/wt) lactalbumin diet containing 50 (L50) or 500 (L500) mg/kg diet of all-rac-α-tocopheryl acetate, or a 20% (wt/wt) lactalbumin diet containing 50 (N50) or 500 (N500) mg/kg of all-rac-α-tocopheryl acetate for 6 wk. A fifth group (P50) was pair-fed to the L50 group with the N50 diet. The L50 and L500 groups showed signs of protein malnutrition such as growth retardation as well as lower hematocrit and plasma protein and albumin concentrations. The α-tocopherol concentrations of plasma, heart, lung, kidney and muscle were significantly lower in the L50 group compared with the N50 group. The L500 group showed significantly less α-tocopherol in heart, kidney, muscle, brain and adipose tissue compared with the N500 group. The α-tocopherol concentrations in liver, testis, spleen and adrenal gland did not significantly differ either between the L50 and N50 groups or between the L500 and N500 groups. Supplementation with 500 mg/kg diet of all-rac-α-tocopheryl acetate resulted in significantly higher tissue α-tocopherol concentration in all tissues except muscle. The tissue α-tocopherol concentrations of the P50 group were not significantly different from those of the N50 group. The results indicated that protein insufficiency resulted in significantly lower α-tocopherol concentrations in most tissues in young growing rats.

Tissue alpha-tocopherol concentrations following supplementation with various forms of vitamin E in sheep.

Tissue alpha-tocopherol concentrations were determined in 40 lambs following oral supplementation of various forms of vitamin E. Lambs were allocated to 8 dietary groups of 5 animals each and supplemented with or without equimolar amounts (300 mg equivalence) of different vitamin E compounds daily for 60 d as follows: 1) control, no supplemental vitamin E; 2) D-alpha-tocopheryl acetate; 3) DL-alpha-tocopheryl acetate; 4) DL-alpha-tocopheryl nicotinate; 5) D-alpha-tocopheryl polyethylene glycol 1,000 succinate (TPGS); 6) DL-alpha-tocopheryl nicotinate+TPGS; 7) D-alpha-tocopheryl acetate+TPGS; and 8) D-alpha-tocopheryl succinate. At the end of the 60 d the lambs were killed and portions of adrenal, fat, heart, kidney, liver, lung, skeletal (brachiocephalicus and gluteus) muscles, pancreas and spleen were removed. Daily supplementation with various vitamin E compounds (equivalence) in lambs resulted in significant differences in tissue alpha-tocopherol concentration in heart, liver, gluteus medius muscle, and spleen. Correlations between the plasma and tissue alpha-tocopherol levels were highly significant for all tissues except adrenal, fat, and pancreas.

Dietary vitamin E concentration and duration of feeding affect tissue α-tocopherol concentrations of channel catfish ( Ictalurus punctatus)

Semipurified diets containing 30% crude protein from casein and gelatin were supplemented with three concentrations of dl- α-tocopheryl acetate (0, 240 or 1000 mg/kg) and fed to channel catfish (initial average weight = 36.4 g) for 6 weeks. Factorial analysis of variance indicated a significant ( P<0.001) effect of dietary vitamin E on α-tocopherol concentrations of plasma, liver and muscle; levels of α-tocopherol in these tissues were directly related to dietary vitamin E levels. Concentrations of α-tocopherol in plasma and liver reached approximate maxima by week 2; whereas, fillets of fish fed diets with 240 and 1000 mg dl- α-tocopheryl acetate/kg had progressively higher concentrations of α-tocopherol after 2, 4, and 6 weeks of feeding. Levels of α-tocopherol in fillet tissue that had previously been shown to improve oxidative stability were achieved after 6 weeks of feeding the diet containing 240 mg α-tocopherol/kg; similar levels were attained within 2 weeks of feeding the diet containing 1000 mg α-tocopherol/kg. This information may be used in developing diet and/or feeding regimes to improve the oxidative stability of channel catfish fillet tissue prior to harvest and processing.