Liver Alpha-tocopherol Concentrations Research Articles

Quantitation, Absorption and Tissue Distribution of Coenzyme Q10 from Pak-wanban (Sauropus androgynus L. Merr.) Leaf and Its Antioxidant Activities

Pak-wanban (Sauropus androgynus L. Merr.), a popular Thai vegetable, has been found to have a high content of Coenzyme Q10 (CoQ10), which is a powerful antioxidant. This study investigated the quantitation, absorption and tissue distribution of CoQ10 from raw and stir-fried Pak-wanban and its antioxidant activities in rats. Male Wistar rats (seven weeks old) were randomly grouped as follows: (1) control, (2) raw Pak-wanban powder of 0.5 mg CoQ10/kg/day, (3) stir-fried Pak-wanban powder of 0.5 mg CoQ10/kg/day, (4) stir-fried Pak-wanban powder of 1.0 mg CoQ10/kg/day, and (5) commercially CoQ10 supplement groups of 0.5 mg CoQ10/kg/day. The results found that stir-fried cooking did not significantly reduce the content of CoQ10 in the Pak-wanban leaves. After 3 weeks of experimentation, the level of CoQ10 in the plasma, liver and spleen was increased in all Pak-wanban groups when compared to the control group. The level of CoQ10 in the stir-fried Pak-wanban group was significantly higher than the raw Pak-wanban group but slightly lower than the CoQ10 supplement group. Liver alpha-tocopherol concentrations were markedly increased in rats that consumed a high dose of CoQ10 from stir-fried Pak-wanban of 1 mg of CoQ10/kg/day when compared with the control group. Plasma antioxidant activities (ORAC: FRAP: DPPH) were significantly increased in both groups of stir-fried Pak-wanban when compared with the control group. We concluded that CoQ10 in Pak-wanban could be well absorbed and improved the plasma antioxidant activities. Furthermore, cooking oil may increase the bioavailability of CoQ10 from vegetables. Therefore, it would be useful for vegetarian people.

Dietary Alpha-Tocopherol Affects Tissue Vitamin E and Malondialdehyde Levels but Does not Change Antioxidant Enzymes and Fatty Acid Composition in Farmed Atlantic Salmon (Salmo salar L.)

In this study the effect of increasing dietary alpha tocopherol on vitamin E tissue concentrations, lipid peroxidation (malondialdehyde), antioxidant enzymes, and fatty acid composition has been investigated in farmed Atlantic salmon. To this end fish (initial body weight ~ 193 g, n = 70 per group) were fed diets based on fish oil (27.5 %), fish meal (15.0 %), wheat gluten (20.6 %), and soy protein concentrate (24.0 %) for 14 weeks. Diets were supplemented with 0 (negative control), 150, and 400 mg/kg vitamin E as all-rac alpha-tocopheryl acetate. Dietary vitamin E did not affect feed conversion efficiency ratio but significantly (p < 0.05) increased alpha-tocopherol concentrations in salmon plasma, liver, and fillet (n = 8 per group each). The increase in fillet alpha-tocopherol was accompanied by a considerable decrease (p < 0.01) in malondialdehyde concentrations at the higher supplementation level. Furthermore, we observed an antagonistic interaction between alpha- and gamma-tocopherol in plasma at the highest supplementation level, since high dietary alpha-tocopherol reduced plasma gamma-tocopherol concentrations. Liver antioxidant enzymes, including glutathione peroxidase and superoxide dismutase, remained largely unchanged in response to dietary alpha-tocopherol. Dietary alpha-tocopherol did not affect eicosapentaenoic acid and docosahexaenoic acid concentrations in salmon fillet. Present data suggest that alpha-tocopherol supplementations beyond dietary recommendations may further improve flesh quality and nutritional value of Atlantic salmon fillet as far as malondialdehyde and vitamin E concentrations are concerned.

The Effect of Carrier for Vitamin E on Liver Concentrations of Vitamin E and Vitamin E Excretion in Broilers ,

Two experiments were conducted to determine the effect of 2 carrier sources of vitamin E on growth performance and excreta and liver vitamin E concentrations of broilers. Chicks were pretested from d 0 to 7 posthatching on a corn-soybean meal diet without vitamin E supplementation, and the experiments lasted from d 7 to 19 posthatching. Each treatment in both experiments was replicated with 6 pens with 5 chicks each. Initial and final BW were 155 and 684 g in experiment 1 and 155 and 691 g in experiment 2. In experiment 1, the dietary treatments were the corn-soybean meal diet with varying concentrations (0, 30, 100, or 300 IU/kg) of supplemental vitamin E either absorbed to verxite (VE) or adsorbed to silica (SE). In experiment 2, the dietary treatments were the 0 and 30 IU/kg of vitamin E as VE or SE. In experiment 1, feed intake decreased and gain:feed increased as concentration of VE increased, but feed intake increased and gain:feed decreased as concentration of SE increased (source x concentration, P < 0.03). Gain, feed intake, and gain:feed were not affected (P > 0.10) by the vitamin E carrier source in experiment 2. The mean excreta vitamin E concentration at d 7 posthatching was 17.2 IU/kg (DM basis). The percentages of vitamin E excreted were based on analyzed vitamin E concentrations in the diet. At 100 and 300 IU/kg of supplemental vitamin E, an average of 94 and 44% of vitamin E intake from broilers fed vitamin E from VE and SE, respectively, was excreted (vitamin E source, P < 0.01; source x concentration, P < 0.08), but at 30 IU/kg of vitamin E, 49 and 45% of vitamin E intake from broilers fed vitamin E from VE and SE was excreted. In experiment 2, 52 and 43% of vitamin E intake from VE and SE was excreted (source, P < 0.02). Liver alpha-tocopherol concentration was not different (P > 0.10) between the sources of vitamin E in either experiment. Increased concentrations of vitamin E increased liver alpha-tocopherol concentrations (P < 0.01). On the basis of the results of excreted vitamin E, vitamin E adsorbed to SE was more available than vitamin E absorbed to VE, but on the basis of liver vitamin E concentration, their availabilities were similar.

Galactosamine-Induced Acute Liver Injury in Rats Reduces Hepatic .ALPHA.-Tocopherol Transfer Protein Production

The liver plays the main role in the secretion of food-derived alpha-tocopherol into the circulation through the functioning of alpha-tocopherol transfer protein (alpha-TTP). However, the effect of liver disease on alpha-TTP level and alpha-tocopherol metabolism has not been clarified. We examined the amount of liver alpha-TTP and its effect on serum alpha-tocopherol concentration in liver injury. Male Wistar rats were injected intraperitoneally with D-galactosamine at 800 mg/kg body weight, and liver and serum lipid concentrations, alpha-tocopherol concentrations, and hepatic alpha-TTP mRNA and protein levels were measured at 24, 48, and 72 h after injection. On the basis of body weight changes and serum transaminase activities, the livers were found to be in an injured state 24 and 48 h after galactosamine injection but had recovered by 72 h. The hepatic alpha-TTP mRNA level was reduced throughout the experimental period, and at 48 h after injection the alpha-TTP protein level had begun to decrease. Lipid and alpha-tocopherol concentrations in the serum were decreased at 24 and 48 h after injection and increased at 72 h. Liver lipid concentrations were increased at 24 and 48 h after injection, but the liver alpha-tocopherol concentration was unchanged. These results show that galactosamine-induced liver injury decreases hepatic alpha-TTP synthesis in rats. Serum alpha-tocopherol concentration was not directly affected by the acute change in hepatic alpha-TTP level, suggesting that the chronic changes in alpha-TTP activity would be necessary to regulate serum alpha-tocopherol concentration.

Combined Lycopene and Vitamin E Treatment Suppresses the Growth of PC-346C Human Prostate Cancer Cells in Nude Mice

Epidemiologic studies have repeatedly associated a high intake of lycopene and vitamin E with reduced prostate cancer risk. The present study examined the ability of the 2 compounds to reduce tumor growth and prostate-specific antigen (PSA) plasma levels in the PC-346C orthotopic mouse model of human prostate cancer. Three days after intraprostatic tumor injection, NMRI nu/nu mice were administered a daily oral dose of synthetic lycopene [5 or 50 mg/kg body weight (BW)], vitamin E in the form of alpha-tocopheryl acetate (5 or 50 mg/kg BW), a mixture of lycopene and vitamin E (5 mg/kg BW each), or vehicle. Intraprostatic tumor volume and plasma PSA concentrations were measured at regular intervals. Mice were killed when the tumor load exceeded 1000 mm(3) or on d 95 when the study was terminated. Prostate and liver were analyzed by HPLC for lycopene isomers and alpha- and gamma, delta-tocopherol concentrations. None of the single treatments significantly reduced tumor volume. In contrast, combined treatment with lycopene and vitamin E, at 5 mg/kg BW each, suppressed orthotopic growth of PC-346C prostate tumors by 73% at d 42 (P < 0.05) and increased median survival time by 40% from 47 to 66 d (P = 0.02). The PSA index (PSA:tumor volume ratio) did not differ between experimental groups, indicating that PSA levels were not selectively affected. Lycopene was detected only in mice supplemented with lycopene. As in humans, most tissue lycopene was in the cis-isomer conformation, whereas 77% trans-lycopene was used in the dosing material. Liver alpha-tocopherol concentrations were increased in mice supplemented with both 50 mg/kg (226%, P < 0.05) and 5 mg/kg vitamin E (41%, P < 0.05), whereas prostate alpha-tocopherol concentrations were increased only by the higher dose (83%, P < 0.05). Our data provide evidence that lycopene combined with vitamin E may inhibit the growth of prostate cancer and that PSA can serve as a biomarker of tumor response for this treatment regimen.

Regulation of the α‐tocopherol transfer protein in mice: Lack of response to dietary vitamin E or oxidative stress

The alpha-tocopherol transfer protein (TTP) plays an important role in the regulation of plasma alpha-tocopherol concentrations. We hypothesized that hepatic TTP levels would be modulated by dietary vitamin E supplementation and/or by oxidative stress. Mice were fed either a High E (1150 mg RRR-alpha-tocopheryl acetate/kg diet) or a Low E (11.5 mg/kg diet) diet for 2 wk. High E increased plasma and liver alpha-tocopherol concentrations approximately 8- and 40-fold, respectively, compared with Low E-fed mice, whereas hepatic TTP increased approximately 20%. Hepatic TTP concentrations were unaffected by fasting (24 h) in mice fed either diet. To induce oxidative stress, chow-fed mice were exposed for 3 d to environmental tobacco smoke (ETS) for 6 h/d (total suspended particulate, 57.4 +/- 1.8 mg/m3). ETS exposure, while resulting in pulmonary and systemic oxidative stress, had no effect on hepatic alpha-tocopherol concentrations or hepatic TTP. Overall, changes in hepatic TTP concentrations were minimal in response to dietary vitamin E levels or ETS-related oxidative stress. Thus, hepatic TTP concentrations may be at sufficient levels such that they are unaffected by either modulations of dietary vitamin E or by the conditions of environmentally related oxidative stress used in the present studies.

Dietary Fat Type Affects Vitamins C and E and Biomarkers of Oxidative Status in Peripheral and Brain Tissues of Golden Syrian Hamsters

Oxidative stress is an important trigger in the complex chain of events leading to neurodegenerative diseases. On the other hand, dietary fatty acids play an essential role in brain function. The objectives of this study were to assess the effect of dietary fat type on vitamin C and vitamin E (alpha-and gamma-tocopherol) concentrations in peripheral and brain tissues and its effect on 8-epiPGF(2)alpha (F(2)-isoprostanes). Male Golden Syrian hamsters (n = 120, 8 wk old) were fed diets enriched in butter, hydrogenated fat (margarine), and canola and soybean oils. After 12 wk, hamsters were deprived of food, anesthetized with isoflurane, and killed via terminal exsanguination. Analyses of vitamins C, E, and 8-epiPGF(2)alpha were performed in peripheral tissues and brain. Hamsters consuming the margarine-enriched diet had lower (P < 0.05) vitamin C and alpha-tocopherol concentrations in liver, plasma, and brain, and higher (P < 0.02) plasma 8-epiPGF(2)alpha than groups fed the butter, and the canola and soybean oil diets. Liver and plasma gamma-tocopherol concentration was higher (P < 0.001) among the groups fed the soybean- and margarine-enriched diets compared with the other groups. alpha-Tocopherol was higher (P < 0.05) and 8-epiPGF(2)alpha lower (P < 0.01) among the groups fed the canola and soybean oil diets compared with the other groups. Across the groups, an inverse correlation between plasma levels of vitamin C and 8-epiPGF(2)alpha (r = -0.37, P = 0.03) and a positive correlation between plasma levels of vitamin C and alpha-tocopherol were observed (r = 0.341, P = 0.003). Hamsters fed the butter-enriched diet had a higher (P < 0.03) plasma uric acid concentration than the other groups. The results of this study provide new evidence concerning the effect of dietary fat on antioxidant status, which is important for the maintenance of good health.

Five Cysteine-Containing Compounds Have Antioxidative Activity in Balb/cA Mice

Balb/cA mice were used to study the in vivo effect of N-acetyl cysteine, S-allyl cysteine, S-ethyl cysteine, S-methyl cysteine and S-propyl cysteine, all derived from garlic, on glutathione (GSH) concentration and catalase and glutathione peroxidase (GPX) activities in plasma, kidney and liver. Cysteine was used for comparison. The effects of these compounds on the levels of fibronectin, triglyceride (TG), cholesterol and alpha-tocopherol were also evaluated. Cysteine or cysteine-containing compounds were added to drinking water at 1 g/L. After 4 wk of treatment, GSH levels in kidney and liver were greater (P<0.05) than in controls. Cysteine decreased catalase and GPX activities in liver, and enhanced both Fe2+- and glucose-induced lipid oxidation in plasma, kidney and liver compared with the control group (P<0.05). However, the administration of the five cysteine-containing compounds enhanced catalase and GPX activities in kidney and liver, and reduced Fe2+- and glucose-induced lipid oxidation in plasma, kidney and liver compared with the control and cysteine-treated groups (P<0.05). Intake of the five cysteine-containing compounds reduced fibronectin, TG and cholesterol concentrations in plasma and liver, and increased the alpha-tocopherol concentration in plasma, kidney and liver compared with the control and cysteine-treated groups (P<0.05). The five cysteine-containing compounds derived from garlic had marked effects on antioxidant enzymes and spared alpha-tocopherol in mice. Furthermore, these compounds reduced fibronectin, TG and cholesterol concentrations in plasma. These data indicate that these compounds have a range of protective effects for cardiovascular disease prevention or therapy.

Effects of Sago Starch Content in the Diet on Lipid Peroxidation and Antioxidative Enzyme Activities in Rats

The effects of sago starch content in diets on the status of lipid peroxidation and antioxidative enzyme activities were examined with rats fed cholesterol-free and cholesterol-enriched diets. Despite the diets with and without supplemental cholesterol, both food intake and the value of plasma thiobarbituric acid reactive substances (TBARS) showed a lower tendency or lower values in the rats fed the diet with a high ratio of sago starch as compared to a low ratio. Liver superoxide dismutase (SOD) and catalase activities, and serum and liver alpha-tocopherol concentrations were higher in the rats fed the cholesterol-free and enriched diets with a high ratio of sago starch as compared to a low ratio. From these results, it was suggested that a higher ratio of sago starch in the diet may be useful to keep the in vivo oxidative status at a lower level.

Evaluating the antioxidant status of weanling pigs fed dietary vitamins A and E

Two experiments evaluated the relationship of vitamin E (source and level) and vitamin A (level) on the apparent absorption and retention of both vitamins in weaned pigs. Both experiments used a combined total of 460 crossbred pigs ([Yorkshire x Landrace] x Duroc), housed in elevated 1.2- x 1.2-m crates containing five pigs per pen. Experiment 1 was a 2 x 2 x 2 factorial arrangement of treatments in a randomized complete block design conducted in seven replicates. Levels of vitamin A (2,200 or 13,200 IU/kg), vitamin E (15 or 90 IU/kg), and two vitamin E sources (D-alpha-tocopheryl acetate [D-TAc] or DL-alpha-tocopheryl acetate [DL-TAc]) were evaluated over a 35-d period. Vitamin A or E levels and the two vitamin E sources did not affect pig performances to 20 kg BW. Serum retinol and alpha-tocopherol concentrations increased (P < 0.01) as the dietary level of each vitamin increased. Serum alpha-tocopherol declined as dietary vitamin E level increased when vitamin A level increased resulting in an interaction (P < 0.05). Serum alpha-tocopherol concentrations were higher (P < 0.05) at 35-d postweaning when D-TAc was the vitamin E source. Experiment 2 was a 3 x 2 factorial arrangement of treatments conducted in six replicates. Three levels of vitamin A (2,200, 13,200, or 26,400 IU/ kg) and two sources of vitamin E (D-TAc or DL-TAc) each provided at 40 IU/kg diet were evaluated over a 35-d period. Pig performances to 35-d postweaning were not affected by the dietary variables. Serum alpha-tocopherol (P < 0.01) and retinol (P < 0.05) concentrations increased as their respective vitamin level increased. Serum (P < 0.05) and liver (P < 0.01) alpha-tocopherol concentrations both declined as dietary vitamin A levels increased resulting in interaction responses. Serum alpha-tocopherol concentration was higher (P < 0.05) at 35-d postweaning when d-TAc was the vitamin E source. Dietary vitamin E sources had no effect on serum or liver retinol concentrations. These results demonstrated that both supplemental vitamin A and vitamin E increased in the blood as their dietary levels increased. However, as dietary vitamin A level increased, serum and liver alpha-tocopherol concentrations declined, suggesting a reduced absorption and retention of alpha-tocopherol when weaned pigs were fed high dietary vitamin A levels.

Feeding unsaponifiable compounds from rice bran oil does not alter hepatic mRNA abundance for cholesterol metabolism-related proteins in hypercholesterolemic rats.

The hypocholesterolemic effect of rice bran oil (RBO) is defined in human and animal experiments which indicate the presence of active component(s) in the unsaponifiable fraction, but the detailed mechanism is not known yet. Exogenously hypercholesterolemic (ExHC) rats were fed for 2 weeks on a 0.5% cholesterol diet supplemented with 10% each of RBO, RBO-simulated oil (RBOSO) in its fatty acid composition, or RBOSO plus 0.25% unsaponifiable compounds (UC) from RBO. Rats fed RBO or the UC resulted in lowing serum and liver cholesterol concentration and preventing reduction of high density lipoproteinic-cholesterol. Dietary RBO or the UC led to an elevation of fecal neutral sterol excretion, but no significant change in fecal bile acid excretion or in hepatic abundance of mRNAs for 3-hydroxy-3-methylglutaryl-CoA reductase, cholesterol-7alpha-hydroxylase, and low density lipoprotein receptor. Besides, serum and liver alpha-tocopherol concentrations were lowered in RBO or the UC-fed rats. These results show that the UC in RBO leads to a decreased serum cholesterol concentration by interrupting the absorption of intestinal hydrophobic compounds rather than by modifying cholesterol metabolism in the liver.

Low Arachidonic Acid Rather than α-Tocopherol Is Responsible for the Delayed Postnatal Development in Offspring of Rats Fed Fish Oil Instead of Olive Oil during Pregnancy and Lactation

This study was designed to compare in rats the effects of dietary fish oil and olive oil during pregnancy and lactation on offspring development, fatty acid profile and vitamin E concentration. From d 0 of pregnancy, female Sprague-Dawley rats were divided into two groups that were fed purified diets that differed only in their nonvitamin lipid components. One diet contained 10 g fish oil/100 g diet (FOD), whereas the other contained 10 g olive oil/100 g diet (OOD). At d 20 of gestation, maternal adipose tissue fatty acid profile did not differ between rats fed the two diets, whereas both maternal and fetal plasma and liver arachidonic acid (AA) contents were proportionally lower and eicosapentaenoic (EPA) and docosahexaenoic (DHA) acid contents were higher in the FOD group than in the OOD group. alpha-Tocopherol concentration was lower in maternal and fetal plasma, liver and brain in the FOD group than in the OOD group. The postnatal increase in body weight and length was less and body and psychomotor maturation indices were delayed in pups from FOD-fed dams compared with those from OOD-fed dams. This difference was maintained when pups were cross-fostered at birth, with the delay in postnatal development present in the pups suckling dams fed FOD during lactation. At age 21 d, pups suckling dams fed FOD had lower AA and higher EPA and DHA concentrations in brain phospholipids. Although alpha-tocopherol in plasma and liver was lower in pups suckling dams fed FOD rather than OOD, brain alpha-tocopherol concentrations did not differ. Milk yield and milk alpha-tocopherol and AA concentrations were lower and EPA and DHA were higher in the milk of dams fed FOD compared with those fed OOD. Postnatal development indices and the proportion of plasma, liver and brain AA concentrations, although not plasma, liver and brain alpha-tocopherol concentrations, recovered to the values found in dams fed OOD when the FOD was supplemented with gamma-linolenic acid. However, postnatal development indices were not recovered when the FOD was supplemented with sufficient exogenous vitamin E to increase plasma and liver alpha-tocopherol concentrations above those in dams fed OOD. Thus, although feeding FOD during pregnancy and lactation decreases both alpha-tocopherol and AA concentrations, the latter deficiency rather than the former seems to be responsible for delayed postnatal development of rat pups.

Sesamin and alpha-tocopherol synergistically suppress lipid-peroxide in rats fed a high docosahexaenoic acid diet.

Docosahexaenoic acid (DHA) is an essential nutrient for human health, but has extremely high oxidative susceptibility. We examined the suppressing effect of sesamin, a sesame seed lignan, on lipidperoxides in rats fed a low alpha-tocopherol and high DHA containing diet. Groups of rats were fed four experimental diets: low alpha-tocopherol (10 mg/kg diet) control diet, low alpha-tocopherol + 0.2% sesamin diet, low alpha-tocopherol + 0.5% DHA diet and low alpha-tocopherol + 0.5% DHA + 0.2% sesamin diet. TBARS concentrations in plasma and liver were significantly increased by DHA, but were completely suppressed by sesamin. Alpha-tocopherol concentrations in plasma and liver decreased by addition of DHA, but with sesamin recovered to the control level. The addition of DHA into the diets caused remarkable increases of DHA concentrations in plasma and liver lipids. Sesamin caused a significant increase of DHA concentrations in the triacylglycerol of plasma.

Alpha-tocopherol and phospholipase A2 in liver and brain of chicks posthatching: the influence of dietary fat and vitamin E.

One of the classical vitamin E deficiency syndromes is nutritional encephalomalacia in broiler chicken. Subject of this study was the influence of dietary fatty acids and vitamin E on phospholipase A2 and alpha-tocopherol concentration in liver, cerebrum and affected cerebellum posthatching. Therefore, chicks were fed either oleic, linoleic or linolenic acid rich fats together with 5, 25, or 125 ppm vitamin E. At the end of 0, 1, 2 and 3 weeks the tocopherol content and phospholipase A2 activity of liver, cerebrum and cerebellum were determined. Dietary fatty acids did not influence tissue alpha-tocopherol and phospholipase A2. In the vitamin E-deficient cerebellum the enzyme activity of cytosolic phospholipase A2 was increased. Due to its low content of vitamin E the cerebellum is the most susceptible tissue to oxidative stress during vitamin E deficiency.

Effect of vitamin E supplementation on immune status and α-tocopherol in plasma of piglets

Twelve (Yorkshire) gilts were assigned to 2 dietary fat supplement groups starting at 57 d of gestation. Group 1 received no fat and Group 2 was supplemented with 5% Canola oil. Each group was supplemented with 0.1 ppm Se and 22 IU of DL-alpha-tocopherol acetate/kg of feed. Colostrum (d 0) and milk (7, 14, 21 and 28 d post partum) were sampled from gilts. At farrowing 3 piglets from each gilt of both groups were injected with alpha-tocopherol at birth (500 IU) and at 7 and 14 d (1,000 IU) of age and 3 piglets were injected with saline and used as control. Blood samples were taken from the newborn piglets at birth and at 7, 14, 21, 28 and 35 d of age. alpha-Tocopherol concentration in the colostrum of gilts was significantly higher than in the milk. Plasma alpha-tocopherol concentrations and antibody titres to Key-hole limpet haemocyanin of piglets injected with vitamin E were significantly higher than the control piglets. Vitamin E injected piglets had significantly higher alpha-tocopherol concentrations in spleen, liver, kidney, heart, lung and hip muscle than the control piglets.

Tissue vitamin E status is compromised by dietary protein insufficiency in young growing rats.

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-alpha-tocopheryl acetate, or a 20% (wt/wt) lactalbumin diet containing 50 (N50) or 500 (N500) mg/kg of all-rac-alpha-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 alpha-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 alpha-tocopherol in heart, kidney, muscle, brain and adipose tissue compared with the N500 group. The alpha-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-alpha-tocopheryl acetate resulted in significantly higher tissue alpha-tocopherol concentration in all tissues except muscle. The tissue alpha-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 alpha-tocopherol concentrations in most tissues in young growing rats.

Serum and tissue tocopherol in sheep after intramuscular injection and(or) dietary vitamin E supplementation

In a 28-d trial, 35 wethers weighing 35 to 60 kg were used to evaluate serum, liver, pancreas, kidney, diaphragm, heart, and neck muscle alpha-tocopherol concentrations after vitamin E administration as i.m. injections and(or) oral supplementation. Treatments (T) were as follows: 1) i.m. DL-alpha-tocopherol(DL-alpha-ol) d 1, 2) i.m. DL-alpha-tocopheryl acetate(DL-alpha-ac) d 1, 3) i.m. DL-alpha-ol d 1, 7, 14, and 21, 4) T 1 and oral supplementation, 5) T 3 and oral supplementation, 6) oral supplementation, and 7) control, no E supplementation. Supplemented wethers received 500 IU via injection and(or) 30 IU/kg of diet (acetate form). In a second 10-d trial, blood was periodically collected from 20 wethers weighing 32 to 47 kg that had been assigned to T as follows: 1) control, 2) i.m. DL-alpha-ol d 1, 3) i.m. DL-alpha-ac d 1, 4) T 2 d 1 and 7, and 5) T 3 d 1 and 7. Results from repeated measures ANOVA in both trials indicated that there were day x T effects (P < .0001) on serum alpha-tocopherol. Pretreatment serum tocopherol concentrations were .58 and .66 microgram/mL for Trials 1 and 2, respectively. In Trial 1, wethers receiving the four alcohol vitamin E forms showed a rapid increase in serum tocopherol between d 1 and 3, followed by a rapid decline to pretreatment concentrations for T 1, whereas T 3, 4, and 5 maintained higher than pretreatment concentrations after the decline.(ABSTRACT TRUNCATED AT 250 WORDS)

Tissue equilibration and subcellular distribution of vitamin E relative to myoglobin and lipid oxidation in displayed beef

Supplementary alpha-tocopheryl acetate (vitamin E) was fed to provide none (E0), 2,000 IU/d (E2000), 5.8 IU/kg live weight (E5.8), or 8.6 IU/kg live weight (E8.6) to steers that were individually fed mainly a corn diet. Three steers were placed on each of 10 treatments: E0, E2000, E5.8, E5.8 to d 126 then E0 to d 266, E0 to d 126 then E5.8 to d 266, E8.6, grazing followed by either E0 or E8.6 all with Holstein steers; and E0 and E2000 with crossbred beef steers. During the last 100 d, vitamin E consumption (International Units/day) averaged 96 for E0, 1,840 for E2000, 2,520 for E5.8, and 3,610 for E8.6. Concentrations of alpha-tocopherol in plasma and in liver and longissimus lumborum biopsy samples obtained every 42 d were elevated (P < .01) by vitamin E supplementation. Tissue saturation was approached at these vitamin E intakes causing similar incorporation of alpha-tocopherol with both per day and per BW supplementation strategies. Maximum accretion or depletion of alpha-tocopherol in plasma and liver occurred before 42 d, but accretion required 120 d and depletion required 180 d in longissimus lumborum. Vitamin E supplementation elevated (P < .01) concentrations of alpha-tocopherol in liver, lung, subcutaneous fat, omental fat, perirenal fat, kidney, diaphragm, spinal cord, longissimus lumborum, and plasma at slaughter with maximum accretion achieved (P < .01) in lung, subcutaneous fat, kidney, diaphragm, and spinal cord. Depletion was not achieved in longissimus lumborum and spinal cord (P < .01), subcutaneous fat (P < .06), and perirenal fat (P < .08) within 140 d. Vitamin E inhibited (P < .01) oxidation at the surface and center of longissimus lumborum steaks displayed for 19 d. Lipid oxidation occurred throughout E0 steaks, but metmyoglobin accumulation occurred more rapidly (P < .01) on the surface than in the center. Myoglobin and lipid oxidation were not concurrent events. Supplementation with vitamin E increased (P < .01) alpha-tocopherol concentrations in longissimus lumborum fractions (mitochondria, microsome, cytoplasm, connective, and remainder) but, except for connective tissue, the proportional distribution of total longissimus lumborum alpha-tocopherol was not affected (P > .1) by vitamin E supplementation. Vitamin E supplementation for at least 44 d at 1,300 IU/d is expected to incorporate adequate amounts of alpha-tocopherol into muscle (3.3 micrograms/g for longissimus lumborum) to produce beef with extended color and lipid stability.

REDUCED CONCENTRATION OF HEPATIC α-TOCOPHEROL IN PATIENTS WITH ALCOHOLIC LIVER CIRRHOSIS

The concentration of alpha-tocopherol was measured in liver biopsy specimens obtained from 83 patients with alcoholic and non-alcoholic liver diseases. The mean hepatic vitamin E content (as alpha-tocopherol) was significantly lower in 23 patients with alcoholic cirrhosis (17.6 +/- 12.1 nmol/mg wet weight liver), compared with 12 patients with normal liver histology (39.2 +/- 29.7 nmol/mg, P less than 0.01). The mean serum concentration of alpha-tocopherol was lower in patients with alcoholic cirrhosis (13.9 +/- 7.0 mumol/l) than in individuals with alcoholic fatty liver (21.3 +/- 9.3 mumol/l, P less than 0.01) and patients with normal liver histology (23.4 +/- 11.6 mumol/l, P less than 0.01). A decreased ratio of serum alpha-tocopherol/total serum lipids was also observed in patients with alcoholic cirrhosis, compared with patients with normal liver histology (P less than 0.05). There was a significant correlation between concentrations of alpha-tocopherol in liver and serum (r = 0.43, P less than 0.001). Furthermore, serum alpha-tocopherol correlated with retinol (r = 0.53, P less than 0.001), selenium (r = 0.45, P less than 0.001), and albumin (r = 0.37, P less than 0.001) in serum. We suggest that the reduced content of hepatic alpha-tocopherol observed in some patients may play a role in ethanol-induced lipid peroxidation.

Assessment of the influence of dietary vitamin E on sows and offspring in three parities: reproductive performance, tissue tocopherol, and effects on progeny

Sixty crossbred (Yorkshire-Hampshire X Duroc) gilts were fed one of four corn-soybean meal diets fortified with .3 ppm Se and 0, 16, 33, or 66 IU of DL-alpha-tocopheryl acetate/kg. The study was conducted over a three-parity period to evaluate sow reproductive performance and the vitamin E tissue status of both sows and progeny at various time periods postcoitum and(or) postpartum. The basal diet averaged 8.4 mg of alpha-tocopherol/kg and .38 ppm of Se. Although litter size at birth was lowest (P less than .15) when sows were fed the basal diet, a higher incidence of agalactia when sows were fed the lower dietary vitamin E levels resulted in an increased (P less than .05) litter size at 7 d postpartum as dietary vitamin E increased. Sow serum alpha-tocopherol increased (P less than .01) at each measurement period as dietary vitamin E level increased. Colostrum and milk alpha-tocopherol concentrations increased (P less than .01) as dietary vitamin E level increased, and colostrum values were three to five times higher than at later milks. Colostrum alpha-tocopherol declined by parity from sows fed less than or equal to 16 IU/kg but was similar at each parity for sows fed greater than or equal to 33 IU/kg, resulting in a dietary vitamin E x parity interaction (P less than .01). The Se content of sow milk declined with parity but was not affected by dietary vitamin E level. Sow liver tocopherol at weaning (28 d postpartum) increased (P less than .01) as dietary vitamin E increased and increased with parity (P less than .05). Pig serum and liver alpha-tocopherol concentrations were elevated at birth and 7 and 28 d of age as sow dietary level of vitamin E increased. Upon weaning, pigs were fed a torula yeast-dextrose diet that contained 3.0 mg of alpha-tocopherol/kg and .32 ppm Se for a 28-d postweaning period. Liver and serum alpha-tocopherol concentrations declined during the postweaning period. Evidence of the vitamin E deficiency occurred at 28 d postweaning in the progeny from sows fed the basal diet or 16 IU of vitamin E; the incidence was more prevalent in the pigs from Parities II and III. These results suggest that a supplemental level of 16 IU of vitamin E/kg of diet was inadequate for the reproducing sow; higher levels are justified, particularly when females are retained in the herd for several parities.