Plasma Α-tocopherol Concentrations Research Articles

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.

Oxidative nutritional stress associated with feeding rancid oils to African catfish, Clarias gariepinus (Burchell) and the protective role of α-tocopherol

Over a 56-day feeding period, during which juvenile African catfish, Clarias gariepinus (Burchell) increased in body weight at least threefold, diets containing fresh or rancid oils (0.352 and 9.133 mmol MDA equivalents per g oil, respectively) at two levels of supplemental vitamin E (20 or 100 mg all-rac-α-tocopheryl acetate kg-1 dry diet) were fed at 3% body weight per day. On termination of the feeding trial, growth performance and food utilization were assessed. Additionally, health criteria such as hepatosomatic index (HSI), haematocrit, plasma haemoglobin and plasma α-tocopherol concentration were determined. Plasma α-tocopherol was seen to increase significantly (P 0.05). Values of other growth parameters and nutrient utilization indices were seen to respond positively to increased vitamin E levels and fresher dietary oils. With respect to other health indices, HSI was strongly correlated (P < 0.05) to dietary vitamin E dose and not oil oxidation state, with catfish fed lower α-tocopherol doses exhibiting larger livers proportional to somatic mass. Haematocrit values were significantly (P < 0.05) lower in fish fed low-tocopherol/fresh-oil diets. Although no measurably significant differences were found between treatments with respect to plasma-haemoglobin concentration, higher mean values for the fish fed rancid oils at the lower α-tocopherol inclusion level may indicate heightened Spontaneous haemolysis in this group. Mechanisms to account for dietary modulation of health indices in catfish under the present dietary regime are postulated. It was concluded that supplemental α-tocopheryl acetate in diets likely to undergo oxidation, would protect catfish from the nutritional stress imposed by rancid oils and increase growth above levels associated with unsupplemented dietary treatments.

Increased oxidation resistance of atherogenic plasma lipoproteins at high vitamin E levels in non-vitamin E supplemented men

The oxidative modification of human low density lipoprotein (LDL) has been widely investigated. However, there are no data concerning the oxidation susceptibility of combined very low density lipoprotein (VLDL), intermediate density lipoprotein (IDL) and low density lipoprotein fraction, although all of them are atherogenic and contain antioxidants such as α-tocopherol. We investigated the oxidation susceptibility and oxidation resistance of VLDL + LDL (including IDL) fraction by induction with CuCl 2 and its relation to plasma α-tocopherol concentration and lipid standardised α-tocopherol concentration in 406 non-vitamin E-supplemented men from eastern Finland. Even thought we did not give oral vitamin E or any other antioxidant supplementation to our study participants, we observed a significant, consistent relationship between measurements of oxidation resistance and plasma content of vitamin E. In the multivariate regression model, a high plasma content of vitamin E or lipid standardised vitamin E concentration were the most important determinants of lag time to maximal oxidation rate (standardised regression coefficient = 0.244, P < 0.0001 for vitamin E and 0.211, P < 0.0001 for lipid standardised vitamin E). After statistical adjustment for age, use of cigarettes, hypolipidemic medication (yes vs. no), month of the measurements, plasma concentrations of total ascorbic acid (ascorbic acid + dehydroascorbic acid), β-carotene and phospholipids, serum concentrations of LDL cholesterol and triglycerides and dietary intake of linoleic acid, the lag time to maximal oxidation rate was 10% (95% C.I. 6.0–13.5%) longer in men in the highest fifth than in the lowest fifth of plasma vitamin E content ( P < 0.0001 for trend). When the fifths of lipid standardised vitamin E were compared, the lag time to maximal oxidation rate was 6% (95% C.I. 1.8–10.1%) longer in men in the highest than in the lowest fifth ( P < 0.0001 for trend). Our data suggest that α-tocopherol is an important antioxidant preventing the in vitro oxidation of VLDL + LDL fraction even in non-supplemented subjects.

Pharmacokinetic Profile of Plasma Tocopherol Following Intramuscular Administration of Acetylated α-Tocopherol to Sheep

Five sheep, with a mean BW of 45kg, were given a single i.m. injection (600 IU) of dl-α-tocopherol acetate. Plasma concentration of α-tocopherol was best fitted to a single-compartment model. Two successive absorption processes were selected. The individual pharmacokinetic parameters were absorption rate constant, Ka1=0.29±0.02/h; the second absorption rate constant, Ka2=0.03±0.002/h; elimination half-life = 42.40±1.70/h; mean residence time = 46±0.92h; and area under the curve = 290±10.77μg/h per ml. During the first absorption process, elimination half-life was 2.46±0.22h, and the second elimination half-life was 21.20±1.72h. The peak concentration of vitamin E plasma (4.78±0.23μg/ml) was observed at 14.6±4.08h after i.m. injection. The increase in vitamin E concentration occurred because of gradual hepatic hydrolysis of the absorbed acetylated tocopherol.

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.

Smoking and low antioxidant levels increase oxidative damage to sperm DNA

Our previous studies have shown that men with low ascorbate intake have markedly increased oxo 8dG in the DNA of their sperm. Because cigarette smoke is high in oxidants and depletes plasma and tissue antioxidants, oxidative DNA damage in sperm and tocopherol and ascorbate levels in seminal plasma were determined in smokers and non-smokers. The level in sperm DNA of oxo 8dG, an oxidative lesion of guanine, was 50% higher in smokers compared to non-smokers ( p = 0.005). The concentration of α-tocopherol in seminal plasma was decreased in smokers by 32% ( p = 0.03). Smoking and low antioxidant levels increase oxidative damage to sperm DNA. We discuss the possibility that paternal smoking causes mutations in sperm that lead to cancer, birth defects, and genetic diseases in offspring.

Randomised controlled trial of vitamin E in patients with coronary disease: Cambridge Heart Antioxidant Study (CHAOS)

Summary Background Vitamin E (α-tocopherol) is thought to have a role in prevention of atherosclerosis, through inhibition of oxidation of low-density lipoprotein. Some epidemiological studies have shown an association between high dietary intake or high serum concentrations of α-tocopherol and lower rates of ischaemic heart disease. We tested the hypothesis that treatment with a high dose of α-tocopherol would reduce subsequent risk of myocardial infarction (MI) and cardiovascular death in patients with established ischaemic heart disease. Methods In this double-blind, placebo-controlled study with stratified randomisation, 2002 patients with angiographically proven coronary atherosclerosis were enrolled and followed up for a median of 510 days (range 3-981). 1035 patients were assigned α-tocopherol (capsules containing 800 IU daily for first 546 patients; 400 IU daily for remainder); 967 received identical placebo capsules. The primary endpoints were a combination of cardiovascular death and non-fatal MI as well as non-fatal Ml alone. Findings Plasma α-tocopherol concentrations (measured in subsets of patients) rose in the actively treated group (from baseline mean 34·2 μmol/L to 51·1 μmol/L with 400 IU daily and 64·5 μmol/L with 800 IU daily) but did not change in the placebo group. α-tocopherol treatment significantly reduced the risk of the primary trial endpoint of cardiovascular death and non-fatal Ml (41 vs 64 events; relative risk 0·53 [95% Cl 0·34-0·83; p=0·005). The beneficial effects on this composite endpoint were due to a significant reduction in the risk of non-fatal Ml (14 vs 41; 0·23 [0·11-0·47]; p=0·005); however, there was a non-significant excess of cardiovascular deaths in the α-tocopherol group (27 vs 23; 1·18 [0·62-2·27]; p=0·61). All-cause mortality was 36 of 1035 α-tocopherol-treated patients and 27 of 967 placebo recipients. Interpretation We conclude that in patients with angiographically proven symptomatic coronary atherosclerosis, α-tocopherol treatment substantially reduces the rate of non-fatal MI, with beneficial effects apparent after 1 year of treatment. The effect of α-tocopherol treatment on cardiovascular deaths requires further study.

Whey from cultured skim milk decreases serum cholesterol and increases antioxidant enzymes in liver and red blood cells in rats

The study was carried out to examine the effect of whey from bovine skim milk fermented with bifidobacteria and lactic acid bacteria on plasma cholesterol and antioxidant enzymes in rats. Rats were maintained for 6 wks on a purified diet (reference diet) and on the purified diet supplemented milk whey or whey from cultured skim milk with Bifidobacterium longum (B. longum), Lactobacillus acidophilus (L. acidophilus) or Streptococcus salivarius subsp. thermophilus (S. thermophilus). Diets containing the product with S. thermophilus resulted in the lowest concentration of plasma cholesterol. The activity of superoxide dismutase (SOD) in red blood cells (RBC) and the activity of catalase in liver were elevated on cultured product-diets compared with the reference diet; in addition, the activity of glutathione peroxidase (GSHPx) in RBC was higher on the L. acidophilus diet compared with the reference diet. Although there were no significant differences in the concentrations of thiobarbituric acid-reactive substances and α-tocopherol in plasma, plasma d<1.063 g/ml lipoprotein fractions prepared from rats fed on the B. longum- and L. acidophilus-diets were resistant to the oxidative stress induced by a transition metal ion when compared with those from rats fed on the reference diet. The non-fermented whey diet was not as effective in lowering plasma cholesterol and in increasing antioxidant enzymes as were the fermentation product diets. These results therefore suggest that wheys from cultured milk may exert spesific effects on hypercholesterolemia and oxidative stress.

Impact of hydrogenated fat consumption on endogenous cholesterol synthesis and susceptibility of low-density lipoprotein to oxidation in moderately hypercholesterolemic individuals

The effects of replacing corn oil with corn oil margarine in stick form on endogenous cholesterol synthesis and susceptibility of low-density lipoprotein (LDL) to oxidation were assessed in 14 middle-aged and elderly men and women aged 63 ± 12 years (mean ± SD) with moderate hypercholesterolemia (mean LDL-cholesterol [LDL-C], 4.24 ± 0.59 mmol/L at the time of recruitment). Subjects consumed each of two diets for 32-day periods, one enriched in corn oil, which contained 30% of energy as fat (7% saturated fatty acid [SFA], 9% monounsaturated fatty acid [MUFA] [0.4% 18:1n9 trans], and 11% polyunsaturated fatty acid [PUFA]) and 85 mg cholesterol/4.2 MJ, and one enriched in stick corn oil margarine, which contained 30% fat (8% SFA, 12% MUFA [4.2% 18:1n9 trans], and 8% PUFA) and 77 mg cholesterol/4.2 MJ. Both diets were isocaloric and supplied by a metabolic research kitchen. Mean total cholesterol levels were lowest ( P = .039) when subjects consumed the corn oil-enriched diet (5.01 ± 0.51 mmol/L) as compared with the margarine-enriched diet (5.30 ± 0.58 mmol/L). LDL-C levels were 3.24 ± 0.51 and 3.50 ± 0.54 mmol/L when subjects consumed corn oil- and margarine-enriched diets, respectively ( P = .058). There were no significant differences in high-density lipoprotein cholesterol (HDL-C) or triglyceride concentrations between the two experimental periods. Consumption of the margarine-enriched diet versus the corn oil-enriched diet tended to result in lower cholesterol fractional synthetic rates ([C-FSRs] 0.0466 ± 0.0175 and 0.0668 ± 0.0298, respectively, P = .080) and cholesterol absolute synthetic rates ([C-ASRs] 1.1761 ± 0.5375 and 1.6954 ± 0.8685, respectively, P = .092); however, differences did not reach statistical significance. Consumption of the margarine-enriched diet versus the corn oil-enriched diet resulted in a significantly higher concentration of α-tocopherol in both plasma and LDL ( P = .004 and P = .011, respectively). LDL particle size tended to be smaller after subjects consumed the margarine-enriched diet versus the corn oil-enriched diet ( P = .103). Susceptibility of LDL to oxidation was similar after consumption of the corn oil- and margarine-enriched diets. These data suggest that an increased rate of endogenous cholesterol synthesis did not contribute to the higher plasma cholesterol concentrations during the period when subjects consumed the margarine-enriched diet. Therefore, the increase in cholesterol concentration resulting from margarine consumption was likely attributable, at least in part, to a decreased catabolic rate of cholesterol. Additionally, susceptibility of LDL to in vitro oxidation was not altered by consumption of hydrogenated fat.

Plasma tocopherol, retinol, and carotenoid concentrations in free-ranging Humboldt penguins (Spheniscus humboldti) in Chile

Plasma retinol and α-tocopherol concentrations were measured in heparinized blood samples collected from 51 free-ranging adult Humboldt penguins (Sphenicus humboldti) residing at two colonies off the Chilean coast. Thirty samples were collected in April 1992 from penguins inhabiting the Ex-islote de los Pajaros Ninos in Algarrobo, Chile. In September 1992, 21 samples were collected from birds inhabiting Isla de Cachagua, Chile. Samples were assayed for retinol, retinyl palmitate, α-tocopherol, γ-tocopherol, lutein, β-cryptoxanthin, lycopene, α-carotene, and β-carotene. Retinol, α-tocopherol, and lutein were detected in all samples, while lycopene and γ-tocopherol were not detected in any. A significantly higher percentage of samples had detectable levels of retinyl palmitate and α-carotene in April (P < 0.001): for β-cryptoxanthin the percentage was higher in September (P < 0.001). Plasma concentrations of α-tocopherol and lutein were higher in September. Alpha-tocopherol concentrations were 1,877.1 ± 99.0 (SEM) μg/dl in April compared to 2.289 ± 122.3 μg/dl in September (P < 0.05); lutein concentrations were 4.16 ± 0.43 μg/dl in April vs. 10.68 ± 1.02 μg/dl in September (P < 0.001). Retinol concentrations were not significantly different (117 ± 8.0 μg/dl in April vs. 105.3 ± 7.6 μg/dl in September). Both physiologic changes associated with season, and the change in locale may have contributed to the differences seen in the assay means and the number of samples with detectable levels. © 1996 Wiley-Liss, Inc.

Plasma tocopherol, retinol, and carotenoid concentrations in free‐ranging Humboldt penguins (Spheniscus humboldti) in Chile

Plasma retinol and α-tocopherol concentrations were measured in heparinized blood samples collected from 51 free-ranging adult Humboldt penguins (Sphenicus humboldti) residing at two colonies off the Chilean coast. Thirty samples were collected in April 1992 from penguins inhabiting the Ex-islote de los Pájaros Niños in Algarrobo, Chile. In September 1992, 21 samples were collected from birds inhabiting Isla de Cachagua, Chile. Samples were assayed for retinol, retinyl palmitate, α-tocopherol, γ-tocopherol, lutein, β-cryptoxanthin, lycopene, α-carotene, and β-carotene. Retinol, α-tocopherol, and lutein were detected in all samples, while lycopene and γ-tocopherol were not detected in any. A significantly higher percentage of samples had detectable levels of retinyl palmitate and α-carotene in April (P < 0.001): for β-cryptoxanthin the percentage was higher in September (P < 0.001). Plasma concentrations of α-tocopherol and lutein were higher in September. Alpha-tocopherol concentrations were 1,877.1 ± 99.0 (SEM) μg/dl in April compared to 2.289 ± 122.3 μg/dl in September (P < 0.05); lutein concentrations were 4.16 ± 0.43 μg/dl in April vs. 10.68 ± 1.02 μg/dl in September (P < 0.001). Retinol concentrations were not significantly different (117 ± 8.0 μg/dl in April vs. 105.3 ± 7.6 μg/dl in September). Both physiologic changes associated with season, and the change in locale may have contributed to the differences seen in the assay means and the number of samples with detectable levels. © 1996 Wiley-Liss, Inc.

α-Tocopherol Concentrations in Milk and Plasma During Clinical Escherichia coli Mastitis

Eighteen cows were challenged by intramammary infusion with Escherichia coli 727 to determine the effects of acute clinical mastitis on α-tocopherol concentrations in plasma and milk. Cows were fed diets supplemented with 1000 IU of vitamin E/d from calving through the experimental period. At challenge, geometric mean DIM was 33 d. Each mammary quarter was diagnosed with an IMI and clinical mastitis at 24 and 48h after challenge. The α-tocopherol concentrations in milk from challenged quarters were approximately 60% greater by 24 and 48h after challenge than concentrations at prechallenge and 168h postchallenge. Plasma α-tocopherol concentrations did not change after intramammary challenge. The α-tocopherol in plasma and milk was correlated at 48 and 168h postchallenge but at prechallenge or 24h postchallenge. Milk α-tocopherol and SCC were correlated positively across all sample periods. Milk fat and milk α-tocopherol concentrations were correlated at each sample period except 24h postchallenge. Increases in milk α-tocopherol during clinical mastitis were not correlated to milk production, DMI, or BSA concentration in milk. Changes in milk α-tocopherol concentration during clinical mastitis were similar to the dynamics of milk SCC.

Vitamin E treatment of weaner sheep. I. The effect of vitamin E supplements on plasma α-tocopherol concentrations, liveweight and wool production in penned or grazing sheep

Effect of vitamin E supplements on liveweight gain and wool production, and their effectiveness in increasing plasma alpha -tocopherol concentrations and preventing nutritional myopathy was investigated. Commercial preparations were compared in pen and grazing experiments in the first part of the study. In a pen experiment, 3 different treatments, intramuscular oily injection, oral drench and dried supplement added to feed, were compared; in grazing sheep, intramuscular oily injection and oral drench were compared. The intramuscular oily injection was slow to increase the plasma concentrations of alpha -tocopherol in pen experiments and did not prevent vitamin E deficiency and development of subclinical myopathy in grazing experiments. Oral treatments increased plasma alpha -tocopherol concentrations in the pen experiment; though repeated oral drench did not increase plasma alpha -tocopherol in the grazing experiment, the development of subclinical nutritional myopathy was prevented. Aqueous preparations of vitamin E and the effect of selenium supplements in grazing sheep were studied in the second part of the study. Aqueous injections of 2000 mg of vitamin E acetate by intramuscular and subcutaneous routes in December and February were successful in rapidly increasing and maintaining plasma alpha -tocopherol concentrations in grazing weaner sheep. Injections of aqueous emulsions of vitamin E acetate could be the most useful preventative treatment for nutritional myopathy if problems of tissue damage can be overcome. None of the vitamin E supplements increased liveweight gain in any of the experiments, and there was no increase in wool quantity or quality in any of the grazing experiments. When selenium and vitamin E supplementation were compared, selenium-supplemented sheep had greater wool length and fibre diameter over summer-autumn than vitamin E-treated or control sheep. Vitamin E supplements are expensive; unless flocks are susceptible to vitamin E-responsive myopathy, it is suggested that there is little economic justification for using vitamin E as a supplement over the summer.

Effects of Supplemental Vitamins E and C on the Immune Responses of Calves

Two experiments were conducted to evaluate the effects of oral supplementation of vitamin C and vitamin E (α-tocopherol), alone and in combination, on immune responses of calves. In Experiment 1, 18 Holstein newborn female calves were supplemented with 0, 1, and 2 g/d of vitamin C from birth to 6 wk of age. Concentrations of ascorbic acid in blood plasma were significantly higher for supplemented calves than for control calves. No significant differences among treatments occurred in the concentrations of IgG1, IgG2, and titer to keyhole limpet hemocyanin. In Experiment 2, effects of oral supplementation of vitamins E and C on immune responses were studied using 18 Holstein female calves. Concentrations of α-tocopherol in blood plasma were significantly higher for supplemented than for control calves. The concentrations increased from birth to wk 1, and then very little change occurred from wk 1 to 6. Differences among treatments in the concentrations of IgG1, IgG2, IgM, and titer to keyhole limpet hemocyanin were not significant; however, concentrations of IgM in calves supplemented with vitamins E and C generally tended to be higher than those of control calves. Antibodies to keyhole limpet hemocyanin were higher at 6 wk than at 4 wk of age.

The effect of dietary fat content on plasma α-tocopherol concentration during vitamin E supplementation: Fanny K. Ennever, Steven Schindler, Daniel J. Zaccaro, Jane Stegner, and [formula omitted], The Bowman Gray School of Medicine, Winston-Salem, NC

The effect of dietary fat content on plasma α-tocopherol concentration during vitamin E supplementation: Fanny K. Ennever, Steven Schindler, Daniel J. Zaccaro, Jane Stegner, and [formula omitted], The Bowman Gray School of Medicine, Winston-Salem, NC

Supplementation with low doses of vitamin E protects LDL from lipid peroxidation in men and women.

There is accumulating evidence that oxidative modification of LDL is an important step in the process of atherogenesis and that antioxidants may protect LDL from oxidation. We and others have previously shown that ingestion of pharmacological doses of the antioxidant D,L-alpha-tocopherol (vitamin E), far above the recommended daily intake (ie, 12 to 15 IU/d for adults), increases the oxidation resistance of LDL. In this study, we ascertained the minimal supplementary dose of vitamin E necessary to protect LDL against oxidation in vitro. Twenty healthy volunteers (10 men and 10 women, aged 21 to 31 years) ingested consecutively 25, 50, 100, 200, 400, and 800 IU/d, D,L-alpha-tocopherol acetate during six 2-week periods. No changes were observed in LDL triglyceride content, fatty acid composition of LDL, or LDL size during the intervention. Concentrations of alpha-tocopherol in plasma and LDL were both 1.2 times the baseline values after the first period (25 IU/d) and 2.6 and 2.2 times, respectively, after the last period (800 IU/d). There was a linear increase in LDL alpha-tocopherol levels up to an intake of 800 IU/d (r = .79, P < .0001) and a good correlation between alpha-tocopherol in plasma and LDL (r = .66, P < .0001). Simultaneously, the resistance of LDL to oxidation was elevated dose-dependently (+28% after the last period) and differed significantly from the baseline resistance time even after ingestion of only 25 IU/d.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of dietary carnosine on plasma and tissue antioxidant concentrations and on lipid oxidation in rat skeletal muscle

The effect of dietary carnosine supplementation on plasma and tissue carnosine and alpha-tocopherol concentrations and on the formation of thiobarbituric acid reactive substances (TBARS) in rat skeletal muscle homogenates was evaluated. Plasma, heart, liver and hind leg muscle was obtained from rats fed basal semipurified diets or basal diets containing carnosine (0.0875%), alpha-tocopheryl acetate (50 ppm), or carnosine (0.0875%) plus alpha-tocopheryl acetate (50 ppm). Dietary carnosine supplementation did not increase carnosine concentrations in heart, liver and skeletal muscle. Dietary supplementation with both carnosine and alpha-tocopherol increased carnosine concentrations in liver 1.56, 1.51- and 1.51-fold as compared with diets lacking carnosine, alpha-tocopherol or both carnosine and alpha-tocopherol, respectively. Dietary supplementation with both carnosine and alpha-tocopherol also increased alpha-tocopherol concentrations in heart and liver 1-38-fold and 1.68-fold, respectively, as compared to supplementation with alpha-tocopherol alone. Dietary supplementation with carnosine, alpha-tocopherol or both carnosine and alpha-tocopherol was effective in decreasing the formation of TBARS in rat skeletal muscle homogenate, with dietary alpha-tocopherol and alpha-tocopherol plus carnosine being more effective than dietary carnosine alone. The data suggest that dietary supplementation with carnosine and alpha-tocopherol modulates some tissue carnosine and alpha-tocopherol concentrations and the formation of TBARS in rat skeletal muscle homogenates.

Leukocyte Functions of Young Dairy Calves Fed Milk Replacers Supplemented with Vitamins A and E

Holstein calves (n = 44) were fed milk replacers from d 3 to 45 with low or high concentrations of vitamin A (7000 or 87,000 IU/kg) and vitamin E (11.2 or 57 IU/kg) to examine the influence of vitamin concentrations on vitamin bioavailability and leukocyte functions. Concentrations of α-tocopherol in plasma reflected increased vitamin E but were unaffected by increased vitamin A. Plasma retinol concentrations were greatest with high supplementation of vitamins A and E at wk 3; however, at wk 6, plasma of calves fed high vitamin A and low vitamin E contained the most retinol. Increased supplementation of vitamin A improved fecal consistency compared with that for calves fed the low vitamin A diet at wk 3 and 4. At wk 3, calves that received increased supplementation of vitamins E and A had enhanced neutrophil bactericidal activity compared with that of calves with increased individual vitamins. Lymphocyte DNA synthesis and chemotactic index were unaffected by dietary treatments. Results indicate that increased vitamin A in milk replacer did not affect plasma vitamin E concentrations, benefited fecal scores regardless of vitamin E concentrations, but was only beneficial to bactericidal activity of neutrophils in conjunction with increased vitamin E.

Consumption of thermally-oxidized sunflower oil by chicks reduces α-tocopherol status and increases susceptibility of tissues to lipid oxidation

The effect of heated sunflower oil consumption on alpha-tocopherol status, fatty acid composition and oxidative stability of chicken tissues was investigated. Chicks were fed on diets containing (g/kg): fresh sunflower oil (FSO) 40, heated sunflower oil (HSO) 40 or heated sunflower oil (40) supplemented with alpha-tocopheryl acetate (HSE) to a similar alpha-tocopherol concentration as the FSO diet. Concentrations of alpha-tocopherol in tissues of chicks fed on HSO and HSE were significantly lower than those of chicks fed on FSO. Significant correlations were observed between plasma alpha-tocopherol concentration and the alpha-tocopherol concentrations of other tissues (r > or = 0.67, P < 0.005) and between log plasma alpha-tocopherol and plasma thiobarbituric acid-reacting substances (TBARS) concentrations (r -0.851, P < 0.001). The concentrations of TBARS in tissues of chicks fed on the various diets were generally very similar before stimulation of peroxidation with Fe-ascorbate. Susceptibility of tissues to Fe-ascorbate-induced lipid peroxidation was increased by feeding HSO. Supplementation with alpha-tocopheryl acetate reduced susceptibility to lipid oxidation to varying degrees, depending on the tissue. The results suggest that chronic ingestion of oxidized lipids may compromise free-radical-scavenging activity in vivo by depleting alpha-tocopherol in the gastrointestinal tract, or possibly in plasma and other tissues.

Glutathione peroxidase activity in tissues of chickens supplemented with dietary selenium

Lipid peroxidation in plasma, blood glucose and plasma α-tocopherol concentrations and glutathione peroxidase (GSHpx) activities in tissues were investigated in chickens supplemented with dietary selenium from baker's yeast (Saccharomyces cerevisiae). There was no significant difference in lipid peroxidation, blood glucose and plasma α-tocopherol concentrations between chickens supplemented with and without dietary selenium. 3. GSHpx activities in erythrocytes, plasma and liver increased significantly in chickens supplemented with dietary selenium.