scholarly journals Effects of protein and vitamin E on haemoglobin formation in rats

1968 ◽  
Vol 22 (4) ◽  
pp. 751-755 ◽  
Author(s):  
J. Bunyan ◽  
J. Green ◽  
M. A. Cawthorne

1. Young rats were given, for 9 weeks, vitamin E-deficient diets containing either 20% or 10% casein, with and without a dietary supplement of 350 ppm D-α-tocopheryl acetate. For the next 5 weeks the casein content of the low-protein diets was decreased to 7%.2. The low-protein diets induced severe growth depression.3. The dialuric acid-induced haemolysis test showed that the rats given the 20% casein vitamin E-deficient diet were depleted of vitamin E, but that the rate of depletion on the lowcasein diet was slower.4. Haemoglobin levels were slightly decreased by the 10% casein diets after 9 weeks, but this difference was not found after 14 weeks, comparing 20% and 7% casein. Dietary vitamin E had no effect on haemoglobin levels or erythrocyte counts.

2008 ◽  
Vol 78 (45) ◽  
pp. 230-237 ◽  
Author(s):  
Wissam Ibrahim ◽  
Vickie Tatumi ◽  
Che-Chung Yeh ◽  
Chuen Bin Hong ◽  
Ching Kuang Chow

The purpose of this study was to determine if moderate levels of carnosine supplement, alone or in combination with vitamin E, enhance antioxidant status and/or provide protection against oxidative stress. Fiftyfour one-month-old male Sprague-Dawley rats were fed a basal vitamin E-deficient diet supplemented with either 0, 200, or 1000 mg L-carnosine, and either 0, 10, or 100 IU vitamin E (as all rec-α-tocopheryl acetate) per kg diet for 15 weeks. The antioxidant and oxidative status were assessed in the skeletal muscle, liver, and blood. Dietary vitamin E, but not carnosine, increased levels of vitamin E, decreased tissue peroxidizability, prevented incidence of myodegeneration, and reduced erythrocyte hemolytic stress. The levels of conjugated dienes, protein carbonyls, ascorbic acid, and nonprotein sulfhydryls, and activities of catalase, glutathione (GSH) peroxidase, and aldehyde dehydrogenase were not significantly altered by dietary carnosine or vitamin E. The results obtained suggest that supplementation of carnosine at levels of up to 1000 mg/kg diet does not significantly affect the antioxidant and oxidative status of rats.


1967 ◽  
Vol 4 (1) ◽  
pp. 1-14 ◽  
Author(s):  
Inger Nafstad

The effects of different protein levels, different fat levels and the supplement of vitamins B1 and E and the amino acids lysine, methionine and tryptophan on the development of gastric ulcers in pigs were studied in three experiments involving 72 pigs. The addition of vitamin B1, amino acids and the feeding of low fat rations did not change the number of stomach lesions observed. A modifying effect of vitamin E on ulcer development was observed. The feeding of low protein diets resulted in no increase of the total number of stomach lesions, but appeared to increase their severity. The pathology of gastric ulcers is described.


1985 ◽  
Vol 53 (1) ◽  
pp. 149-157 ◽  
Author(s):  
J. G. Bell ◽  
C. B. Cowey ◽  
J. W. Adron ◽  
Aileen M. Shanks

1. Duplicate groups of rainbow trout (Salrno gairdnert) (mean weight 11 g) were given for 40 weeks one of four partially purified diets that were either adequate or low in selenium or vitamin E or both.2. Weight gains of trout given the dually deficient diet were significantly lower than those of trout given a complete diet or a diet deficient in Se. No mortalities occurred and the only pathology seen was exudative diathesis in the dually deficient trout.3. There was significant interaction between the two nutrients both with respect to packed cell volume and to malondialdehyde formation in the in vitro NADPH-dependent microsomal lipid peroxidation system.4. Tissue levels of vitamin E and Se decreased to very low levels in trout given diets lacking these nutrients. For plasma there was a significant effect of dietary vitamin E on Se concentration.5. Glutathione (GSH) peroxidase (EC 1. 1 1. 1.9) activity in liver and plasma was significantly lower in trout receiving low dietary Se but was independent of vitamin E intake. The ratios of hepatic GSH peroxidase activity measured with cumene hydroperoxide and hydrogen peroxide were the same for all treatments. This confirms the absence of a Se-independent GSH peroxidase activity in trout liver.6. Se deficiency did not lead to any compensatory increase in hepatic GSH transferase (EC 2. 5. 1. 18) activity; values were essentially the same in all treatments.7. Plasma pyruvate kinase (EC 2. 7. 1.40) activity increased significantly in the trout deficient in both nutrients. This was thought to be due to leakage of the enzyme from the muscle and may be indicative of incipient (subclinical) muscle damage.


2001 ◽  
Vol 72 (3) ◽  
pp. 529-534 ◽  
Author(s):  
S. Y. Shiau ◽  
L. F. Shiau

AbstractA 10-week feeding trial was conducted to re-evaluate the level of dietary vitamin E (DL- α-tocopheryl acetate) that was adequate for juvenile tilapia Oreochromis niloticus ✕ O. aureus given diets containing two dietary lipid concentrations. Purified diets with eight levels of vitamin E (0, 25, 50, 75, 100, 150, 200, 400 mg/kg diet) at either 50 or 120 g lipid per kg were each given to three replicate groups of tilapia (mean weight: 0·69 (s.e.0·02) g) reared in a closed, recirculating system. Food efficiency and protein deposition were significantly (P < 0·05) higher in fish given 50 mg vitamin E per kg diet and 75 mg/kg diet in the 50 and 120 g lipid per kg groups respectively, compared with fish given the unsupplemented control diet. Mortality of fish was not affected by dietary treatment. Weight gain and liver microsomal ascorbic acid-stimulated lipid peroxidation data analysed by broken-line regression indicated that the optimum dietary vitamin E requirements in juvenile tilapia are 42 to 44 mg vitamin E per kg and 60 to 66 mg vitamin E per kg in 50 and 120 g lipid per kg diets, respectively.


1984 ◽  
Vol 52 (2) ◽  
pp. 335-349 ◽  
Author(s):  
R. V. Juhani Hakkarainen ◽  
Jouko T. Työppönen ◽  
Saifeldin Hassan ◽  
Gösta Bengtsson ◽  
S. R. Lennart Jönsson ◽  
...  

1. Investigations were carried out to establish the total biopotency of the natural vitamin E isomers in barley compared with that of DL-α-tocopheryl acetate.2. The chick was used as an experimental animal. Prevention of nutritional encephalomalacia (NE) and chick liver-storage and plasma-storage assays of vitamin E were the methods used in the study. The individual tocopherols and tocotrienols, both in the tissue samples and in the grain and barley oil, were analysed using high-pressure liquid chromatography (HPLC) with fluorescence detection. The diagnosis of NE was based on careful clinical and histopathological observations.3. It can be concluded from the results that full protection against NE in the chicks was obtained with a supplementation level of 7.5 mg DL-α-tocopheryl acetate/kg diet (i.e. a total vitamin E content of 11.20 mg/kg diet) or with a supplement of 8.7 g barley oil/kg diet (i.e. a total vitamin E content of 22.99 mg from barley oil/kg diet). This gave a biopotency factor of 0.49 for barley for prevention of NE of the chicks, as compared to that of DL-α-tocopheryl acetate.4. Using regression analysis a statistically linear relationship could be observed between the total dietary vitamin E level and the response, as measured by the total vitamin E content in the liver and plasma, both in the groups supplemented with DL-a-tocopheryl acetate and in the groups supplemented with corresponding amounts of vitamin E in barley oil. The liver and plasma responses to the total vitamin E in the barley-oil diet compared with those of the DL-a-tocopheryl acetate reference diet gave identical values for the regression coefficients, i.e. in both liver-storage and plasma-storage assays the value for slopes of dose-response lines was 0.37. This means that the biopotency of the total vitamin E in barley was 37% of that of dietary DL-a-tocopheryl acetate. Thus, barley is not as rich a source of vitamin E as could be supposed on the basis of the chemical determination of its total vitamin E content.5. It was possible to verify this experimentally established biopotency of 0.37 for the total vitamin E in barley by converting the chemically determined amounts of the vitamin E isomers in barley into DL-α-tocopheryl acetate equivalents by multiplying them with internationally accepted potency factors for the individual natural isomers (DL-α-tocopheryl acetate 1.00, D-α-tocopherol 1.49, D-β-tocopherol 0.60, D-gamma;-tocopherol 0.1 5, D-α-tocotrienol 0.37).6. In spite of the high proportion of α- and β-tocotrienols in the barley-oil diets (about 60% of the total vitamin E content), only traces of these isomers could be detected in the plasma and none could be detected in the liver. On the other hand, calculation of the individual hiopotencies for the different isomers in the barley-oil diet by comparing the dose responses, diet: liver, separately for each isomer with those of DL-α-tocopheryl acetate, resulted in biopotency values for α- and β-tocopherol which were twice as high as the internationally accepted conversion factors. These results of the present study tempted the authors to draw the conclusion that there may have been a chemical reduction of the α- and β-tocotrienols to the corresponding tocopherols before entering the liver.


1968 ◽  
Vol 22 (1) ◽  
pp. 133-143 ◽  
Author(s):  
M. A. Cawthorne ◽  
J. Bunyan ◽  
A. T. Diplock ◽  
Elspeth A. Murrell ◽  
J. Green

1. The effect of vitamin E on the metabolism, utilization and storage of vitamin A has been studied in the rat.2. Male weanling rats were given a vitamin A-deficient, vitamin E-deficient diet until growth had ceased for 3 days, and each rat was then given 50 i.u. vitamin A palmitate. The rats were divided into four groups and given the diet with the addition of 10% methyl oleate or 10% cod-liver oil methyl esters, or either of these diets supplemented with 100 ppm D-α-tocopheryl acetate. There was no increase in maximum weight-gain response in the two groups given vitamin E. There was a significantly lower weight-gain response in the groups given cod-liver oil methyl esters. This effect was not influenced by the presence of vitamin E in the diet.3. Weanling rats of both sexes were made deficient in vitamins A and E and then divided into two groups. One group received, every other day, 1·75 i.u. vitamin A palmitate and 0·6 mg D-α-tocopherol given together; the second group received the two vitamins, in the same amounts, on alternate days. After 28 days there was no difference in the growth of the two groups of rats, irrespective of sex.4. Vitamin A-depleted, vitamin E-deficient rats were given 17·51 μg ‘14C-carbinol’retinyl acetate and then a vitamin A-deficient, vitamin E-deficient diet or that diet supplemented with 100 ppm D-α-tocopheryl acetate. After 6 days, the total remaining ‘14C’retinol and its lipidsoluble metabolites were measured in the carcasses of the rats. Vitamin E administration did not affect the metabolism of the vitamin A dose or its effect on growth.5. Vitamin E-deficient rats were given vitamin A until their liver reserves exceeded 30000 i.u. and were then divided into two groups. One group received a diet deficient in vitamins A and E and the other received, in addition to this diet, a weekly oral supplement of 1 mg D-α-tocopheryl acetate. The vitamin E supplement significantly decreased the rate of vitamin A depletion from the liver during the next 6 weeks. This effect, which was not found to occur when the initial liver reserves were only 3000 i.u., suggests a role for vitamin E in connexion with the capacity of the liver to bind vitamin A.6. The relationship between vitamin A and vitamin E in vivo cannot, in the light of these results, be regarded as that between an antioxidant and a peroxidizable substrate.


2020 ◽  
Vol 103 (5) ◽  
pp. 1288-1292
Author(s):  
Brendon D Gill ◽  
Harvey E Indyk

Abstract Background α-Tocopherol can exist as eight possible stereoisomers due to the presence of three chiral carbons. Regulations and industry guidelines necessitate that dietary vitamin E intakes be based on the vitamin E activity of RRR-α-tocopherol. Food products fortified with synthetic all-rac-α-tocopherol or all-rac-α-tocopheryl acetate during manufacturing will require chiral separation of the α-tocopherol stereoisomers for accurate estimation of vitamin E activity. Objective The development of an HPLC method utilizing a chiral column for the chromatographic separation of RRR-α-tocopherol from other α-tocopherol stereoisomers. Method Normal phase liquid chromatographic separation using a polysaccharide-based chiral column with fluorescence detection of α-tocopherol stereoisomers. Results The described chromatographic method achieves baseline resolution of RRR-α-tocopherol from its stereoisomers. Method selectivity, precision, and robustness were evaluated and acceptable performance was achieved. Conclusions The chromatographic method was found to be suitable for application where both RRR-α-tocopherol content and total α-tocopherol content are required for routine compliance testing. Highlights A robust and precise chomatographic method for the baseline resolution of RRR-α-tocopherol from its stereoisomers was acheived.


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