scholarly journals On the relationship between vitamin A and vitamin E in the rat

1968 ◽  
Vol 22 (1) ◽  
pp. 133-143 ◽  
Author(s):  
M. A. Cawthorne ◽  
J. Bunyan ◽  
A. T. Diplock ◽  
Elspeth A. Murrell ◽  
J. Green
Keyword(s):  
Weight Gain ◽  
Vitamin E ◽  
Vitamin A ◽  
Methyl Esters ◽  
Tocopheryl Acetate ◽  
Cod Liver Oil ◽  
Deficient Diet ◽  
Weanling Rats ◽  
The Relationship

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.

scholarly journals Vitamin E and stress

1967 ◽  
Vol 21 (4) ◽  
pp. 845-864 ◽  
Author(s):  
J. Green ◽  
I. R. Muthy ◽  
A. T. Diplock ◽  
J. Bunyan ◽  
M. A. Cawthorne ◽  
...  
Keyword(s):  
Vitamin E ◽  
Vitamin A ◽  
Dietary Vitamin ◽  
Dietary Pufa ◽  
Weanling Rats ◽  
Depletion Rate ◽  
Gastro Intestinal Tract ◽  
The Relationship ◽  
Liver Vitamin

1. The nature of the relationship between vitamins A and E has been studied in the rat and the chick.2. Stress induced by diets rich in polyunsaturated fatty acids (PUFA) was found to have no effect on the liver vitamin A reserves of vitamin E-deficient rats given dietary vitamin A or repeated small oral doses of vitamin A.3. Dietary PUFA did not affect the liver vitamin A reserves of young rats given necrogenic diets deficient in vitamin E and selenium, nor were these reserves affected by the onset of liver necrosis or its prevention by Se.4. The effect of dietary PUFA on the rate of depletion of liver vitamin A reserves in weanling rats or rats depleted initially of vitamins A and E and then given a single large dose of vitamin A was studied over periods from 2 to 12½ weeks. In three experiments the dietary PUFA did not significantly accelerate vitamin A depletion. In one experiment the depletion rate was increased, but this was not reversed by dietary vitamin E and thus could not be attributed to an enhancement of peroxidation in vivo but rather to a toxic effect. The effect of vitamin E in these experiments was not consistent but, in general, it slightly decreased the rate of depletion.5. Large doses of vitamin A did not affect the metabolism of small amounts of [14C]D-α-tocopherol in the vitamin E-deficient rat or chick, when interaction of the two vitamins in the gastro-intestinal tract was avoided.6. Large doses of vitamin A (40000 i.u. in total) given to vitamin E-deficient chicks receiving a diet containing 1% linoleic acid (as maize oil esters) did not accelerate the onset of encephalomalacia and therefore failed to exert a pro-oxidative effect on tissue tocopherol.7. The conclusion drawn from these experiments was that any relationship that may exist in vivo between vitamins A and E is not concerned with an effect of vitamin E in preventing oxidation of vitamin A. A critical review of the literature on the nature of the relationship in general supports this view.

scholarly journals Vitamin E and stress

1967 ◽  
Vol 21 (1) ◽  
pp. 115-125 ◽  
Author(s):  
A. T. Diplock ◽  
J. Green ◽  
J. Bunyan ◽  
D. Mchale ◽  
I. R. Muthy
Keyword(s):  
Vitamin E ◽  
Terminal Illness ◽  
Methyl Esters ◽  
Tocopheryl Acetate ◽  
Liver Necrosis ◽  
Deficient Diet ◽  
Weanling Rats ◽  
High Incidence ◽  
Gastro Intestinal Tract ◽  
Oxidant Effect

1. When weanling rats were given a vitamin E-deficient diet and 0.15% (w/v) silver acetate in their drinking water, there was a high incidence of liver necrosis and death after 2–4 weeks. This was prevented by 120 ppm D-α-tocopheryl acetate in the diet, was partially prevented by selenium at 1 ppm but not at 0.05 ppm and was only marginally prevented by 0.15% DL-methionhe.2. All these effects were observed when the diet was free of fat and when it contained either methyl oleate or polyunsaturated methyl esters. The polyunsaturated lipid slightly increased the velocity of the terminal illness.3. In spite of the ‘anti-vitamin E’ effect of Ag and the clear demonstration that α-tocopherol played a major part in preventing toxicity, experiments with tracer amounts of [5-Me-14C]-D-α-tocopherol showed that rather than there being any destruction of tocopherol in the critical period preceding the onset of disease, there was an increase in tocopherol in the liver due to Ag administation. The metabolism of tocopherol in the remainder of the animal was unaffected during the pre-necrotic phase.4. The results are inconsistent with the view that the stress induced by Ag is caused by a pro-oxidant effect, either in the gastro-intestinal tract or in the tissues of the rat. They show that lipid peroxidation is not a causal factor in the aetiology of Ag-induced liver necrosis and suggest that stress in the vitamin E-deficient animal probably raises the requirement for tocopherol.

scholarly journals The effect of vitamin A deficiency on hepatic, renal and pulmonary glutathione S-transferase activities in the rat

1980 ◽  
Vol 188 (3) ◽  
pp. 889-893 ◽  
Author(s):  
Z H Siddik ◽  
E G Mimnaugh ◽  
M A Trush ◽  
T E Gram
Keyword(s):  
Vitamin A ◽  
Vitamin A Deficiency ◽  
Nutritional State ◽  
Glutathione S Transferase ◽  
Chemical Carcinogens ◽  
Deficient Diet ◽  
Liver Cytosol ◽  
Weanling Rats ◽  
Glutathione S Transferases ◽  
The Relationship

Feeding male weanling rats on a vitamin A-deficient diet for 6 weeks resulted in significant increases (44-57%) in glutathione S-aryl-, S-aralkyl- S-alkyl- and S-epoxidetransferase activities in the liver cytosol. Only the S-aralkyl- (27%) and S-alkyltransferase (14%) activities were significantly increased in the kidney as a result of deficiency. There was no effect on any of the pulmonary glutathione S-transferase activities. The increases in hepatic transferase activities were due primarily to increases (25-96%) in the apparent Vmax. There were no changes in the apparant Km of any of the four drug substrates employed. With 3,4-dichloronitrobenzene as the second substrate, the apparent Km for glutathione was increased by over 2-fold in vitamin A-deficient livers as compared with controls. The relationship between these results and enhanced susceptibility to chemical carcinogens in vitamin A deficiency is briefly discussed, and comparison is made between the effects of this nutritional state and pretreatment with drug inducers on the glutathione S-transferases.

scholarly journals Vitamin E and stress

1967 ◽  
Vol 21 (3) ◽  
pp. 725-730 ◽  
Author(s):  
A. T. Diplock ◽  
J. Green ◽  
J. Bunyan ◽  
M. A. Cawthorne ◽  
Jean Dawson
Keyword(s):  
Vitamin E ◽  
Vitamin A ◽  
Fatty Acid Methyl Esters ◽  
Methyl Esters ◽  
Dietary Lipid ◽  
Stress Effect ◽  
Deficient Animal ◽  
Oxidative Reactions ◽  
Liver And Kidney

1. The effects of iron overloading and unsaturation of dietary lipid on the metabolism of α-tocopherol in the rat were studies.2. Young adult male vitamin E-deficient rats were given 1000 i.u. of vitamin A and 100 μg of [14C-5-Me]D-α-tocopherol and then given diets containing 5% methyl oleate or 5% cod-liver oil fatty-acid methyl esters. Rats from each group were given intramuscular injections of iron-dextran (50 mg Fe/kg rat) at 48 h intervals for 15 days, and compared with controls given dextran. After this time, liver, kidney and the remainder of the carcass were analysed for [14C]α-tocopherol, and liver and kidney were also analysed for vitamin A.3. There was no evidence that Fe overloading caused any increase in the destruction of either tocopherol or vitamin A in vivo, whether or not the diet contained polyunsaturated fatty acids. Indeed, treatment with Fe significantly decreased the metabolism of the radioactive tocopherol dose in all three tissues studied.4. These experiments show that the stress effect of Fe in the vitamin E-deficient animal is unrelated to an increase in oxidative reactions. They provide further evidence that ‘lipid peroxidation’ is not causally concerned in ‘anti-vitamin E’ stress conditions and that α-tocopherol does not function, in vivo, as an antioxidant.

scholarly journals Vitamin E and stress

1967 ◽  
Vol 21 (1) ◽  
pp. 69-101 ◽  
Author(s):  
J. Green ◽  
A. T. Diplock ◽  
J. Bunyan ◽  
D. Mchale ◽  
I. R. Muthy
Keyword(s):  
Fatty Acids ◽  
Ascorbic Acid ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Vitamin E ◽  
Dietary Fat ◽  
Methyl Esters ◽  
Cod Liver Oil ◽  
Deficient Diet

1. A critical analysis of the biological antioxidant theory of vitamin E function has been made and the implications of the theory have been tested.2. When small amounts of [5-Me-14C]α-tocopherol were present in lipid systems subject to autoxidation in vitro, it was found that, whether the tocopherol was the sole antioxidant or was in synergistic combination with a secondary antioxidant (ascorbic acid), peroxidation did not occur without concomitant destruction of the tocopherol. This was so, whether a simple fat substrate or a liver homogenate (subject to catalysis) was used. The decomposition of tocopherol took place even when the secondary antioxidant was in large excess, as would occur under physiological conditions in the vitamin E-deficient animal, and accelerated as the induction period neared its end.3. When [5-Me-14C,3H]α-tocopherol and ascorbic acid were used as a synergistic antioxidant couple in vitro, tocopherol recovered from the peroxidizing system always had the same isotopic ratio as the starting material. This means that regeneration of tocopherol by the secondary antioxidant cannot involve, as an intermediate, a tocopherol carbon radical formed by loss of hydrogen from the 5-methyl group. Such radicals probably dimerize before they can be regenerated. The same result was found when doubly labelled α-tocopherol was given to the rat and recovered later from its tissues.4. In a series of experiments, rats were rigorously depleted of vitamin E for periods up to 7 months and then given as little as 50 μg [14C]D-α-tocopherol. They were then given, either by stomach tube daily or by dietary addition, large amounts of methyl linoleate or vitamin E-free polyunsaturated fatty acid methyl esters prepared from cod-liver oil and compared with controls given methyl oleate for up to 31 days. When the possibility of interaction between the lipid and tocopherol in the gut was eliminated, analyses of liver, kidney, testis, adrenal, adipose tissue, whole carcass and faeces showed that there was no effect of the polyunsaturated fatty acids on either the metabolism or recovery of [14C]α-tocopherol in any of the animals.5. When interaction between the administered fatty acid esters and tocopherol in the gut was allowed to take place, a marked destruction of [14C]α-tocopherol in the tissues was observed in animals given the polyunsaturated esters. The importance of oxidative destruction of tocopherol in the gut before absorption was demonstrated in a nutritional trial, in which cod-liver oil and lard were compared and the degrees of resistance of rats' erythrocytes to dialuric acid-induced haemolysis was used as an index of vitamin E depletion.6. Similar experiments with [14Cα-tocopherol in weanling rats given large amounts of cod-liver oil methyl esters also showed little effect. Although there was a suggestion that prolonged feeding of partly peroxidized polyunsaturated esters could lead to a slight depression of tissue tocopherol concentrations, no significant differences were usually obtained.7. Fourteen-day-old rats were given a vitamin E-deficient diet and received three weekly doses of 0.5 mg α-tocophcryl acetate. The dosage was stopped, the rats were then given a deficient diet containing 4% of either vitamin E-free linseed oil fatty acids or oleic acid, and the rate of their tocopherol depletion was measured by the erythrocyte haemolysis test. No effect of the polyunsaturated fatty acids was found. Nor was there any effect on the concentrations of ‘secondary antioxidants’ (glutathione and ascorbic acid) in liver, kidney, testis, muscle or adipose tissue.8. The results of the experiments in vivo contrast strongly with those in vitro. They lead to the conclusion that lipid peroxidation, if it occurs in the living animal, is irrelevant to the problem of vitamin E function. This conclusion has been substantiated by a critical review of the literature on the quantitative aspects of the vitamin E-dietary fat relationship.9. The effects of dietary fat stress in vitamin E-deficient animals are, we believe, due to two causes: (1) destruction of tocopherol in the diet or in the gastro-intestinal tract of the animal, and (2) the existence of an increased requirement for vitamin E for the metabolism of certain long-chain fatty acids. The specific effects of certain of these substances in producing or accelerating some vitamin E deficiency diseases may be related to the toxic states known to be induced in vitamin E-deficient animals by other stress factors.

Allergic contact dermatitis from tocopheryl acetate (vitamin E) and retinol palmitate (vitamin A) in a moisturizing cream

1994 ◽  
Vol 31 (5) ◽  
pp. 324-324 ◽  
Author(s):  
Diego Manzano ◽  
Antonio Aguirre ◽  
Jesus Gardeazabal ◽  
X. Eizaguirre ◽  
Jose Luis Díaz Pérez
Keyword(s):  
Vitamin E ◽  
Contact Dermatitis ◽  
Vitamin A ◽  
Allergic Contact Dermatitis ◽  
Tocopheryl Acetate ◽  
Allergic Contact

Vitamin E Deficiency Fails to Affect Myocardial Performance During In Vivo Ischemia-Reperfusion

2000 ◽  
Vol 70 (6) ◽  
pp. 293-300 ◽  
Author(s):  
Jeff Coombes ◽  
Scott Powers ◽  
Haydar Demirel ◽  
Karyn Hamilton ◽  
James Jessup ◽  
...  
Keyword(s):  
Vitamin E ◽  
Corn Oil ◽  
Ischemia Reperfusion ◽  
Control Diet ◽  
Cardiac Performance ◽  
In Vivo Model ◽  
Vitamin E Deficiency ◽  
Deficient Diet ◽  
Protein Thiols

Vitamin E content, of cardiac tissue, has been proposed to play a major, role in the damage caused by myocardial ischemia-reperfusion (I-R). Previous studies using in vitro models have examined vitamin E deficiency and I-R-induced myocardial damage with equivocal results. The purpose of this study was to use an in vivo model of myocardial I-R to determine the effects of vitamin E deficiency on myocardial I-R-induced damage. Female Sprague-Dawly rats (4-mo old) were assigned to either: 1) control diet (CON), or 2) vitamin E deficient diet (VE-DEF). The CON diet was prepared to meet AIN-93M standards, which contains 75 IU vitamin E/kg diet. The VE-DEF diet was the AIN-93M diet prepared with tocopherol stripped corn oil and no vitamin E. Following a 14-week feeding period, significant differences (p < 0.05) existed in mean myocardial VE levels between groups (mean values ± SEM: CON = 48.2 ± 3.5; VE-DEF = 12.4 ± 1,4 mug VE/g wet weight). Animals from both experimental groups were subjected to an in vivo I-R protocol consisting of 25 minutes of left coronary artery occlusion followed by 10 minutes of reperfusion. No group differences (p > 0.05) existed in cardiac performance (peak arterial pressure or ventricular work) or the incidence of ventricular arrhythmias during the I-R protocol. VE-DEF animals had significantly higher (p < 0.05) levels of myocardial lipid peroxidation and lower (p < 0.05) protein thiols following I-R compared to the CON animals. These data suggest that although vitamin E deficiency increases oxidative damage resulting from myocardial I-R, it does not affect cardiac performance during the insult.

scholarly journals The histology and in vivo sulphate uptake of epiphyseal cartilage in protein-depleted rats

1977 ◽  
Vol 38 (3) ◽  
pp. 513-518 ◽  
Author(s):  
B. Shapiro ◽  
B. Pimstone
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Alcian Blue ◽  
Crystal Violet ◽  
Intraperitoneal Injection ◽  
Linear Growth ◽  
Hormonal Factors ◽  
Weanling Rats ◽  
Testicular Hyaluronidase

1. Weanling rats, aged 21 d, given a 40 g casein/kg diet for 25 d were compared with ‘age-matched’ controls given a 200 g casein/kg diet and with ‘weight-matched’ weanling controls.2. The protein-malnourished rats demonstrated failure of weight gain and linear growth, hypoproteinaemia, hypoalbuminaemia and fatty liver.3. Autoradiography of the tibia was carried out 24 h after intraperitoneal injection of Na235SO4 (0.1, 1.0, 2.0, 5, 10 μCi/g body-weight). Sections of tibia, humerus and costochondral junction were stained by haematoxylin and eosin, resorcin-crystal violet and picro-fuchsin, Alcian Blue at pH 0.1 and pH 2.5, Alcian Blue at pH 5.7 with magnesium chloride (0.1, 0.7, 1.0 m), and by Alcian Blue after ovine testicular hyaluronidase (EC 3.2.1.35) digestion. The width of the upper tibial epiphysis was measured and the histological and histochemical features of the epiphyses studied.4. The incorporation of 35SO4 into the epiphyses of the protein-malnourished animals was markedly reduced. The chondrocytes were small and flattened with frequent pyknotic nuclei. The staining characteristics of the cartilagenous matrix was qualitatively similar in all animals. The epiphyses in malnutrition were found to be thin, all zones being affected. The upper tibial epiphyses (mean±sd; μm) were 202 ±46 for the protein-malnourished animals, 367±52 for age-matched controls and 578±40 for weight-matched controls.5. The changes found resemble those after hypophysectomy and the possible hormonal factors are discussed.

scholarly journals Effect of vitamin E- and selenium-deficiency on rat liver chemiluminescence

1987 ◽  
Vol 242 (2) ◽  
pp. 383-386 ◽  
Author(s):  
C G Fraga ◽  
R F Arias ◽  
S F Llesuy ◽  
O R Koch ◽  
A Boveris
Keyword(s):  
Vitamin E ◽  
Glutathione Peroxidase ◽  
Selenium Deficiency ◽  
Serum Levels ◽  
Hepatic Necrosis ◽  
Deficient Diet ◽  
Control Value ◽  
Weanling Rats

The role of vitamin E and selenium as protective agents against oxidative stress was evaluated by measuring liver chemiluminescence in situ. Weanling rats fed a vitamin E- and selenium-deficient diet showed liver chemiluminescence that was increased 60 and 100% over control values at 16 and 18 days respectively after weaning. At day 21, the double deficiency led to hepatic necrosis, as observed by optical and electron microscopy, and increased serum levels of lactate dehydrogenase and alanine aminotransferase. Single deficiencies, in either vitamin E or selenium, did not produce liver necrosis but increased liver chemiluminescence. Vitamin E deficiency led to a 23 and 50% increase in liver emission at days 18 and 20 respectively; selenium deficiency produced a 64% increase at day 16. The activity of liver selenium-glutathione peroxidase diminished to 13% of the control value in the rats fed doubly deficient and selenium-deficient diets. Activities of superoxide dismutase, catalase and non-selenium-glutathione peroxidase were not modified by the different diets. These results suggest that oxy-radical generation may play a major role in hepatic necrosis in vitamin E- and selenium-deficiency.

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