scholarly journals On the postulated peroxidation of unsaturated lipids in the tissues of vitamin E-deficient rats

1968 ◽  
Vol 22 (1) ◽  
pp. 97-110 ◽  
Author(s):  
J. Bunyan ◽  
J. Green ◽  
Elspeth A. Murrell ◽  
A. T. Diplock ◽  
M. A. Cawthorne
Keyword(s):  
Adipose Tissue ◽  
Vitamin E ◽  
Methyl Esters ◽  
Lipid Peroxide ◽  
Lipid Peroxides ◽  
Dietary Vitamin ◽  
Unsaturated Lipids ◽  
Peroxide Values ◽  
Dietary Concentration ◽  
Exogenous Lipid

1. The micro-iodimetric method has been used to study some factors affecting the concentration of lipid peroxides in the adipose tissue of vitamin E-deficient rats.2. Cod-liver oil methyl esters (CLOME) or maize oil methyl esters (MOME) with peroxide values ranging from 3 to 330 μ-equiv./g were given by mouth to vitamin E-deficient rats deprived of food before and after the dose. Lipid peroxides did not accumulate in the adipose tissue of these rats.3. Experiments with dietary CLOME and MOME of varying peroxide values (2–230 μ-equiv./g) showed that exogenous lipid peroxide accumulates in the adipose tissue when the rats received these lipids at 10% in the diet for 4 weeks, but not if the dietary concentration was only 4% or if the diet with 10% lipid was given for 5 days only.4. Rats were given dietary CLOME for 4 weeks. Their adipose tissue was then found to contain about 50 μ-equiv. lipid peroxide/g. They were divided into three groups. One group was given a fat-free diet and, after 10 days, the adipose tissue concentration of lipid peroxide had decreased to about 10 μ-equiv./g. The other groups were given the fat-free basal diet supplemented with vitamin E or DPPD (N,N′-diphenyl-p-phenylenediamine). Neither supplement significantly affected the rate of disappearance of the peroxides from the adipose tissue.5. It was shown that neither α-tocopherol nor DPPD reacted with the lipid peroxides of CLOME or MOME in vitro, at room temperature or even after 65 h at 37°.6. It was concluded that unsaturated lipids do not become peroxidized after incorporation into the adipose tissue of vitamin E-deficient rats. Lipid peroxides taken up from the diet into the adipose tissue are not of fleeting existence, having a half-life of about 6 days. Dietary vitamin E probably prevents the accumulation of exogenous lipid peroxides in the adipose tissue by reinforcing the barrier to their absorption in the gut.7. These studies provide further evidence that current concepts of lipid peroxidation in vitamin E-deficient animals are incorrect. In fact, vitamin E-deficient animals have low concentrations of peroxide in their adipose tissue, unless they have received large amounts of unsaturated lipid for long periods, and the role of vitamin E in controlling this concentration is not due to any effect on peroxidation in vivo.

scholarly journals On the existence and significance of lipid peroxides in vitamin E-deficient animals

1967 ◽  
Vol 21 (2) ◽  
pp. 475-495 ◽  
Author(s):  
J. Bunyan ◽  
Elspeth A. Murrell ◽  
J. Green ◽  
A. T. Diplock
Keyword(s):  
Adipose Tissue ◽  
Vitamin E ◽  
Peroxide Value ◽  
Lipid Peroxide ◽  
Lipid Peroxides ◽  
Dietary Lipid ◽  
Acetate Solution ◽  
Liver Necrosis ◽  
Peroxide Content ◽  
Peroxide Values

1. A micro-adaptation of the iodimetric method has been used to determine lipid peroxides in the tissues of vitamin E-deficient rats and chicks.2. No increases in lipid peroxide were found in liver, kidney or adipose tissue of rats with nutritional liver necrosis due to deficiency of vitamin E and selenium. When liver necrosis was induced by giving rats a casein diet and silver acetate solution to drink, the peroxide value of the adipose tissue was not increased.3. Degeneration of the testes of vitamin E-deficient rats was not accompanied by a rise in the peroxide value of the tissue lipids.4. There was an increase in cathepsin activity of the kidneys of rats displaying the phenomenon of renal autolysis (post mortem), but there was no increase in lipid peroxide content.5. No rise in lipid peroxide was found in dystrophic chick breast muscle, in cerebellum, brain and adipose tissue of chicks with encephalomalacia nor in the liver of chicks with exudative diathesis.6. In rat liver, kidney, testis and leg muscle, peroxide values in the range 10–40 µ-equiv./g lipid were found, and these values were not altered either by a substantial change in the degree of unsaturation of the dietary lipid or by the addition of vitamin E to the diet. Dietary addition of N, N'-diphenyl-p-phenylenediamine (DPPD) or 6-ethoxy-1, 2-dihydro-2,2,4-trime-thylquinoline (ethoxyquin) also failed to affect the peroxide value of liver. The possibility that lipid peroxide is a normal metabolite of these tissues is discussed.7. Peroxide values of rat adipose tissue were never found to be greater than 40 µ-equiv./g lipid and were readily decreased by the addition of vitamin E to the diet or by a decrease in the unsaturation of the dietary lipid. The peroxide content of this tissue may depend upon the up-take of peroxidized dietary lipid.8. The conclusion from this study of true lipid peroxides in animal tissues is that the biological role of vitamin E is not connected with lipid peroxidation in vivo, in agreement with our previous studies on the metabolism of the fatty acid substrates of peroxidation and of α-tocopherol and other postulated biological antioxidants.

Effects of Vitamin E Administration on Platelet Function and Serum Lipid Peroxides in DOCA-Salt Hypertensive Rats

1991 ◽  
Vol 65 (04) ◽  
pp. 411-414 ◽  
Author(s):  
Keizo Umegaki ◽  
Hiromi Saegusa ◽  
Masato Kurokawa ◽  
Tomio Ichikawa
Keyword(s):  
Vitamin E ◽  
Platelet Function ◽  
Serum Lipid ◽  
Lipid Peroxide ◽  
Lipid Peroxides ◽  
Hypertensive Rats ◽  
Serotonin Content ◽  
Serum Lipid Peroxide ◽  
Salt Hypertension

SummaryEffects of vitamin E on platelet function and serum lipid peroxide levels were investigated in DOCA-salt hypertensive rats. In the hypertensive rats, ADP- and collagen-induced platelet aggregation in whole blood were markedly attenuated and accompanied by a reduction of serotonin content as compared with the normotensive controls. These facts indicated the appearance of exhausted platelets, which have already been activated in vivo, due to the hypertension. Platelet vitamin E levels were decreased by 50%, while serum lipid peroxide levels were increased 3.6-fold in the hypertensive rats. Vitamin E administration (10 times the dietary intake) during the experimental periods did not influence either the aggregability or the serotonin content of platelets from the hypertensive rats. However, vitamin E administration significantly prevented the elevation of serum tipid peroxides due to the hypertension. These results suggest that vitamin E administration has little effect on platelet activation in vivo due to DOCA-salt hypertension.

THE PROTECTIVE ACTION OF TOCOPHEROL AGAINST HEMOLYSIS OF RAT ERYTHROCYTES BY DIALURIC ACID

1960 ◽  
Vol 38 (9) ◽  
pp. 957-964 ◽  
Author(s):  
C. C. Tsen ◽  
H. B. Collier
Keyword(s):  
Protective Action ◽  
Lipid Peroxide ◽  
Lipid Peroxides ◽  
Thiobarbituric Acid ◽  
Peroxide Formation ◽  
Rat Erythrocytes ◽  
Thiobarbituric Acid Test ◽  
Unsaturated Lipids ◽  
Acid Test ◽  
Test Treatment

Erythrocytes from rats on tocopherol-deficient and tocopherol-supplemented diets gave similar low values for lipid peroxides by the thiobarbituric acid test. Treatment of the cells from tocopherol-deficient rats with dialuric acid caused a marked increase in lipid peroxides and this closely paralleled the degree of hemolysis. Shaking of the red cells from tocopherol-deficient animals in an atmosphere of oxygen also resulted in a slow lipid peroxidation which again paralleled the degree of hemolysis. Addition of α-tocopherol to a suspension of erythrocytes from tocopherol-deficient rats decreased or completely prevented (depending upon concentration) hemolysis by dialuric acid and also decreased lipid peroxide formation.It is concluded that dialuric acid probably acts by catalyzing the formation of lipid peroxides in the unsaturated lipids of the membrane of erythrocytes from tocopherol-deficient animals. Tocopherol presumably inhibits peroxide formation, and therefore hemolysis, by virtue of its antioxidant action.

scholarly journals Effects of dietary n-3 polyunsaturated fatty acids, breed and dietary vitamin E on the fatty acids of lamb muscle, liver and adipose tissue

2004 ◽  
Vol 91 (4) ◽  
pp. 551-565 ◽  
Author(s):  
G. Demirel ◽  
A. M. Wachira ◽  
L. A. Sinclair ◽  
R. G. Wilkinson ◽  
J. D. Wood ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Vitamin E ◽  
Fish Oil ◽  
Live Weight ◽  
Dietary Fatty Acids ◽  
Polar Lipids ◽  
Dietary Vitamin ◽  
Lipid Fractions

The effect of feeding n-3 PUFA on the fatty acid composition of muscle, adipose tissue and liver of lambs was investigated. Groups of eight ram lambs per breed, Suffolk×Lleyn (24kg live weight) and Scottish Blackface (18kg live weight), were each fed one of six diets containing one of three fat sources (50g fatty acids/kg DM; Megalac® (calcium soap of palm fatty acid distillate; Volac Ltd, Royston, Herts., UK) and formaldehyde-treated whole linseed (Trouw Nutrition UK, Northwich, Ches., UK) either alone or with fish oil (1:1, w/w) and either 100 or 500mg α-tocopheryl acetate/kg DM. Feed was offered ad libitum until slaughter at approximately half breed mature live weight. The type of dietary fat had no effect on intake, growth rate or feed conversion ratio. The 3·0-fold higher concentration of 18:3n-3 in the linseed compared with the Megalac® diet approximately doubled (P<0·001) the concentration in the neutral and polar lipid fractions of musculus semimembranosus and liver, and in adipose tissue it increased 2·5-fold. Feeding protected linseed also increased (P<0·001) concentrations of 20:5n-3 and 22:5n-3 in muscle polar lipids and both lipid fractions of liver. The linseed–fish oil raised the 20:5n-3 concentrations above those for the linseed diet and also increased 22:6n-3. Scottish Blackface lambs had lower concentrations of 18:3n-3 in all lipids compared with Suffolk x Lleyn lambs, but more 20:5n-3 in the polar lipids of muscle and liver. High levels of dietary vitamin E were associated with small decreases in the concentration of monounsaturated fatty acids and increases in PUFA. Linseed raised the PUFA:saturated fatty acid ratios in liver and adipose tissue but not in muscle, and improved the n-6:n-3 fatty acid ratio, as did the linseed–fish oil. Different combinations of dietary fatty acids and better protection against rumen biohydrogenation are required to improve muscle PUFA:saturated fatty acids ratios.

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.

scholarly journals Optimal dietary concentration of vitamin E for alleviating the effect of heat stress on performance, thyroid status, ACTH and some serum metabolite and mineral concentrations in broilers

2012 ◽  
Vol 47 (No. 4) ◽  
pp. 110-116 ◽  
Author(s):  
K. Sahin ◽  
O. Kucuk ◽  
N. Sahin ◽  
M. F Gursu
Keyword(s):  
Heat Stress ◽  
Vitamin E ◽  
Management Practice ◽  
Live Weight ◽  
Basal Diet ◽  
Dietary Vitamin ◽  
Broiler Chicks ◽  
Serum Concentrations ◽  
Dietary Concentration ◽  
Vitamin E Supplementation

An experiment utilizing Cobb-500 male broilers was conducted to evaluate the effects of vitamin E (d1--to- copheryl acetate) supplementation at various concentrations (0, 62.5, 125, 250, or 500 mg/kg of diet) on performance and serum concentrations of Triiodothyronine (T<sub>3</sub>), Thyroxin (T<sub>4</sub>), Adrenocorticotropine Hormone (ACTH), and some metabolites and minerals in broilers reared under heat stress (32&deg;C). One day-old 150 male broilers were randomly assigned to 5 treatment groups, 3 replicates of 10 birds each. The birds received either a basal diet or basal diet supplemented with vitamin E at 62.5, 125, 250, or 500 mg/kg of diet. Increased supplemental vitamin E linearly increased feed intake (P = 0.01), live weight gain (P = 0.01), and improved feed efficiency linearly (P = 0.001). Increasing dietary vitamin E supplementation also resulted in linear increases in serum T<sub>3 </sub>and T<sub>4</sub> concentrations (P = 0.01) but, linear decreases in ACTH concentration (P = 0.01). Serum glucose, uric acid, triglycerides, and cholesterol concentrations decreased linearly (P = 0.001) while, protein and albumin concentrations increased linearly (P = 0.001) when dietary vitamin E supplementation increased. Serum activities of Serum Glutamic Oxalate Transaminase (SGOT) and Serum Glutamic Pyruvate Transaminase (SGPT) were not influenced by dietary vitamin E supplementation (P &gt; 0.10). However, serum activity of Alkaline Phosphatase (AP) increased linearly (P = 0.001) with increasing dietary vitamin E supplementation. Increasing dietary vitamin E supplementation also caused linear increases (P = 0.001) in serum concentrations of Ca and P. Results of the present study conclude that a 250 mg/kg of vitamin E provides an optimal performance in broiler chicks reared under heat stress, and vitamin E supplementation at such a level can be considered as a protective management practice in a broiler diet, reducing the negative effects of heat stress.

THE PROTECTIVE ACTION OF TOCOPHEROL AGAINST HEMOLYSIS OF RAT ERYTHROCYTES BY DIALURIC ACID

1960 ◽  
Vol 38 (1) ◽  
pp. 957-964 ◽  
Author(s):  
C. C. Tsen ◽  
H. B. Collier
Keyword(s):  
Protective Action ◽  
Lipid Peroxide ◽  
Lipid Peroxides ◽  
Thiobarbituric Acid ◽  
Peroxide Formation ◽  
Rat Erythrocytes ◽  
Thiobarbituric Acid Test ◽  
Unsaturated Lipids ◽  
Acid Test ◽  
Test Treatment

Erythrocytes from rats on tocopherol-deficient and tocopherol-supplemented diets gave similar low values for lipid peroxides by the thiobarbituric acid test. Treatment of the cells from tocopherol-deficient rats with dialuric acid caused a marked increase in lipid peroxides and this closely paralleled the degree of hemolysis. Shaking of the red cells from tocopherol-deficient animals in an atmosphere of oxygen also resulted in a slow lipid peroxidation which again paralleled the degree of hemolysis. Addition of α-tocopherol to a suspension of erythrocytes from tocopherol-deficient rats decreased or completely prevented (depending upon concentration) hemolysis by dialuric acid and also decreased lipid peroxide formation.It is concluded that dialuric acid probably acts by catalyzing the formation of lipid peroxides in the unsaturated lipids of the membrane of erythrocytes from tocopherol-deficient animals. Tocopherol presumably inhibits peroxide formation, and therefore hemolysis, by virtue of its antioxidant action.

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