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.

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.

Effect of dietary lipid peroxides on metabolism of serum chylomicrons in rats

1993 ◽  
Vol 264 (3) ◽  
pp. G561-G568 ◽  
Author(s):  
I. Staprans ◽  
X. M. Pan ◽  
M. Miller ◽  
J. H. Rapp
Keyword(s):  
Lipid Peroxide ◽  
Lipid Peroxides ◽  
Hepatic Uptake ◽  
Dietary Lipid ◽  
Hydrolysis Rate ◽  
Liver Uptake ◽  
Peroxide Content ◽  
Initial Plasma ◽  
Heart Perfusion ◽  
High Peroxide

We have found that in rats the peroxide content of chylomicrons (CM) is determined by the lipid peroxide concentration in the diet, indicating that dietary lipid peroxides are incorporated into the lymph CM. Moreover, these incorporated lipid peroxides influence the normal CM metabolism. When radiolabeled CM were injected into rats, there was no difference in the initial plasma removal between CM prepared from oil with low peroxide content (control CM) and CM prepared from oil with high peroxide content (oxidized CM). However, the tissue distribution of the labels indicated that the hepatic uptake of CM decreased with increasing lipid peroxide content of CM. At 10 min after injection of CM, liver uptake of cholesterol label was 48.39 +/- 3.08% for control CM and 31.41 +/- 10.73% for oxidized CM. Vitamin E enrichment of control CM increased their hepatic uptake to 61.07 +/- 0.83%. Additionally, binding of oxidized CM to the heart endothelium increased from 2.55 to 3.60% compared with binding of control CM. When the hydrolysis of control and oxidized CM by endothelial lipoprotein lipase (LPL) was tested in a heart perfusion system, we found that after 30 min, 56.51 +/- 5.81% of control and 76.82 +/- 1.75% of oxidized CM were not hydrolyzed and remained in the perfusate. Thus our results indicate that the altered metabolism of oxidized CM may be related to a reduced hydrolysis rate by endothelial LPL.

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.

scholarly journals Vitamin E and stress

1967 ◽  
Vol 21 (3) ◽  
pp. 671-679 ◽  
Author(s):  
M. A. Cawthorne ◽  
A. T. Diplock ◽  
I. R. Muthy ◽  
J. Bunyan ◽  
Elspeth A. Murrell ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Ascorbic Acid ◽  
Vitamin E ◽  
Lipid Peroxide ◽  
Toxic Effects ◽  
Peroxide Content ◽  
In Vitro Techniques ◽  
Sulphydryl Compounds

1. Vitamin E-deficient rats were found to be more susceptible than vitamin E-supplemented controls to the toxic effects of hyperbaric oxygen (60 lb/in.2 for 20 min). This agrees with the findings of other workers.2. Hyperbaric O2 treatment did not increase the metabolic destruction of a small amount (46.65 μg) of [14C-5-Me]D-α-tocopherol given to adult vitamin E-deficient rats 24 h previously. The O2 treatment also did not affect the soluble sulphydryl compounds and ascorbic acid of rat liver, nor the percentag haemolysis in vivo of rat blood.3. Hyperbaric O2 treatment did not increase the true lipid peroxide content of rat brain, compared to control rats treated with hyperbaric air, which has no toxic effects. Increases in ‘lipid peroxidation’ reported by previous workers are considered to have been due to the use of inadequate controls (untreated rats) and of in vitro techniques that are open to criticism.4. The toxic effects of hyperbaric O2 in the vitamin E-deficient rat cannot be attributed to peroxidation in vivo.5. Vitamin E was not found to protect rats against the effects of reduced O2 tension (anoxic anoxia). This finding contrasts with some reports by earlier workers. Reduced O2 tension had no effect on the metabolism of radioactive tocopherol, on blood haemolysis in vivo, or on the soluble sulphydryl compounds and ascorbic acid of liver.

scholarly journals Nutritional effects of autoxidized fats in animal diets

1966 ◽  
Vol 20 (1) ◽  
pp. 113-122 ◽  
Author(s):  
J. L. L'estrange ◽  
K. J. Carpenter ◽  
C. H. Lea ◽  
L. J. Parr
Keyword(s):  
Vitamin E ◽  
Vitamin A ◽  
Peroxide Value ◽  
Liver Weight ◽  
Dietary Lipid ◽  
Feed Conversion ◽  
Nutritional Effects ◽  
High Peroxide ◽  
Lower Vitamin ◽  
Oxidized Fat

1. Beef fat oxidized to a peroxide value of 109 μmoles/g (218 m-equiv./kg), with a reduction in iodine value of 3.4 units, was incorporated at a 5% level in the diet of day-old chicks (diet 2) and stored for 8 weeks at room temperature during feeding. Similar diets containing fresh fat (diet 1, peroxide value zero) or oxidized fat in which the peroxide had been largely destroyed by heating (diet 3, peroxide value 2 μmoles/g) were also used. The diets contained adequate but not excessive levels of all vitamins, including stabilized vitamin A, except that for half of the chicks the supplement of stabilized vitamin E was omitted. 2. No further oxidation of the dietary lipid occurred during storage, and the initially high peroxide value in diet 2 decreased rapidly. The natural vitamin E decreased by more than 50% in diet 2, but remained unaffected in diets 1 and 3. 3. The chicks grew normally, with no difference in weight gain or feed conversion between the groups, the only differences attributable to the diets being marginally lower vitamin A levels accumulated in the livers of the birds on diet 2 and ajustdetectablyhigher liver weight in the birds on diet 3. 4. One of the twelve chicks receiving oxidized fat (diet 2) without synthetic vitamin E developed encephalomalacia. There was no other suggestion of performance being inferior as a consequence of the absence of the vitamin E supplement. 5. No difference could be detected in the flavour of the chickens, either freshly roasted or reheated.

scholarly journals Vitamin E and stress

1967 ◽  
Vol 21 (2) ◽  
pp. 497-506 ◽  
Author(s):  
J. Green ◽  
A. T. Diplock ◽  
J. Bunyan ◽  
I. R. Muthy ◽  
D. Mchale
Keyword(s):  
Fatty Acid ◽  
Linoleic Acid ◽  
Vitamin E ◽  
Fatty Acid Methyl Esters ◽  
Essential Fatty Acids ◽  
Methyl Esters ◽  
Dietary Lipid ◽  
Liver Necrosis ◽  
Torula Yeast ◽  
Acid Methyl

1. Liver necrosis was produced in rats given diets deficient in selenium and vitamin E and the metabolism of [5-Me-14C]D-α-tocopherol was studied during the development of the disease. 2. When a torula yeast diet (containing sufficient of the yeast to provide essential fatty acids) was used, the addition of 5 % cod-liver oil fatty acid methyl esters produced only a slight decrease in the time taken to produce the disease, compared to controls given methyl oleate; methionine had little protective effect. The metabolism of the radioactive tocopherol was unaffected by dietary lipid, Se or methionine and was not influenced by the development of necrosis. 3. When a casein diet (devoid of fat and containing insufficient Se to prevent liver necrosis) was used, the addition of small amounts of linoleic acid to the diet (as 2 % maize oil fatty acid methyl esters) decreased the time taken to produce the disease and increased its incidence. However, the metabolism of the radioactive tocopherol was independent of dietary lipid or Se. 4. It would appear that either Se or vitamin E may be necessary for effective utilization of the ratapos;s requirement for linoleic acid.

Approaches Undertaken for Betterment of Stability and Acceptability of Cooking Soybean Oil

2017 ◽  
Vol 54 (4) ◽  
pp. 427
Author(s):  
Prodip Kumar Baral ◽  
Md Aqib Hossain Khan ◽  
Md Prince Mahmud ◽  
Sakina Sultana
Keyword(s):  
Vitamin E ◽  
Soybean Oil ◽  
Peroxide Value ◽  
Normal Condition ◽  
Acid Value ◽  
Storage Conditions ◽  
Clear Trend ◽  
Peroxide Values ◽  
Periodic Interval

In the present study storage conditions ensuring better stability of Soybean oil over a period of 180 days were investigated. The study was carried out on 12 samples (4x3) of three brands namely brand A, B and C. After periodic interval of time ‘acid value’ and ‘peroxide value’ for each sample were determined. The result showed that in every case, darkness decreased degradation in oil over the normal condition over the period of experiments. Results were expressed in terms of acid value and peroxide value. For example peroxide values for samples of brand A stored under normal condition and in the dark were 0.88 on first day where the value came up to 128.64 and 33.3 at the end of 180 days respectively. The trend remained the same for the samples of brand B and brand C. In this study an attempt was made to decrease autooxidation in oils when vitamin E was added (1 ml of 200IU d-α-tocopherol per 100 ml of oil). Samples with and without vitamin E were stored under normal condition and in the dark. Results were expressed in terms of peroxide values. Results failed to show a clear trend of decreasing auto oxidation at the end of 180 days irrespective of the nature of storing condition.

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