Vitamin E and stress

Abstract

I. When chicks were given a fat-free casein-gelatin diet and, after z weeks of age, 0.15 % silver acetate in the drinking water, they were found to have colourless exudates mainly in the pectoral region and partly in the peritoneal and pericardial spaces. Vitamin E and selenium, separately and together, failed to prevent this condition. Vitamin E was required together with methionine to prevent the condition. Methionine itself induced green staining of a few of the exudates.2. When lard was added to the casein-gelatin diet and the chicks were also given Ag, some green exudates were found in addition to the colourless ones. Addition of vitamin E or Se or both prevented the green exudates, but raised the incidence of colourless exudates.Methionine enhanced the green exudate condition, but again when combined with vitamin E prevented both types of exudate.3. A similar condition characterized by colourless exudates was induced by giving chicks diets based upon gelatin, yeast BPC, a-protein (with extra salts) or a-protein with gelatin. A torula yeast diet induced green exudates and haemorrhages. 4. All the basal diets, which wcre deficient in sulphur amino acids, produced dystrophy of the breast muscle. Four of these diets contained no fat. Some diets also induced dystrophy of the gizzard. Vitamin E and Se protected against both these lesions. Methionine was protective in all except the torula yeast diet.5 . Ethionine induced muscular dystrophy in chicks given a vitamin E-deficient diet adequate in sulphur amino acids. Additional methionine or vitamin E was protective, but cystine was not. Ethionine also produced a small incidence of green exudates and slight haemorrhages. This condition was prevented by vitamin E but not by methionine. The liver damage due to ethionine was not prevented by vitamin E, methionine or cystine. .Liver necrosis was induced in rats by giving them an 8.3 yo casein diet and Ag, 130-1000 ppm, in the drinking water or the diet. Necrosis was produced even in the absence of dietary fat. Vitamin E and DPPD (N,N'-diphenyl-p-phenylenediamine) prevented necrosis, but adenine sulphate (025 %), methionine (0.1 5 yo) and IONOX 330 (2,4,6-tri-(3',5'-ditert.-butyl-4'-hydroxybenzyl) mesitylene) did not. Se, 0.05 ppm, protected against 130 ppm Ag, but 1000 ppm Ag overcame the protective effect of I ppm Se. Similarly, 3 ppm cyanocobalamin was partly protective against 130 ppm Ag, but not against the higher concentration. Gold chloride (1000 ppm Au) had a mildly necrotic effect against which vitamin E did not protect. Neither copper sulphate (500 ppm Cu) not arsanilic acid (70 ppm As) induced liver necrosis. 7. A high intake of Se (20 ppm as sodium selenate) was necrogenic in rats given a 10% casein diet; vitamin E and methionine did not protect. Vitamin E and cystine raised the low incidence of an exudative condition found in rats given 20 ppm Se. Methionine opposed this action of vitamin E.8. It was concluded that exudative diathesis in chicks could be resolved into a simple exudative condition and a super...

Dietary fat composition and tocopherol requirement: I. Lack of correlation between nutritional indices and results of in vitro peroxide hemolysis tests

“…The results of our studies are in agreement with those reported by Bunyan etal. (31,32) who found that unsaturated lipids do not become peroxidized after incorporation into the adipose tissue of vitamin E deficient rats. They also reject the in vivo antioxidant theory of vitamin E activity proposed by others (4,26,33-36) since the existence of peroxidation in vivo in the vitamin E deficient animal has not been substantiated (31,32).…”

“…(31,32) who found that unsaturated lipids do not become peroxidized after incorporation into the adipose tissue of vitamin E deficient rats. They also reject the in vivo antioxidant theory of vitamin E activity proposed by others (4,26,33-36) since the existence of peroxidation in vivo in the vitamin E deficient animal has not been substantiated (31,32). In further support for our studies, Barber (37) has shown that the in vitro hemolysis test simply reveals the effective balance of pro-and antioxidant components in a system which is not related to conditions in vivo.…”

Absorption and metabolism of 1‐14C‐methyl linoleate hydroperoxide

“…Andrews et al (2) were unable to find evidence for the absorption of peroxides and therefore concluded that their toxic action took place on the intestinal wall. Other investigators also have concluded that intact peroxides are not absorbed (3)(4); still others (5)(6) have reported that feeding peroxides to rats leads to appreciable concentrations in the tissues. Nishida and Kummerow (7) obtained spectral evidence of diene conjugation in the lymph of rats dosed with methyl linoleate hydroperoxide and concluded therefore that some peroxide was absorbed.…”

Metabolism of 1‐14C‐methyl linoleate hydroperoxide in the rabbit

“…Whether fatty acid peroxides are formed in animal tissues in vivo has been a controversial question for some years (1)(2)(3)(4)(5)(6). Substances which presumably are derived from peroxides or their degradation products have been detected in tissue extracts (7)(8)(9)(10), but it is difficult to prove their existence in the live organism.…”