Etiology of Muscular Dystrophy in the Lamb and Chick

Erwin, E. S.; Sterner, W; Gordon, Rebecca; Machlin, L. J.; Tureen, Louis L.

doi:10.1093/jn/75.1.45

Cited by 15 publications

(5 citation statements)

References 13 publications

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“…a similar observation has been made by others (Wright and Bell, 1964; Hopkins ~_!l., 1964). As all diets contained ethoxyquin, it is apparent that it was also without effect upon this phenomenon, which is contrary to the findings in young lambs made by Kuttler and Marble (1959) and Erwin~~• (1961). However, Erwin~ !l_.…”

Section: •-I-mentioning

confidence: 62%

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Effects of Vitamin E and Selenium Deficiencies in Sheep Fed a Purified Diet during Growth and Reproduction

Buchanan-Smith

Nelson

Osburn

et al. 1969

Journal of Animal Science

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Section: •-I-mentioning

confidence: 62%

“…Corn oil was used in a skim milk diet for lambs, in which clin'ical signs of dystrophy were produced that did not respond to vitamin E (Boyd, 1968). The dystrophy in lambs produced by Erwin et al ( 1961) with coconut oil could be prevented by the --. antioxidant, ethoxyquin.…”

Section: Nutrition: Generalmentioning

confidence: 99%

Effects of Vitamin E and Selenium Deficiencies in Sheep Fed a Purified Diet during Growth and Reproduction

Buchanan-Smith

Nelson

Osburn

et al. 1969

Journal of Animal Science

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“…Hopkins et at. [1964] and another group [Erwin et al, 1961] have produced selenium-deficient lambs by using a somewhat similar dietary approach to our own. However, Erwin and his collaborators did not study the condition in detail histopathologically.…”

Section: Discussionmentioning

confidence: 99%

Abnormal Electrocardiograms, Blood Pressure Changes, and Some Aspects of the Histopathology Ofselenium Deficiency in Lambs

Godwin

Fraser

1966

Exp Physiol

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Experimental selenium deficiency has been studied in a group of lambs weaned early on to a semi-synthetic diet. Nineteen lambs were used; eleven became selenium deficient, the remaining eight were supplemented with selenium and remained normal. Well-defined differences, in terms of histopathological changes, developed between the two groups. The dystrophic lesions were mainly found in skeletal and cardiac muscle, and to a lesser extent in the pancreas and diaphragm.Electrocardiograms showed the progressive development of a characteristic abnormality, after the animals had been on the deficient diet for a few weeks. Just before death the ECG pattern became grossly abnormal in some cases, a rise in the T-wave giving way to an elevated S-T segment, similar to that seen frequently in myocardial infaretion in man.Paralleling these changes, at least in time, there was a fall in blood pressure especially marked in the limbs, but present to a lesser degree in the rest of the systemic circulation. Taken together, these observations point to the possibilitv that the fundamental change occurring in selenium deficiency may be circulatory failure.Finally, comparison of the histopathological picture of the lamb and the rat, when both species are reared on the same diet, indicates that entirely different syndromes appear, at first sight, to develop. However, ECG changes previously studied in rats are somewhat similar to those reported here. Skeletal muscle is severely dystrophic in both species. Perhaps subsequent studies will demonstrate that even though the final outcome of selenium deficiency in different species is variable, the initial lesions are closely comparable.AT a recent symposium on the metabolism of vitamin E and related substances [Karrer et al., 19621, it was re-emphasized that though the metabolic functions of selenium and vitamin E are apparently closely related, neither can invariably take the place of the other. As their functions are as yet not clearly understood, the metabolic origins of certain well defined metabolic lesions are at present unsatisfactory. Muscular dystrophy induced by feeding large quantities of unsaturated fatty acids to lambs, for instance, responds well to vitamin E supplementation, though not to selenium [Welch et al., 1960]. On the other hand muscular dystrophy produced in poultry by feeding a diet low in selenium and vitamin E is prevented completely by selenium supplementation but is unaffected by additional vitamin E [Scott, 1962].'The following experiments were designed to produce in lambs and rats an uncomplicated selenium-deficiency syndrome, so that means could be sought to recognize the symptoms of the condition in its early stages.One of the striking features of vitamin E deficiency is the great variation of the pathological state which results in different species. Schwarz [1961] 94

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“…The position with the dystrophies of vitamin E deficiency is even more obscure. In contrast to dystrophy in the chick, nutritional myopathies in the lamb (Erwin, Sterner, Gordon, Machlin & Tureen, 1961), the rat (Witting & Horwitt, 1964) and the rabbit (Bunyan, Green & Diplock, unpublished observations) are hardly affected by dietary sulphur amino acids. Furthermore, the effect of Se on enzootic nutritional myopathies varies from species to species.…”

Section: Vol 21mentioning

confidence: 99%

Vitamin E and stress

et al. 1967

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I. 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-'*C]a-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]a-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 a-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 pg [14C]n-a-tocopherol. They were then given, either by stomach tube daily or by dietary addition, large amounts of methyl linoleate or vitamin Efree polyunsaturated fatty acid methyl esters prepared from cod-liver oil and compared with controls given methyl oleate for up to 3 I 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 ['4C]or-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]a-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 codliver 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 [14C]cr-tocopherol in weanling rats given large amounts of codliver 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-ol...

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Etiology of Muscular Dystrophy in the Lamb and Chick

Cited by 15 publications

References 13 publications

Effects of Vitamin E and Selenium Deficiencies in Sheep Fed a Purified Diet during Growth and Reproduction

Effects of Vitamin E and Selenium Deficiencies in Sheep Fed a Purified Diet during Growth and Reproduction

Abnormal Electrocardiograms, Blood Pressure Changes, and Some Aspects of the Histopathology Ofselenium Deficiency in Lambs

Vitamin E and stress

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