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The anemia of vitamin E deficiency in swine: An experimental model of the human congenital dyserythropoietic anemias
Author(s) -
Lynch R. E.,
Hammar S. P.,
Lee G. R.,
Cartwright G. E.
Publication year - 1977
Publication title -
american journal of hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/ajh.2830020206
Subject(s) - erythropoiesis , vitamin e deficiency , anemia , vitamin e , vitamin , medicine , pathogenesis , ineffective erythropoiesis , abnormality , endocrinology , biology , physiology , biochemistry , psychiatry , antioxidant
Abstract The ultrastructural and erythrokinetic characteristics of vitamin E deficiency in swine were investigated in an effort to evaluate the suitability of the swine disorder as a model of the human congenital dyserythropoietic anemias. The dominant erythrokinetic abnormality in vitamin E deficient pigs, as in the CDAs, is ineffective erythropoiesis. As in some patients with CDA, the activity of a number of erythrocyte enzymes was increased. Distinctive ultrastructual changes previously described in patients with CDA were found in normoblasts from vitamin E deficient pigs. The morphologic, erythrokinetic, biochemical and ultrastructural similarities between vitamin E deficiency in swine and the CDAs in man appear to justify the study of the animal disorder as a model of the human disease. A complete hematologic response was elicited by the administration not only of vitamin E, but also, as in the previous studies of vitamin E deficiency in monkeys, by hexahydrocoenzyme Q 4 . The partial hematologic response occurring after deletion of tocopherol stripped corn oil from the diet indicates that factors other than the dietary lack of vitamin E are important in the pathogenesis of this disorder.