Document Type



The literature concerning teratogeny that is attributable to faulty nutrition of laboratory induced origin was reviewed in a previous publication (Thomas and Cheng: 1952). Any review of this subject leads to the conclusion that there are numerous conditions of nutritional insufficiency which produce congenital abnormalities. Until reported recently (Thomas and Cheng, 1952) none had been ascribed to avitaminosis E. The usual abnormality in reproduction which prevails among pregnant rats in an advanced state of avitaminosis E is fetal resorption. Adequate vitamin E therapy administered promiscuously is not sufficient to circumvent reproductive difficulties. Timing of therapy is an exceedingly important limiting condition. Therapy that is adequate when given during the first week of gestation in the rat frequently will fail if delayed until the second and third weeks of gestation. When given during the second week uterine responses will be variable. Thus, in a single uterus some feti will be resorbed, others will have developed congenital abnormalities, and still others will appear externally morphologically normal. When therapy is given during the third week the embryological contents of the uterus will be partially or completely resorbed. The purpose of this report is to show more specifically than was possible at the time of our original announcement (Thomas and Cheng, 1952) the relationship of time of therapy to incidence of teratogeny in nutritional avitaminosis E. Also, data are presented summarizing the incidence of the different types of abnormalities thus far observed which are a part of this syndrome.

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Proceedings of the Iowa Academy of Science





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©1953 Iowa Academy of Science, Inc.



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