Abstract
It has been suggested that zinc deficiency may interfere with fatty acid metabolism, possibly by increasing the rate of lipid peroxidation. The hypothesis was investigated that the teratogenicity of zinc deficiency might be alleviated by vitamin E supplementation. Sprague-Dawley rats were fed during pregnancy a complete purified diet containing either 100μg zinc/gram diet (control) or <0.4 μg zinc/gram diet (deficient). Half of the animals in each diet group received supplemental vitamin E (200 x control). At term, fetuses were removed, examined for malformations, resorption sites were counted, and maternal and fetal tissues were analyzed for zinc concentration. Vitamin E supplementation of the control diet did not produce teratogenic effects. The number of total sites affected (resorptions + malformed fetuses) in the zinc-deficient groups was not influenced by vitamin E supplementation. Tissue zinc was significantly lower in the zinc-deficient groups, but vitamin E supplementation had no effect. These results show that vitamin E supplementation does not ameliorate the teratogenicity of zinc deficiency.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 1875-1877 |
| Number of pages | 3 |
| Journal | Journal of Nutrition |
| Volume | 113 |
| Issue number | 9 |
| State | Published - 1983 |
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ASJC Scopus subject areas
- Food Science
- Medicine (miscellaneous)
Cite this
The effects of vitamin E on zinc deficiency teratogenesis in rats. / Hurley, L. S.; Dungan, D. D.; Keen, Carl L; Lonnerdal, B.
In: Journal of Nutrition, Vol. 113, No. 9, 1983, p. 1875-1877.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - The effects of vitamin E on zinc deficiency teratogenesis in rats
AU - Hurley, L. S.
AU - Dungan, D. D.
AU - Keen, Carl L
AU - Lonnerdal, B.
PY - 1983
Y1 - 1983
N2 - It has been suggested that zinc deficiency may interfere with fatty acid metabolism, possibly by increasing the rate of lipid peroxidation. The hypothesis was investigated that the teratogenicity of zinc deficiency might be alleviated by vitamin E supplementation. Sprague-Dawley rats were fed during pregnancy a complete purified diet containing either 100μg zinc/gram diet (control) or <0.4 μg zinc/gram diet (deficient). Half of the animals in each diet group received supplemental vitamin E (200 x control). At term, fetuses were removed, examined for malformations, resorption sites were counted, and maternal and fetal tissues were analyzed for zinc concentration. Vitamin E supplementation of the control diet did not produce teratogenic effects. The number of total sites affected (resorptions + malformed fetuses) in the zinc-deficient groups was not influenced by vitamin E supplementation. Tissue zinc was significantly lower in the zinc-deficient groups, but vitamin E supplementation had no effect. These results show that vitamin E supplementation does not ameliorate the teratogenicity of zinc deficiency.
AB - It has been suggested that zinc deficiency may interfere with fatty acid metabolism, possibly by increasing the rate of lipid peroxidation. The hypothesis was investigated that the teratogenicity of zinc deficiency might be alleviated by vitamin E supplementation. Sprague-Dawley rats were fed during pregnancy a complete purified diet containing either 100μg zinc/gram diet (control) or <0.4 μg zinc/gram diet (deficient). Half of the animals in each diet group received supplemental vitamin E (200 x control). At term, fetuses were removed, examined for malformations, resorption sites were counted, and maternal and fetal tissues were analyzed for zinc concentration. Vitamin E supplementation of the control diet did not produce teratogenic effects. The number of total sites affected (resorptions + malformed fetuses) in the zinc-deficient groups was not influenced by vitamin E supplementation. Tissue zinc was significantly lower in the zinc-deficient groups, but vitamin E supplementation had no effect. These results show that vitamin E supplementation does not ameliorate the teratogenicity of zinc deficiency.
UR - http://www.scopus.com/inward/record.url?scp=0020961844&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0020961844&partnerID=8YFLogxK
M3 - Article
C2 - 6886830
AN - SCOPUS:0020961844
VL - 113
SP - 1875
EP - 1877
JO - Journal of Nutrition
JF - Journal of Nutrition
SN - 0022-3166
IS - 9
ER -