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 100 micrograms zinc/gram diet (control) or less than 0.4 microgram 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.