Helene Swenerton

Congenital Malformations Resulting from Zinc Deficiency in Rats.

Summary A mild but specific zinc deficiency was produced in female rats by the use of a purified diet lacking the element and by stringent elimination of sources of zinc contamination from the environment. Almost all of the full-term fetuses produced under such conditions showed gross congenital malformations encompassing a wide variety of organ systems, including skeletal, brain, eye, heart, lung, and urogenital defects. The fetuses from zinc-deficient females contained less zinc than did their controls, suggesting that the congenital anomalies resulted from a direct effect of lack of zinc in the fetal tissues.

Zinc-Deficient Embryos: Reduced Thymidine Incorporation

The 12-day-old embryos of rats with a deficiency of zinc showed a reduced uptake of tritiated thymidine when compared with controls, as shown by liquid scintillation and autoradiography. The high incidence of gross congenital malformations resulting from zinc deficiency may thus be caused by DNA impaired DNA synthesis.

Teratogenic Effects of a Chelating Agent and Their Prevention by Zinc

Ingestion of a chelating agent (ethylenediaminetetraacetic acid) by female rats during pregnancy impaired reproduction and resulted in congenitally malformed young. When ethylenediaminetetraacetic acid was fed from days 6 to 21 of gestation, all of the full-term young had gross congenital malformations. These effects were prevented by simultaneous supplementation with 1000 parts per million of dietary zinc.

Lactic and Malic Dehydrogenases in Testes of Zinc-Deficient Rats

Summary The activities of LDH and MDH were evaluated in the testes of zincdeficient and control rats by both spectrophotometric and histochemical methods. There was no significant decrease in the activities of these enzymes by either method in the testes of rats fed the zinc-deficient ration for 28 days as compared with rats fed the zincsupplemented diet ad libitum or in restricted amounts. Histological changes were observed in the testes of zinc-deficient rats consisting of decreased tubule size, spermatogonic arrest, nuclear chromatolysis in spermatids and secondary spermatocytes, and pyknotic epithelial cells. The testes of restricted or ad libitum-fed controls appeared normal. The evidence presented does not support the hypothesis that reduced activity of these enzymes is a primary cause of the physiological and morphological changes observed in zinc deficiency.