Maternal zinc deficiency, but not copper deficiency or diabetes, results in increased embryonic cell death in the rat: Implications for mechanisms underlying abnormal development

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Abstract
The mechanism underlying the teratogenicity of maternal copper deficiency, zinc deficiency, and diabetes are largely unknown. Here we investigated whether these insults are associated with altered patterns of cell death in gestation day (GD) 11.0 rat embryos. Four weeks prior to mating, rats in the copper‐deficient group (CuD) were fed a copper‐deficient diet supplemented with the chelator, triethylenetetramine, to facilitate the depletion of tissue copper stores. Rats in this group were switched to a triethylenetetramine‐free copper‐deficient diet 1 week prior to mating. Dams in the diabetic and control groups were fed a control (8μg copper, 25 μg zinc/g) diet throughout the study. On GD 3.0, one subset of the control dams was assigned to the zinc‐deficient group (ZnD) and fed a zinc‐deficient diet. A second subset of control dams was assigned to a restricted fed group and fed the control diet in quantities consumed by the zinc‐deficient dams. Litters were taken by cesarean section on GD 11.0 Embryos were examined for gross morphology and assessed for patterns of cell death using Nile blue sulfate. Embryos from the CuD dams were characterized by edematous hindbrain. Embryos from the diabetic group were characterized by delayed development. Altered patterns of cell death were only detected in embryos from the ZnD dams. Within the ZnD group, embryos were either characterized by small size, edematous head region, and control patterns of cell death, or normal size, normal morphology, and increased cell death. These different patterns of morphology and cell death in the embryos of ZnD dams were associated with different patterns of maternal food intake. These results support the concept that abnormal cell death may contribute to zinc deficiency‐induced teratogenesis.
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