MATERNAL ZINC-DEFICIENCY, BUT NOT COPPER DEFICIENCY OR DIABETES, RESULTS IN INCREASED EMBRYONIC-CELL DEATH IN THE RAT - IMPLICATIONS FOR MECHANISMS UNDERLYING ABNORMAL-DEVELOPMENT
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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DOI：
10.1002/tera.1420510207
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发表时间：
1995-02-01
期刊：
影响因子：
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通讯作者：
KEEN, CL
中科院分区：
文献类型：
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作者：
JANKOWSKI, MA;URIUHARE, JY;KEEN, CL
母体铜缺乏、锌缺乏和糖尿病的致畸性机制在很大程度上是未知的。在这里，我们调查这些侮辱是否与妊娠（GD）11.0天的大鼠胚胎细胞死亡模式的改变有关。在交配前四周，在铜缺乏组（CuD）的大鼠喂食铜缺乏的饮食补充螯合剂，三亚乙基四胺，以促进组织铜储存的消耗。该组大鼠在交配前1周转为不含三乙烯四胺的铜缺乏饮食。在整个研究过程中，糖尿病组和对照组的母鼠喂食对照（8 μ g铜，25 μ g锌/g）饮食。GD 3.0时，将对照母鼠的一个子集分配至缺锌组（ZnD），并饲喂缺锌饲料。将对照母鼠的第二个子集分配到限制饲喂组，并以缺锌母鼠消耗的量饲喂对照饲料。在GD 11.0通过剖宫产取窝。检查胚胎的大体形态，并使用尼罗蓝硫酸盐评估细胞死亡模式。来自CuD母鼠的胚胎的特征为后脑水肿。糖尿病组胚胎发育迟缓。仅在来自ZD母鼠的胚胎中检测到细胞死亡模式的改变。在锌组，胚胎的特点是小尺寸，水肿的头部区域，和控制模式的细胞死亡，或正常的大小，正常的形态，和增加细胞死亡。这些不同模式的形态和细胞死亡的胚胎中的锌Dams与不同模式的母亲的食物摄入量。这些结果支持的概念，异常细胞死亡可能有助于缺锌诱导的致畸作用。(C)1995 Wiley-Liss，Inc.
The mechanisms 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 (8 mu g copper, 25 mu g 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. (C) 1995 Wiley-Liss, Inc.