CHANGES IN THE FETAL TIBIAL GROWTH PLATE SECONDARY TO MATERNAL ZINC-DEFICIENCY IN THE RAT - A HISTOLOGICAL AND HISTOCHEMICAL-STUDY
CHANGES IN THE FETAL TIBIAL GROWTH PLATE SECONDARY TO MATERNAL ZINC-DEFICIENCY IN THE RAT - A HISTOLOGICAL AND HISTOCHEMICAL-STUDY
复制标题
DOI：
10.1002/tera.1420440410
复制
发表时间：
1991-10-01
期刊：
影响因子：
--
通讯作者：
ELIZAGA, IV
中科院分区：
文献类型：
--
作者：
FERREIRA, RMCD;GONZALEZ, JLR;ELIZAGA, IV
缺锌（ZD）对大鼠有致畸作用，胎儿骨骼缺陷也很突出。 为了进一步阐明母体 ZD 对胎儿骨骼的影响，我们对 ZD 大鼠胎儿的胫骨生长板（GP）进行了形态学和组织化学研究。 组织化学研究包括鉴定钙、与钙化过程相关的水解酶以及与能量产生和蛋白聚糖合成相关的氧化酶。 怀孕的Sprague-Dawley大鼠被喂养（1）随意的对照饮食（76.4-mu-g Zn/g饮食）（C组），（2）随意的缺锌饮食（0-mu-g/g）（ZD组），或（3）与ZD大鼠配对喂养的对照饮食（PF组）。 妊娠第21天，进行剖腹手术，取出胎儿，获取胎儿胫骨。 样本用苏木精-伊红 (H&E) 和 Masson Trichrome 染色，并进行处理以鉴定碱性磷酸酶、三磷酸腺苷酶、琥珀酸脱氢酶、NADH 脱氢酶和钙。 ZD 胎儿胫骨中发现的形态模式表明与骨代谢有关的各种细胞类型存在缺陷。 水解酶染色显示 ZD 胎儿基质囊泡大小和分布的变化以及 ATP 酶染色较弱。 ZD 胎儿胫骨中氧化酶的染色总体上更强烈。 ZD 胎儿还表现出不规则且有缺陷的钙化。 这些发现表明，严重的母体 ZD 会导致胎儿骨 GP 的结构和功能改变，导致软骨内骨化缺陷。
Zinc deficiency (ZD) is teratogenic in rats, and fetal skeletal defects are prominent. To elucidate further the effects of maternal ZD in the fetal skeleton, we performed a morphological and histochemical study of tibial growth plate (GP) in ZD rat fetuses. The histochemical study included the identification of calcium, of hydrolytic enzymes associated with the process of calcification, and of oxidative enzymes related to energy production and to the synthesis of proteoglycans. Pregnant Sprague-Dawley rats were fed (1) a control diet (76.4-mu-g Zn/g diet) ad libitum (group C), (2) a zinc-deficient diet (0-mu-g/g) ad libitum (group ZD), or (3) the control diet pair-fed to the ZD rats (group PF). On day 21 of gestation, laparotomies were performed, the fetuses were removed, and fetal tibiae obtained. Specimens were stained with hematoxylin-eosin (H&E) and Masson Trichrome and were processed for identification of alkaline phosphatase, adenosine triphosphatase, succinic dehydrogenase, NADH dehydrogenase, and calcium. The morphologic patterns found in ZD fetal tibiae indicated defects in various cell types implicated in bone metabolism. Staining for hydrolytic enzymes revealed alterations in the size and distribution of matrix vesicles and a weaker staining for ATPase in ZD fetuses. Staining for oxidative enzymes was overall more intense in ZD fetal tibiae. ZD fetuses also presented irregular and defective calcification. These findings indicate that severe maternal ZD in the rat results in structural and functional alterations in the GP of fetal bone, leading to a defective endochondral ossification.