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母体甲状腺功能减退和放射性碘对大鼠胚胎发育的影响:甲状腺C细胞。

The influence of maternal hypothyroidism and radioactive iodine on rat embryonal development: thyroid C-cells.

作者信息

Usenko V S, Lepekhin E A, Lyzogubov V V, Kornilovska I N, Apostolov E O, Tytarenko R G, Witt M

机构信息

Morphological Laboratory BIONTEC, 320000 Dnepropetrovsk, Ukraine.

出版信息

Anat Rec. 1999 Sep 1;256(1):7-13. doi: 10.1002/(SICI)1097-0185(19990901)256:1<7::AID-AR2>3.0.CO;2-O.

DOI:10.1002/(SICI)1097-0185(19990901)256:1<7::AID-AR2>3.0.CO;2-O
PMID:10456980
Abstract

There have been no works devoted to the study of the influence of (131)I and maternal (131)I-induced hypothyroidism on the state of the C-cells in the thyroid gland of the developing embryos. A study was made on the effect of a dose of 150 microCi (131)I (0.5 Gy) leading to hypothyroidism in rats, on 35 mother rats and 168 newborn pups. The mother rats were divided into control and four treated groups which were injected with (131)I before pregnancy, on gestation days 5, 10, and 16, respectively. Immunohistochemically, the thyroid gland was examined for calcitonin-positive cells. Maternal hypothyroidism induced by (131)I leads to the development of hyperplasia and hyperthrophy of calcitonin-positive cells in the pups at the time of birth. The discovery of separate C-cells in the peripheral zone of the thyroid lobe may be evidence of an unbalance in the development of the medial and lateral source of the thyroid. There is a verifiable increase in the quantity of C-cells per 1 mm(2) field of the localization in the central zone of the gestation days 10 and 16 groups. This might be a compensatory mechanism for regulating the activity of the thyroid gland under induced hypothyroidism. Thus, in cases when there is a breakdown in the normal external regulation of the embryonic morphogenesis, a reduction in the level of maternal thyroid hormones and also direct exposure to (131)I, there is also a change in the foetus' internal regulatory systems. A change in C-cell system could lead to the appearance of endocrinological disorders later in life.

摘要

尚未有关于(131)I 以及母体(131)I 诱发的甲状腺功能减退对发育中胚胎甲状腺 C 细胞状态影响的研究。对 35 只母鼠和 168 只新生幼崽进行了一项研究,观察剂量为 150 微居里(131)I(0.5 戈瑞)致使大鼠甲状腺功能减退的效果。母鼠被分为对照组和四个处理组,分别在怀孕前、妊娠第 5 天、第 10 天和第 16 天注射(131)I。通过免疫组织化学方法检查甲状腺中的降钙素阳性细胞。(131)I 诱发的母体甲状腺功能减退会导致幼崽出生时降钙素阳性细胞增生和肥大。在甲状腺叶周边区域发现单个 C 细胞可能是甲状腺内侧和外侧来源发育不平衡的证据。在妊娠第 10 天和第 16 天组的中央区域,每 1 平方毫米定位区域内 C 细胞数量有可证实的增加。这可能是在诱发甲状腺功能减退情况下调节甲状腺活动的一种补偿机制。因此,在胚胎形态发生的正常外部调节出现故障、母体甲状腺激素水平降低以及直接接触(131)I 的情况下,胎儿的内部调节系统也会发生变化。C 细胞系统的变化可能导致日后生活中出现内分泌紊乱。

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The influence of maternal hypothyroidism and radioactive iodine on rat embryonal development: thyroid C-cells.母体甲状腺功能减退和放射性碘对大鼠胚胎发育的影响:甲状腺C细胞。
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