The influence of maternal hypothyroidism and radioactive iodine on rat embryonal development: Thyroid C-cells
✍ Scribed by Usenko, Vasilij S. ;Lepekhin, Eugene A. ;Lyzogubov, Valerij V. ;Kornilovska, Iryna N. ;Apostolov, Eugene O. ;Tytarenko, Ruslana G. ;Witt, Martin
- Publisher
- John Wiley and Sons
- Year
- 1999
- Tongue
- English
- Weight
- 267 KB
- Volume
- 256
- Category
- Article
- ISSN
- 0003-276X
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✦ Synopsis
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 µCi 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.