{'fraction_non_alphanumeric': 0.02346041055718475, 'fraction_numerical': 0.031085043988269796, 'mean_word_length': 4.842465753424658, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
The influence of maternal hypothyroidism and radioactive iodine on rat embryonal development: Thyroid C‐cells

There have been no works devoted to the study of the influence of 131I and maternal 131I‐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 131I (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 131I before pregnancy, on gestation days 5, 10, and 16, respectively. Immunohistochemically, the thyroid gland was examined for calcitonin‐positive cells. Maternal hypothyroidism induced by 131I 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 mm2 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 131I, 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. Anat Rec 256:7–13, 1999. © 1999 Wiley‐Liss, Inc.