放射性碘诱导的甲状腺机能减退会干扰未成熟雌性大鼠青春期生殖器官的成熟。

IF 1.6 4区 医学 Q4 TOXICOLOGY
Toxicological Research Pub Date : 2022-08-09 eCollection Date: 2023-01-01 DOI:10.1007/s43188-022-00147-z
Jihyun Keum, Ki-Young Ryu, Jaesook Roh
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引用次数: 0

摘要

动物和人体研究表明,甲状腺激素可能在卵巢的发育过程中起着至关重要的作用。例如,甲状腺缺乏会分别破坏新生儿和成年女性的卵巢微结构和月经周期。因此,可以想象甲状腺缺乏可能会破坏围青春期的性成熟。为了研究放射性碘诱导的甲状腺缺乏对整个青春期生殖器官的影响,我们在未成熟的雌性大鼠出生后的第22天和第29天给它们喂食两次含有放射性碘(0.37 MBq/g体重)的水。放射性碘引起的甲状腺功能减退表现为游离甲状腺素水平低。甲状腺素缺乏会推迟阴道开始张开的时间,减少卵巢重量和中等大小卵泡的数量,并导致子宫变长。但对发情周期或子宫绝对重量没有影响。我们的结论是,放射性碘诱导的甲状腺缺乏会推迟围青春期大鼠的性成熟,并改变卵巢的正常生长。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Radioactive Iodine-induced hypothyroidism interferes with the maturation of reproductive organs during puberty in immature female rats.

Animal and human studies suggest that thyroid hormone may have critical roles in the development of the ovary. For example, thyroid deficiency disrupts the ovarian microarchitecture and menstrual cycle in neonate and adult women, respectively. Therefore, it is conceivable that thyroid deficiency might disrupt sexual maturation during the peri-pubertal period. To investigate the impact of radioactive iodine-induced thyroid deficiency on reproductive organs throughout puberty, immature female rats were given water containing radioactive iodine (0.37 MBq/g body weight) twice, on postnatal days 22 and 29. Radioactive iodine-induced hypothyroidism was revealed by low free thyroxin levels. Thyroid deficiency delayed the onset of vaginal opening, reduced ovarian weight and the number of medium-sized follicles and led to elongated uteri. However, there was no effect on the estrous cycle or absolute uterus weight. We conclude that radioactive iodine-induced thyroid deficiency delays sexual maturation and alters normal ovarian growth in peri-pubertal rats.

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来源期刊
CiteScore
4.20
自引率
4.30%
发文量
39
期刊介绍: Toxicological Research is the official journal of the Korean Society of Toxicology. The journal covers all areas of Toxicological Research of chemicals, drugs and environmental agents affecting human and animals, which in turn impact public health. The journal’s mission is to disseminate scientific and technical information on diverse areas of toxicological research. Contributions by toxicologists, molecular biologists, geneticists, biochemists, pharmacologists, clinical researchers and epidemiologists with a global view on public health through toxicological research are welcome. Emphasis will be given to articles providing an understanding of the toxicological mechanisms affecting animal, human and public health. In the case of research articles using natural extracts, detailed information with respect to the origin, extraction method, chemical profiles, and characterization of standard compounds to ensure the reproducible pharmacological activity should be provided.
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