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小鼠模型口服 I-131 后放射性碘呼出情况

Radioiodine Exhalation Following Oral I-131 Administration in a Mouse Model.

作者信息

Schomäcker Klaus, Fischer Thomas, Sudbrock Ferdinand, Strohe Daniela, Weber Sebastian, Zimmermanns Beate, Dietlein Felix, Krapf Philipp, Schicha Harald, Dietlein Markus, Drzezga Alexander

机构信息

Department of Nuclear Medicine, Faculty of Medicine and University Hospital Cologne, University of Cologne, Kerpener Str. 62, 50937 Cologne, Germany.

Practice for Gynecology and Prenatal Medicine, Dres. med. Horz-Wilhelm/Strohe, Römerfeld 1, 50129 Bergheim, Germany.

出版信息

Biomedicines. 2025 Apr 8;13(4):897. doi: 10.3390/biomedicines13040897.

Abstract

: The exhalation of radioiodine following radioiodine therapy (RIT) presents a challenge in radiation protection, though the mechanisms remain incompletely understood. Previous studies have indicated that radioiodine is predominantly exhaled in an organically bound form in humans. : This study investigates the chemical composition and exhaled amounts of radioiodine, as well as the impact of thyroid-targeted pharmacological interventions, using a controlled mouse model. Female Balb/c mice (25 g) were administered oral doses of radioiodine (0.1, 1, 2, 10, and 23 MBq per animal) with and without prior treatment using thyroid-blocking agents (stable iodine, perchlorate) or antithyroid drugs (carbimazole). Exhaled radioiodine was collected in metabolic cages, separating chemical forms (aerosolized iodine, elemental iodine, organically bound iodine), and quantified via scintillation counter. : The exhaled radioiodine activity was proportional to the administered dose (0.2-0.3%). Thyroid-blocking agents increased exhalation, shifting toward elemental iodine. Antithyroid drugs reduced exhalation but increased aerosol formation, particularly at higher I-131 doses. Organically bound iodine remained the predominant exhaled species in all groups. : These results highlight the critical role of the thyroid in radioiodine organification. The blockade of thyroid uptake disrupted the formation of organically bound iodine, suggesting that iodine organification requires passage through the thyroid. Additionally, the results support the hypothesis that iodine metabolism outside the thyroid is less efficient, contributing to the formation of organic iodine species. Radical formation is likely a key factor in generating these volatile iodine species, with radiation-induced iodine and methyl radicals playing a role in their formation.

摘要

放射性碘治疗(RIT)后呼出放射性碘对辐射防护提出了挑战,尽管其机制仍未完全明确。先前的研究表明,在人类中,放射性碘主要以有机结合形式呼出。本研究使用可控小鼠模型,研究放射性碘的化学成分、呼出量以及甲状腺靶向药物干预的影响。对雌性Balb/c小鼠(25克)口服给予放射性碘剂量(每只动物0.1、1、2、10和23兆贝可),并在有或没有事先使用甲状腺阻断剂(稳定碘、高氯酸盐)或抗甲状腺药物(卡比马唑)治疗的情况下进行。在代谢笼中收集呼出的放射性碘,分离化学形式(雾化碘、元素碘、有机结合碘),并通过闪烁计数器进行定量。呼出的放射性碘活度与给药剂量成正比(0.2 - 0.3%)。甲状腺阻断剂增加呼出量,并向元素碘方向转变。抗甲状腺药物减少呼出量,但增加气溶胶形成,特别是在较高的I - 131剂量下。有机结合碘在所有组中仍然是呼出的主要成分。这些结果突出了甲状腺在放射性碘有机化中的关键作用。甲状腺摄取的阻断破坏了有机结合碘的形成,表明碘有机化需要通过甲状腺。此外,结果支持以下假设:甲状腺外的碘代谢效率较低,有助于有机碘物种的形成。自由基形成可能是产生这些挥发性碘物种的关键因素,辐射诱导的碘和甲基自由基在其形成过程中起作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9261/12025149/dc3b54f52ea8/biomedicines-13-00897-g001.jpg

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