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唾液腺功能是否随放射性碘剂量成比例下降?

Does Salivary Function Decrease in Proportion to Radioiodine Dose?

机构信息

Department of Otolaryngology, Inha University, School of Medicine, Incheon.

Department of Nuclear Medicine, National Cancer Center, Goyang, Republic of Korea.

出版信息

Laryngoscope. 2020 Sep;130(9):2173-2178. doi: 10.1002/lary.28342. Epub 2019 Nov 25.

DOI:10.1002/lary.28342
PMID:31765488
Abstract

OBJECTIVES

This study was conducted to investigate the dose-response characteristics of radioiodine on salivary glands and to investigate the mechanism responsible for radioiodine-induced salivary glands toxicity.

METHODS

Twenty-four mice were divided into six groups: 0, 0.05, 0.10, 0.20, 0.40, and 0.80 mCi/20 g mouse, administered orally. Mortalities were noted 12 months after radioiodine administration. Body weights, gland weights, salivary lag times, flow rates, and changes in Tc pertechnetate were recorded. Histopathological changes and mRNA expressions were also evaluated, and immunohistochemical analysis and apoptotic assays were performed.

RESULTS

Survival rates, body weights, gland weights, and flow rates decreased, and lag times increased on increasing radioiodine dose. Animals administered radioiodine showed acinar atrophy, striated duct dilations, and lymphocytic infiltration in glands and irregular destruction of epithelial surfaces of tongue. The uptake and excretion of Tc pertechnetate were impaired by radioiodine. Immunohistochemical analysis showed that numbers of salivary epithelial, myoepithelial, and endothelial cells decreased and that numbers of ductal cells increased with radioiodine dose. Oxidative stress biomarker levels increased; reactive oxygen species scavenger levels decreased; and numbers of apoptotic cells increased in animals exposed to higher radioiodine doses.

CONCLUSION

These dose-related, long-term effects on salivary gland should be taken into account when determining radioiodine doses.

LEVEL OF EVIDENCE

NA Laryngoscope, 130:2173-2178, 2020.

摘要

目的

本研究旨在探讨放射性碘对唾液腺的剂量反应特征,并研究放射性碘诱导唾液腺毒性的机制。

方法

将 24 只小鼠分为 6 组:0、0.05、0.10、0.20、0.40 和 0.80 mCi/20 g 小鼠,口服给予。在给予放射性碘 12 个月后记录死亡率。记录体重、腺体重量、唾液延迟时间、流量和放射性碘摄取的变化。还评估了组织病理学变化和 mRNA 表达,并进行了免疫组织化学分析和凋亡测定。

结果

随着放射性碘剂量的增加,存活率、体重、腺体重量和流量降低,延迟时间增加。给予放射性碘的动物表现出腺泡萎缩、纹状导管扩张和腺体中的淋巴细胞浸润以及舌上皮表面不规则破坏。放射性碘摄取和排泄受损。免疫组织化学分析显示,随着放射性碘剂量的增加,唾液上皮细胞、肌上皮细胞和内皮细胞数量减少,而导管细胞数量增加。氧化应激生物标志物水平升高;活性氧清除剂水平降低;暴露于较高放射性碘剂量的动物中凋亡细胞数量增加。

结论

在确定放射性碘剂量时,应考虑到这些与剂量相关的唾液腺长期影响。

证据水平

无。喉镜,130:2173-2178,2020。

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