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甲状腺细胞生长:鞘磷脂代谢作为太空飞行过程中细胞损伤的非侵入性标志物。

Thyroid cell growth: sphingomyelin metabolism as non-invasive marker for cell damage acquired during spaceflight.

机构信息

Department of Clinical and Experimental Medicine, Physiopathology Section, University School of Medicine, Perugia, Italy.

出版信息

Astrobiology. 2010 Oct;10(8):811-20. doi: 10.1089/ast.2010.0461.

DOI:10.1089/ast.2010.0461
PMID:21087161
Abstract

Prolonged spaceflights are known to elicit changes in human cardiovascular, musculoskeletal, and nervous systems, whose functions are regulated by the thyroid gland. It is known that sphingomyelin metabolism is involved in apoptosis (programmed cell death) of thyroid cells induced by UVC radiation, but at present no data exists with regard to this phenomenon, which occurs during space missions. The aim of this study was to analyze, for the first time, the effect of spaceflight on the enzymes of sphingomyelin metabolism, sphingomyelinase, and sphingomyelin synthase, and to determine whether the ratio between the two enzymes might be used as a possible marker for thyroid activity during space missions. Both quiescent thyroid cells and thyroid cells stimulated to proliferate with thyrotropin (TSH) were cultured during the Eneide and Esperia missions on the International Space Station. The results show that during space missions the cells treated with TSH grew only 1.5 ± 0.65-fold and, thus, behave similarly to quiescent cells, while on the ground the same cells, maintained in experimental conditions that reproduced those of the flight, grew 7.71 ± 0.67-fold. Comparison of the sphingomyelinase/sphingomyelin-synthase ratio and the levels of Bax, STAT3, and RNA polymerase II in proliferating, quiescent, pro-apoptotic, or apoptotic cells demonstrated that thyroid cells during space missions were induced into a pro-apoptotic state. Given its specificity and the small amount of cells needed for analysis, we propose the use of the sphingomyelinase/sphingomyelin-synthase ratio as a marker of functional status of thyroid cells during space missions. Further studies could lead to its use in real time during prolonged spaceflights.

摘要

众所周知,长时间的太空飞行会引起人体心血管、肌肉骨骼和神经系统的变化,而这些系统的功能是由甲状腺调节的。已知鞘磷脂代谢参与 UVC 辐射诱导的甲状腺细胞凋亡(程序性细胞死亡),但目前尚无关于这一现象的数据,而这一现象发生在太空任务期间。本研究的目的是首次分析太空飞行对鞘磷脂代谢酶、鞘磷脂酶和鞘磷脂合成酶的影响,并确定这两种酶之间的比值是否可作为太空任务期间甲状腺活性的可能标志物。在国际空间站上的 Eneide 和 Esperia 任务期间,对静止的甲状腺细胞和被促甲状腺激素(TSH)刺激增殖的甲状腺细胞进行了培养。结果表明,在太空飞行期间,用 TSH 处理的细胞仅生长了 1.5±0.65 倍,因此与静止细胞的行为相似,而在地面上,处于实验条件下(复制飞行条件)的相同细胞生长了 7.71±0.67 倍。比较增殖、静止、促凋亡或凋亡细胞中的鞘磷脂酶/鞘磷脂合成酶比值和 Bax、STAT3 和 RNA 聚合酶 II 的水平表明,在太空飞行期间,甲状腺细胞被诱导进入促凋亡状态。鉴于其特异性和分析所需的细胞数量较少,我们建议使用鞘磷脂酶/鞘磷脂合成酶比值作为太空飞行期间甲状腺细胞功能状态的标志物。进一步的研究可能会导致在长时间的太空飞行中实时使用它。

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