Endothelial cell damage after gamma-irradiation in vitro: impaired uptake of alpha-aminoisobutyric acid.
Endothelial cell damage after gamma-irradiation in vitro: impaired uptake of alpha-aminoisobutyric acid.
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体外伽玛射线照射后内皮细胞损伤：α-氨基异丁酸的摄取受损。
DOI：
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发表时间：
1982
期刊：
影响因子：
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通讯作者：
B. Fanburg
中科院分区：
文献类型：
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作者：
L. Kwock;W. Douglas;P. Lin;W. Baur;B. Fanburg
用铯-137源对从牛肺动脉中分离的内皮细胞进行γ-照射，并保持在培养物中。表征这些细胞的剂量-反应存活曲线的放射生物学参数（表示为平均值+/- SD）为n = 1.6 +/- 0.2，Dq = 71 +/- 13 rads，Do = 161 +/- 35 rads，表明这些细胞积累或修复辐射损伤的能力相对较低。增加辐射剂量导致内皮细胞对[14 C]2-氨基异丁酸（AIB）（一种Na+依赖性和非代谢性氨基酸）的摄取减少。500拉德的剂量对细胞存活造成显着抑制，导致照射后6小时AIB吸收减少45%，24小时吸收减少69%。光镜下观察24 h后细胞形态未见异常。另一方面，牛肺动脉成纤维细胞在暴露于高达5，000拉德的辐射剂量后24小时对AIB的摄取没有显着损害。内皮细胞对[14 C]1-氨基环戊烷-1-羧酸（一种通过Na+非依赖性过程转运的氨基酸）的摄取不受5，000拉德辐射的影响。我们的研究表明，内皮细胞对辐射敏感，受损的Na+依赖性摄取AIB代表了辐射损伤内皮细胞的早期事件。
The effects of gamma-irradiation with a cesium-137 source were assessed on endothelial cells isolated from bovine pulmonary arteries and maintained in culture. The radiobiologic parameters that characterize the dose-response survival curve for these cells, expressed as mean +/- SD were found to be n = 1.6 +/- 0.2, Dq = 71 +/- 13 rads, and Do = 161 +/- 35 rads, indicating a relatively low capacity of these cells to accumulate or repair radiation damage. Increasing doses of radiation led to decreasing uptake by endothelial cells of [14C]2-aminoisobutyric acid (AIB), a Na+-dependent and nonmetabolizable amino acid. A dose of 500 rads, which caused marked inhibition of cell survival, resulted in a 45% decrease in AIB uptake at 6 h and a 69% decrease in uptake at 24 h after irradiation. No morphologic abnormality was noted in these cells by light microscopy at 24 h after this dose of radiation. Bovine pulmonary artery fibroblasts, on the other hand, showed no significant impairment in uptake of AIB 24 h after exposure to doses of radiation as high as 5,000 rads. The uptake by endothelial cells of [14C]1-aminocyclopentane-1-carboxylic acid, an amino acid transported by a Na+-independent process, was not influenced by 5,000 rads of radiation. Our studies show that endothelial cells are sensitive to radiation and that impaired Na+-dependent uptake of AIB represents an early event in radiation damage to the endothelial cell.