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通过超高剂量率电子辐射在体内的氧气消耗取决于基线组织氧化

Jacob P Sunnerberg¹, Armin D Tavakkoli², Arthur F Petusseau¹

¹Thayer School of Engineering, Dartmouth College, Hanover, New Hampshire.

International journal of radiation oncology, biology, physics

|October 26, 2024

概括

超高剂量速率 (UHDR) 辐射显著影响组织氧气消耗,影响因氧气水平而异. 控制组织氧气对于临床前和临床FLASH放射治疗至关重要.

科学领域:

辐射瘤学辐射瘤学
生物物理学的生物物理.
临床前研究临床前研究

背景情况:

超高剂量速率 (UHDR) 辐射,包括FLASH放射治疗,显示出有希望的结果,但其生物效应尚未完全理解.
已知组织氧气水平 (pO2) 影响辐射反应,但它们在超高强度辐射中的特定作用需要进一步研究.

研究的目的:

评估组织氧气水平如何影响小鼠在UHDR电子辐射期间的氧气消耗.
为了确定在UHDR范围内的剂量速率变化是否会改变这种依赖氧的反应.

主要方法:

使用光火的实时氧度测量和Oxyphor PdG4被用来测量皮肤pO2在UHDR辐射期间.
通过调整吸入氧气和/或血管压缩来调节组织pO2.
用Mobetron线性加速器在UHDR范围 (25-1170 Gy/s) 中改变剂量速率.

主要成果:

在UHDR条件下,氧气消耗g值 (gO2) 显著增加,基线pO2在UHDR条件下高达20mmHg,停滞在0.26mmHg/Gy.
剂量速率和脉冲参数的变化没有显著改变gO2.
传统的剂量速率辐射显示pO2.0没有显著变化.

结论:

超高强度辐射在缺氧与氧气充足的组织中表现出明显的辐射化学效应.
观察到的趋势表明,pO2-依赖的gO2背后存在着保存的化学机制,这可能解释了FLASH效应.
基线pO2在动物间的显著变异性突显了在UHDR和FLASH研究和应用中需要精确的氧气监测的需要.

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