Grau C, Overgaard J
Department of Experimental Clinical Oncology, Radiumstationen, Aarhus C, Denmark.
Radiat Res. 1990 Jun;122(3):309-15.
The variation in hypoxic fraction as a function of time after various priming doses of radiation has been investigated in a C3H mouse mammary carcinoma in situ. The hypoxic fraction was calculated from data for local tumor control. Untreated tumors were found to contain 4.8% radiobiologically hypoxic cells. Within minutes after a priming dose of 20 Gy given in air, the hypoxic fraction increased to a value not significantly different from 100%. After 4 h, reoxygenation was complete (hypoxic fraction 1.3%), and the hypoxic fraction stabilized at a level significantly below the untreated value. Following a priming dose of 40 Gy the reoxygenation pattern was different: The hypoxic fraction stayed above the pretreatment value for 4 h, and pronounced reoxygenation occurred after 12 h (hypoxic fraction 0.4%). At longer time intervals the hypoxic fraction again increased to--and slightly above--the oxygenation level of untreated tumors. The present findings show that reoxygenation in solid tumors is a function of radiation dose, and the data suggest that mechanisms other than a decrease in tumor cell O2 consumption are involved in tumor reoxygenation.
在C3H小鼠原位乳腺癌模型中，研究了不同预照射剂量后乏氧分数随时间的变化。乏氧分数根据局部肿瘤控制数据计算得出。未治疗的肿瘤中发现含有4.8%放射生物学上的乏氧细胞。在空气中给予20 Gy的预照射剂量后几分钟内，乏氧分数增加到与100%无显著差异的值。4小时后，再氧合完成（乏氧分数1.3%），且乏氧分数稳定在显著低于未治疗值的水平。给予40 Gy的预照射剂量后，再氧合模式不同：乏氧分数在4小时内保持高于预处理值，12小时后出现明显的再氧合（乏氧分数0.4%）。在更长的时间间隔后，乏氧分数再次增加到并略高于未治疗肿瘤的氧合水平。目前的研究结果表明，实体瘤中的再氧合是辐射剂量的函数，数据表明除肿瘤细胞耗氧量减少之外的其他机制参与了肿瘤再氧合。
