Szeinfeld D
Research Institute for Medical Biophysics, South African Medical Research Council, Tygerberg.
Oncology. 1989;46(6):400-4. doi: 10.1159/000226760.
The response of adenosine-5'-triphosphate (ATP) levels in implanted murine CaNT tumours, 2.5 h after 10 Gy X-rays (100 kVp) was measured in vivo using various tumour volumes. It is probable that the concentration of ATP, which increased after X-irradiation, plays a major role in energy supply associated with cellular repair processes. Nevertheless, when ATP levels in irradiated tumours were plotted against tumour volume in the range 150-550 mm3, a monotonically decreasing relation was found. This is interpreted as reflecting the degree of hypoxia and changes in the tumour metabolic status. In addition effects of vascular occlusion and artificial hypoxia have been studied after clamping the tumour for 15 min, followed by a radiation dose of 10 Gy and maintaining the clamp for a further 2.5 h. This showed a drastic decrease in the ATP levels 2.5 h after the irradiation, compared with controls in normoxia. It is thought this is due to induction of hypoxia which is produced throughout the tumour volume, resulting in the depletion of cellular ATP. This implies that the clamped tumour cells are less capable of generating a metabolic response following radiation damage.
利用不同的肿瘤体积,在体内测量了10 Gy X射线(100 kVp)照射2.5小时后植入的小鼠CaNT肿瘤中三磷酸腺苷(ATP)水平的反应。X射线照射后增加的ATP浓度可能在与细胞修复过程相关的能量供应中起主要作用。然而,当将照射后肿瘤中的ATP水平与150 - 550 mm³范围内的肿瘤体积作图时,发现了单调递减关系。这被解释为反映了缺氧程度和肿瘤代谢状态的变化。此外,在夹住肿瘤15分钟后,给予10 Gy的辐射剂量,并再保持夹住状态2.5小时,研究了血管闭塞和人工缺氧的影响。与常氧对照组相比,这显示出照射后2.5小时ATP水平急剧下降。据认为,这是由于在整个肿瘤体积中产生的缺氧诱导,导致细胞ATP耗竭。这意味着被夹住的肿瘤细胞在辐射损伤后产生代谢反应的能力较弱。