Lambin P, Scalliet P, Coster B, M'Vondo J C, Vynckier S, Gueulette J, Wambersie A
Unité de Radiobiologie, Université Catholique de Louvain, Bruxelles, Belgium.
Radiother Oncol. 1993 Jan;26(1):73-5. doi: 10.1016/0167-8140(93)90029-8.
The hypothesis that cisplatinum (c-DDP) interacts with radiation by inhibiting the cellular repair capacities, was tested by comparing the interaction of c-DDP with low-LET (60Co gamma-rays) and high-LET radiation (d(50) + Be neutrons) in mice. The biological endpoint was lethality, 6 days after total body irradiation (early intestinal tolerance). The dose modifying factor was 1.80 +/- 0.25 for c-DDP plus 60Co gamma-rays, and 1.97 +/- 0.3 for c-DDP plus neutrons. As less repairable damage is induced by fast neutrons than by photons, this suggests that, in this system, the interaction between radiation and c-DDP is not explained by repair inhibition but is purely additive.
通过比较顺铂(c-DDP)与低线性能量传递(60Coγ射线)和高线性能量传递辐射(d(50)+铍中子)在小鼠体内的相互作用,对顺铂通过抑制细胞修复能力与辐射相互作用的假说进行了检验。生物学终点是全身照射6天后的致死率(早期肠道耐受性)。顺铂加60Coγ射线的剂量修正因子为1.80±0.25,顺铂加中子的剂量修正因子为1.97±0.3。由于快中子诱导的可修复损伤比光子少,这表明,在该系统中,辐射与顺铂之间的相互作用不能用修复抑制来解释,而是纯粹的相加作用。