Miyazaki N, Shinohara K
Department of Radioisotope, Tokyo Institute of Psychiatry, Japan.
Radiat Res. 1993 Feb;133(2):182-6.
The lethal effects induced by the decay of 125I in synchronized L5178Y cells were studied by suicide experiments. We used 125I-antipyrine, which is freely diffusible in cells, and 125I-bovine serum albumin (BSA), which remains outside the cells. Synchronized cells mixed with either 125I-antipyrine or 125I-BSA were frozen and stored at -196 degrees C for various periods to accumulate 125I decays. A clonogenic assay was used to measure the killing of these stored cells. Cells in G1-S and G2-M phases were more sensitive than those in late S phase for both 125I treatments. The ratio of survival in late S to that in G1-S (late S/G1-S) obtained by the decay of 125I-antipyrine, however, was much smaller than that obtained by the decay of 125I-BSA in the dose range examined. These results suggest that Auger electrons emitted from 125I-antipyrine cause a high-LET-type effect. The reason for the high-LET effect must be the intracellular localization of 125I-antipyrine and its closer contact with DNA.
通过自杀实验研究了同步化的L5178Y细胞中125I衰变诱导的致死效应。我们使用了可在细胞中自由扩散的125I - 安替比林，以及保留在细胞外的125I - 牛血清白蛋白（BSA）。将与125I - 安替比林或125I - BSA混合的同步化细胞冷冻并在-196℃下储存不同时间以积累125I衰变。采用克隆形成试验来测定这些储存细胞的杀伤情况。对于两种125I处理，处于G1 - S期和G2 - M期的细胞比处于S期后期的细胞更敏感。然而，在检测的剂量范围内，由125I - 安替比林衰变获得的S期后期与G1 - S期的存活比（后期S/G1 - S）远小于由125I - BSA衰变获得的存活比。这些结果表明，125I - 安替比林发射的俄歇电子会引起高传能线密度（LET）型效应。产生高LET效应的原因必定是125I - 安替比林的细胞内定位及其与DNA更紧密的接触。
