CELL KILLING INDUCED BY DECAY OF I-125 DURING THE CELL-CYCLE - COMPARISON OF I-125 ANTIPYRINE WITH I-125 BOVINE SERUM-ALBUMIN
被引:12
|
作者:
MIYAZAKI, N
论文数: 0引用数: 0
h-index: 0
机构:
TOKYO METROPOLITAN INST MED SCI, DEPT RADIAT RES, BUNKYO KU, TOKYO 113, JAPANTOKYO METROPOLITAN INST MED SCI, DEPT RADIAT RES, BUNKYO KU, TOKYO 113, JAPAN
MIYAZAKI, N
[1
]
SHINOHARA, K
论文数: 0引用数: 0
h-index: 0
机构:
TOKYO METROPOLITAN INST MED SCI, DEPT RADIAT RES, BUNKYO KU, TOKYO 113, JAPANTOKYO METROPOLITAN INST MED SCI, DEPT RADIAT RES, BUNKYO KU, TOKYO 113, JAPAN
SHINOHARA, K
[1
]
机构:
[1] TOKYO METROPOLITAN INST MED SCI, DEPT RADIAT RES, BUNKYO KU, TOKYO 113, JAPAN
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°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.