인체 임파양세포에서 G₂기 염색체의 방사선 감수성

• 영문명: Radiation Induced G2 Chromatid Break and Repair kinetics in Human Lymphoblastoid Cells
• 발행기관: 대한방사선종양학회
• 저자명: 성진실(Jinsil Seong)
• 간행물 정보: 『대한방사선종양학회지』제11권 제2호, 193~203쪽, 전체 11쪽
• 주제분류: 의약학 > 종양학
• 파일형태: PDF
• 발행일자: 1993.12.29

영문 초록

In understanding radiosensitivity a new concept of inherent radiosensitivity based on individuality and heterogeneity within a population has recently been explored. There has been some discussion of possible mechanism underlying differences in radiosensitivity between cells. Ataxia telangiectasia (AT), a rare autosomal recessive genetic disorder, is characterized by hypersensitivity to ionizing radiation and other DNA damaging agents at the cellular level. There have been a lot of efforts to describe the cause of this hypersensitivity to radiation. At the cellular level, chromosome repair kinetics study would be an appropriate approach. The purpose of this study was to better understand radiosensitivity En an approach to investigate kinetics of induction and repair of G_2 chromatic bleaks using normal, AT heterozygous (ATH), and AT homozygous lymphoblastoid cell lines. In an attempt to estimate initial damage, 9-beta-D-arabinosyl-2-fluoroadenine, an inhibitor of DNA synthesis and repair, was used in this study. It was found from this study that radiation induces higher chromatid breaks in AT than in normal and ATH cells. There was no significant differences of initial chromatid breaks between normal and ATH cells. Repair kinetics was the same for all. So the higher level of breaks in AT G_2 cells is thought to be a reflection of the increased initial damage. The amount of initial damage correlated well with survival fraction at 2 Gy of cell survival curve following radiation. Therefore, the difference of radiosensitivity in terms of G_2 chromosomal sensitivity is thought to result from the difference of initial damage.

키워드

Choromosomal radiosensitivity Lymphoblastoid cells 9-beta-D-arabinosyl-2-fluoroadenine