title: Adaptive response to ionizing radiation induced by low doses of gamma rays in human cell lines.
abstract: OBJECTIVE
  The aim of this study was to investigate whether the adaptive response could be induced in human lymphoblastoid cell lines and human tumor cell lines. The time necessary for the expression of the adaptive response was also investigated.
  
  
  METHODS
  Three lymphoblastoid cell lines from ataxia telangiectasia (AT) homozygote (GM 1526), AT heterozygote (GM 3382), and normal individual (3402p) and two hepatoma cell lines, Hep G2 and Hep 3B, were used in this study. Experiments were carried out by delivering 0.01 Gy followed by 0.5 Gy of gamma radiation to the exponentially growing cells. The time necessary for the expression of the adaptive response was determined by varying the time interval between the two doses from 1 to 72 h. In some experiments, 3-aminobenzamide, a potent inhibitor of poly (ADP-ribose) polymerase, was added immediately after the 0.5 Gy exposure. The cultures were fixed 30 min (for the G2 chromatid) and 6 h (for the S chromatid) after the 0.5 Gy exposure. Metaphase chromosome assay was carried out to score chromatid breaks as an end point.
  
  
  RESULTS
  A prior exposure to 0.01 Gy of gamma rays significantly reduced the number of chromatid breaks induced by subsequent higher doses (0.5 Gy) in all the tested cell lines. The magnitude of the adaptive response was similar among the cell lines despite their different radiosensitivities. In the G2 chromatids, the adaptive response was observed both at short-time intervals, as early as 1 h, and at long-time intervals. In the S chromatids, however, the adaptive response was shown only at long-time intervals. When 3-aminobenzamide was added after the 0.5 Gy, the adaptive responses were abolished in all the experimental groups.
  
  
  CONCLUSIONS
  The adaptive response was observed in human lymphoblastoid cell lines and hepatoma cell lines. The magnitude of the adaptive response did not seem to be related to the radiosensitivity of the cells. The elimination of the adaptive response with 3-aminobenzamide is consistent with the proposal that this adaptive response is the result of the induction of a certain chromosomal repair mechanisms.
authors.affiliation: Department of Radiation Oncology, Yonsei University College of Medicine, Yonsei Cancer Center, Seoul, Korea.
authors.forename: J
authors.initials: J
authors.lastname: Seong
authors.forename: C O
authors.initials: CO
authors.lastname: Suh
authors.forename: G E
authors.initials: GE
authors.lastname: Kim
mesh_terms: D000222:Adaptation, Physiological / Q000187:drug effects; D001260:Ataxia Telangiectasia; D001549:Benzamides / Q000494:pharmacology; D006528:Carcinoma, Hepatocellular; D002461:Cell Line, Transformed; D002842:Chromatids / Q000528:radiation effects*; D004249:DNA Damage; D004260:DNA Repair; D016195:G2 Phase; D006801:Humans; D011829:Radiation Dosage; D011836:Radiation Tolerance / Q000187:drug effects / Q000502:physiology*; D011838:Radiation-Sensitizing Agents / Q000494:pharmacology; D013997:Time Factors
chemical_list: D001549:Benzamides; D011838:Radiation-Sensitizing Agents; C025160:3-aminobenzamide