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Volume 37 (1996)
- Issue 4 Pages 235-
- Issue 3 Pages 151-
- Issue 2 Pages 71-
- Issue 1 Pages 1-
Volume 37, Issue 4
Displaying 1-4 of 4 articles from this issue
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NAN MEI, HAJIME IMADA, SATOSHI NOMOTO, NAOKI KUNUGITA, TOSHIYUKI NORIM ...1996 Volume 37 Issue 4 Pages 235-245
Published: December 15, 1996
Released on J-STAGE: March 28, 2006
JOURNAL FREE ACCESSTo investigate individual variation and age dependency in normal cell radiosensitivity, we measured the in vitro radiosensitivity of cultured peripheral blood T-lymphocytes derived from 56 healthy male blood donors. Dose-survival tests using colony formation assay were done with exponential growing T-cells (day 3, PHA-stimulated cells). 6-Thioguanine (6-TG)-resistant mutation assays at the hypoxanthine phosphoribosyl transferase (HPRT) locus were done with G0 phase T-cells (day 0, unstimulated cells). The mean inactivation dose (MID) computed by integration of the fitted survival curves was 1.25 ± 0.23 Gy (mean ± SD). The X-ray dose required to kill 90% of the cells (D10) was 2.81 ± 0.51 Gy. The MID ranged from 0.82 to 1.86 Gy with a coefficient of variation (CV) of 18%. The induced mutation frequencies (MF) per 106 cells at 2 Gy of X-rays ranged from 9.10 to 54.80 with a mean ± SD value of 24.63 ± 12.51 and a CV of 51%. It appears that the radiosensitivity of cell killing and mutagenicity varies among individuals. Although the spontaneous MF at the HPRT locus increases with age, the induced MF after exposure to 2 or 4 Gy of X-rays was not associated with age. Moreover, there were no significant correlations between age and MID values or the other dose-survival parameters. The findings indicate there is significant inter-individual variation in cellular radiosensitivity, but that in human T-lymphocytes aging does not affect the cytotoxic and mutagenic effects of X-irradiation.View full abstractDownload PDF (543K) -
HIROSHI KIMURA, MAKOTO IKEBUCHI, MASATO FUSHIKI, KENSHI KOMATSU1996 Volume 37 Issue 4 Pages 247-255
Published: December 15, 1996
Released on J-STAGE: March 28, 2006
JOURNAL FREE ACCESSThe repair of slowly repairing potentially lethal damage (PLD) in radiosensitive cells from the severe combined immunodeficient (scid) mouse was compared with that in Balb/c 3T3 cells with "wild-type" radiosensitivity and that in RD13B2 cells derived from scid cells whose sensitivity is normal because of the presence of fragments of human chromosome 8. Treatment with 0.23 M NaCl was used for fixation of slowly repairing PLD. The scid cells repaired PLD sensitive to 0.23 M NaCl to a great extent whin 3-4 h, similary to Balb/c 3T3 and RD 13132 cells. This indicates that the scid mutation hardly affects the repair of PLD sensitive to 0.23 M NaCl. On the other hand, as reported previously, the rapidly repairing PLD that is sensitive to 0.5 M NaCl was repaired only slowly (3-4 h) in scid cells, in contrast to the rapid repair (within 1 h) seen with Balb/c 3T3 and RD13B2. This suggests that scid mutation is responsible for this repair at reduced rate. To confirm the independence of repair of 0.23 M NaCl-sensitive PLD from that of 0.5 M NaCl-sensitive PLD, both treatments with 0.23 M NaCl and 0.5 M NaCl were combined in each line. It is found that the repair of either PLD was not affected by the other treatment. The scid mutation impaired only the repair of 0.5 M NaCl-sensitive PLD.View full abstractDownload PDF (395K) -
ATSUKO MATSUOKA, KIYOMI YAMADA, MAKOTO HAYASHI, TOSHIO SOFUNI1996 Volume 37 Issue 4 Pages 257-265
Published: December 15, 1996
Released on J-STAGE: March 28, 2006
JOURNAL FREE ACCESSChromosome painting by fluorescence in situ hybridization (FISH) with a whole chromosome-specific DNA probe was used to detect chromosomal aberrations in lymphocytes from cancer patients given partial-body fractionated X-ray therapy. Six male patients with cancer of the stomach, prostate, lung, or hepatocellular carcinoma, received X-rays in total doses of 40.5 to 70.08 Gy. Lymphocytes were cultured for 50 h with phytohemagglutinin. The mean frequency of aberrant cells detected by chromosome 4 painting varied from 1.57% to 14.34% in the patients and was markedly higher than in healthy controls (mean=0.12%). Chromosome painting effectively detected chromosomal aberrations in lymphocytes from cancer patients.
Equivalent biological doses extrapolated from a dose-response curve obtained in an in vitro human lymphocyte X-ray irradiation study are discussed as an indicator of the cytogenetic damage inducible by radiotherapy in cancer patients.View full abstractDownload PDF (355K) -
YING CHEN, EIKO KUBO, TOSHIHIKO SADO, MASAHIRO MUTO1996 Volume 37 Issue 4 Pages 267-276
Published: December 15, 1996
Released on J-STAGE: March 28, 2006
JOURNAL FREE ACCESSTo investigate the relationship between radiation-induced chromosomal instability and lymphomagenesis, the incidences of chromosome aberrations and of cells with abnormal chromosome complements in the thymuses of B10.Thy 1.1 and STS/A strains which have shown marked differences in susceptibility to radiation-induced lymphomagenesis were compared at an early time (12-33 days) after whole-body X-irradiation (1.61 Gy X 4). Numerical and structural aberrations of chromosome in B10.Thy 1.1 mice were higher than those in STS/A mice. The average incidence of trisomy 15 was 37.5% (12/32 mice) from 12 days to 32 days after irradiation in B10.Thy 1.1 mice, whereas none was found (0/38 mice) in STS/A mice. Frequencies of aberrations in chromosomes 11, 12, 15 of the thymocytes from irradiated B10.Thy 1.1 mice were higher than those from irradiated STS/A mice, and especially, the most frequent translocations occurred in the E-F regions of chromosome 12.
Using B10.Thy 1 congenic mice, we found that in many cases (8/13), the chromosome aberrations detected in the thymocytes from B10.Thy 1.1 mice at an early time after irradiation could also be observed in the donor-type (Thy 1.1) lymphomas developed from recipient mice 4-5 months after intrathymic injection, suggesting that these chromosome aberrations have some role in lymphomagenesis. The difference of chromosome instability detected at an early time after irradiation might be due to genetic background with regard to genomic instability induced by radiation.View full abstractDownload PDF (375K)
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