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Volume 27 (1986)
- Issue 4 Pages 325-
- Issue 3 Pages 255-
- Issue 2 Pages 141-
- Issue 1 Pages 99-
Volume 27, Issue 4
Displaying 1-6 of 6 articles from this issue
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JUMPEI AMAGASA1986 Volume 27 Issue 4 Pages 325-338
Published: December 15, 1986
Released on J-STAGE: June 16, 2006
JOURNAL FREE ACCESSThe photodynamic inactivation of amino acid (phenylalanine) accepting ability of transfer RNA (tRNA) sensitized with acridine orange (AO) was investigated placing a special emphasis on the dye binding to nucleic acid. The dye binding to tRNA was found to be a prerequisite for the photodynamic inactivation of tRNA. The photodynamic efficiencies of AO were compared between two types of tRNA-AO complexes. Based on the calculated quantum yields for the inactivation, the intercalated (monomer) dye was about four times more efficient than the bound dye aggregate. Increasing the number of bound dyes in intercalated form from one to five showed only small variations of the quantum yields, implying that the binding sites in the tRNA is not important insofar as they receives AO in the intercalated form.View full abstractDownload PDF (484K) -
JUMPEI AMAGASA1986 Volume 27 Issue 4 Pages 339-351
Published: December 15, 1986
Released on J-STAGE: June 16, 2006
JOURNAL FREE ACCESSThe photodynamic inactivation of acridine orange (AO)-sensitized tRNA was investigated with respect to the type of photochemical pathways and the base damage leading to the inactivation. The diagnostic tests for singlet oxygen (1O2), namely the enhancement effect of deuterium oxide (D2O) and the inhibition effect by sodium azide, indicated that 1O2 was involved as the reactive intermediate in the photoinactivation (the Type II mechanism). Furthermore, the D2O effect was more pronounced at high ionic strength and under low dye to RNA ratio conditions, indicating that monomerically bound AO acts exclusively through the Type II mechanism. With respect to base damage, the present studies show that guanine is destroyed and tRNA-AO occurs as a photoadduct. The formation of photoadduct was enhanced under N2, and little affected by D2O, excluding the possibility that the photoadduct is responsible for the photoinactivation. Conversely, effects of D2O and azide on the photoinactivation, in conjunction with the predominance of the Type II mechanism in the known cases of guanine destruction by AO-photosensitization, indicate that the destruction of guanine by 1O2 is the most probable critical damage in the photodynamic inactivation of tRNA.View full abstractDownload PDF (550K) -
NOBUO KUBOTA, KENGO MATSUI, TOSHIHIKO TANAKA1986 Volume 27 Issue 4 Pages 352-361
Published: December 15, 1986
Released on J-STAGE: June 16, 2006
JOURNAL FREE ACCESSThe development and decay of thermotolerance were studied in spheroids of HMV-I human malignant melanoma cells and exponentially growing monolayer cells. Thermotolerance was induced by an initial heat treatment at 44° for 15 min. At varying times after preheating, spheroids and monolayer cells were subjected to graded doses of second heating at 44°, and cell survival was assayed by colony formation.
The thermosensitivity of monolayer cells rapidly decreased after preheating, reaching a maximum decrease at 3 and 6 hr. However, more marked thermotolerance developed in spheroids at 1 and 6 hrs compared to that of monolayer cells. Thereafter, the thermotolerance decayed gradually in an exponential manner for a few days. It appears that the kinetics of tolerance decay was almost the same in the spheroids and monolayer cells, in contrast to the difference in development of thermotolerance in the two.View full abstractDownload PDF (365K) -
EI-ICHI TAKAHASHI, KOKI SATO, IZUO TOBARI1986 Volume 27 Issue 4 Pages 362-370
Published: December 15, 1986
Released on J-STAGE: June 16, 2006
JOURNAL FREE ACCESSAn X-ray-sensitive mutant LX830, isolated from mouse lymphoma L5178Y cells, was examined for chromosomal aberrations induced by γ-rays and 4-nitroquionoline-l-oxide (4NQO), as compared with a methyl methanesulphonate (MMS) and X-ray-sensitive mutant M10 and their parental L5178Y cells. Spontaneous incidence of chromosomal aberrations in LX830 cells was 2.5 times higher than that in L5178Y cells, but lower than that in M10 cells. In the first mitosis of LX830 cells after 1.0 Gy γ-irradiation, the frequencies of chromosome- and chromatid-type aberrations were significantly higher than those in L5178Y cells. In addition, chromatid exchanges, particularly triradials, isochromatid breaks, and chromatid gaps and breaks were markedly enhanced at G1 phase of LX830 cells. These results are very similar to those in M10 cells. After 4NQO treatment (50 ng/ml), chromatid-type aberrations were induced more frequently at late fixation times. The maximal frequency of chromatid-type aberrations in LX830 cells was about 1.7 times higher than that in L5178Y cells, but LX830 cells were less susceptible to 4NQO than M10 cells. These results indicate that there exist some heterogeneity in the response to 4NQO among ionizing radiation-sensitive mouse cell mutants.View full abstractDownload PDF (383K) -
IWAO TSUKIYAMA, SUNAO EGAWA, AKIYOSHI KUMAZAWA, YUU IINO1986 Volume 27 Issue 4 Pages 371-377
Published: December 15, 1986
Released on J-STAGE: June 16, 2006
JOURNAL FREE ACCESSEffects of neutrons and x-rays on mouse skin which had been previously irradiated with x-rays were investigated.
Two tattoo marks were placed in the hairless legs of mice at intervals of 15 mm. The legs were exposed to various doses of x-ray and neutrons to determine the relative biological effectiveness (RBE) using the contraction of the skin as an index. The RBE was 0.93 - 1.73. The legs of the mice were preexposed to 25 Gy of x-ray, and exposed 4 months later. The contraction of the skin began earlier than after the first irradiation. RBE was 2.18 - 2.47. This RBE was higher than that in untreated mice. These results suggest that previously irradiated normal tissues are much more sensitive to neutrons than to x-rays.View full abstractDownload PDF (200K) -
KOKI SATO, AKEMI ITO, NAOKO HIEDA-SHIOMI, TADAHIRO SHIOMI, HIROKO HAMA ...1986 Volume 27 Issue 4 Pages 378-385
Published: December 15, 1986
Released on J-STAGE: June 16, 2006
JOURNAL FREE ACCESSTwo independently isolated radiation-sensitive mutants, M10 and LX830, of mouse L5178Y cells were compared for their sensitivity to various DNA-damaging agents. These two mutants share hypersensitivity to gamma rays, bleomycin, arabinofuranosyl cytosine (Ara-C) and aphidicolin. But they differ in that M10 is more sensitive to killing by methyl methanesulfonate (MMS) than LX830 or L5178Y, whereas LX830 is more sensitive to inactivation by hydroxyurea and 3-aminobenzamide than M10 or L5178Y. The response to mitomycin C (MMC) and 4-nitroquinoline-l-oxide (4NQO) is the most pronounced in M10, the least in L5178Y and intermediate in LX830. The complementation tests between M10 and LX830 showed that the X-ray survival curves of M10-LX830 hybrid cells were similar to those of M10 or LX830. An MMS-resistant clone was found among MMS-sensitive M10 cells and proved to be just as sensitive to killing by X-rays as the original M10 cells. These results indicate that M10 and LX830 have a common defect in the repair of damage caused by X rays, bleomycin, Ara-C and aphidicolin but a different defect in the repair of MMS-, MMC-, 4NQO-, hydroxyurea and 3-aminobenzamide-damage.View full abstractDownload PDF (223K)
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