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Biomedical subjects

H Takebe

Publications and source records attributed to H Takebe.

144 records · Page 8Linked to original sources
PubMed1977

DNA repair characteristics and skin cancers of xeroderma pigmentosum patients in Japan.

Fifty xeroderma pigmentosum patients in Japan were examined for clinical characteristics and DNA repair of their cells, Skin cancers developed in 22 patients. Most of the patients without skin cancers were children, except for 5 older patients who had intermediate or nearly normal levels of DNA repair in their cells. All patients younger than 10 years old had no or very low activity of unscheduled DNA synthesis after ultraviolet light irradiation. Three genetic complementation groups, A, D, and E, and variants were found. Many Group A patients and no Group C patients characterized Japanese patients, compared with those in Europe and the United States, where Group C patients were most frequent. The high frequency of patients with low DNA repair capacities in their cells may account for the apparent high frequency of xeroderma pigmentosum patients in Japan. Age distribution of the cancer-bearing patients and their DNA repair characteristics suggest that almost all xeroderma pigmentosum patients will develop skin cancers unless their cells have nearly normal levels of DNA repair.

Adolescent↗
PubMed1975

Excision-repair of 4-nitroquinolin-1-oxide damage responsible for killing, mutation, and cancer.

Excision-repair of DNA base damage produced by 4-nitroquinoline-1-oxide (4NQO) was compared in Escherichia coli, human cells, and mouse cells. Paper chromotography of acid hydrolysates of DNA extracted from cells treated with 3H-labeled 4NQO revealed four peaks; two kinds of 4NQO-guanine adduct, one kind of 4NQO-adenine adduct, and free 4-aminoquinoline-1-oxide (4AQO). About 80% of the initially formed 4NQO-purine adducts were excised from DNA in E. coli uvrA+ cells during 60 min postincubation, but not at all in uvrA- (excisionless for uv damage) cells. Normal human cells excised about 60% of 4NQO-purine adducts during 24 hr postincubation, but xeroderma pigmentosum (excisionless) cells did not. A mouse cell line susceptible to repair of 4NQO-induced pretransformational damage also showed excision-repair ability for the 4NQO adducts. From these and other results, we conclude that the 4NQO-purine adducts and unstable 4NQO-guanine products (which release 4AQO) are, like pyrimidine dimers, repairable by excision-repair universal among E. coli, mouse, and human being, and that unexcised ones are probably the major cause of killing, mutation, and cancer.

4-Nitroquinoline-1-oxide↗
PubMed1969

Action spectrum for growth delay induced in Escherichia coli B-r by far-ultraviolet radiation.

An action spectrum for growth delay induced in Escherichia coli B/r by far-ultraviolet radiation (230 to 295 nm) was obtained. It resembles the action spectrum for killing obtained in the same experiments, indicating that the chromophore for growth delay is probably the same as the chromophore for killing. Another action spectrum for killing, obtained under conditions more suitable for chromophore identification, suggests that nucleic acid, either deoxyribonucleic acid or ribonucleic acid, is the chromophore for growth delay induced by far ultraviolet. Isoprenoid quinones, which seem to be important chromophores for growth delay induced by near-ultraviolet radiation (above 300 nm), appear to play a negligible role in growth delay induced by wavelengths below 300 nm.

DNA, Bacterial↗
PubMedDate not supplied

Comparative studies on photoreactivation of ultraviolet light-induced T4 endonuclease susceptible sites and sister-chromatid exchanges in Potorous cells.

Photoreactivation (PR) of T4 endonuclease-susceptible sites (ESS) and sister-chromatid exchanges induced by ultraviolet light was investigated in Potorous tridactylis Pt K2 cells, using monochromatic light from a grating monochromator. Both ESS and SCE showed maximum PR at 350 nm and the action spectra of PR essentially overlapped between ESS and SCE at 350, 400 and 450 nm. Exposure to 325-nm light after UV irradiation induced additional ESS and SCE, but reduction of ESS was shown by increasing exposure to 325-nm light, and further induction of SCE was observed by the same treatment. A possible difference in mechanisms between induction of ESS and SCE is suggested at 325 nm, while similar causes for ESS and SCE, presumably pyrimidine dimers, are suggested by UV (254-nm) irradiation.

Animals↗
PubMedDate not supplied

Protective effects of sodium selenite on killing and mutation by N-methyl-N'-nitro-N-nitrosoguanidine in E. coli.

Sodium selenite was found to protect Escherichia coli cells against killing and mutagenic effects of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). Such protective effects were not observed when cells were treated with N-methyl-N-nitrosourea (MNU). The protection by sodium selenite was not controlled by the ada gene, which is responsible for the repair of alkylated damage in DNA. A reduction of the amount of glutathione was found when cells were treated with sodium selenite, and glutathione is known to be involved in the methylation of DNA by MNNG, not by MNU. Reduced methylation by MNNG due to the reduction of the amount of glutathione caused by abundant sodium selenite was suggested to be the mechanism of protection.

Escherichia coli↗
PubMedDate not supplied

Difference in O6-methylguanine methyltransferase activity among transformed NIH3T3 cell clones.

We examined the sensitivity to the lethal effects of methylating agents and the O6-methylguanine methyltransferase (MTR) activities of in vitro transformed NIH3T3 cell clones. The sensitivities to the lethal effects of MNNG were not different among all 49 transformed cell clones examined and do not correlate with the MTR activities. All 8 spontaneously transformed cell clones showed the same sensitivities to ACNU as the parental cell line. 2 of 20 transformants induced by UV or MNNG showed higher sensitivities to the ACNU although the MTR activity was normal. One cell clone transformed by UV was sensitive to ACNU and showed about half MTR activity. 5 of 19 cell clones transformed by oncogenes (Ha-ras or SV40 ori-) were sensitive to the lethal effects of ACNU and showed the low MTR activities, but were not as much sensitive as a Ha-MuSV transformed cell clone, Ha821.

Animals↗
PubMedDate not supplied

Excision repair of mouse and human fibroblast cells, and a factor affecting the amount of UV-induced unscheduled DNA synthesis.

Excision-repair ability and the amount of unscheduled DNA synthesis (UDS) after UV irradiation of fibroblast cells (in vitro passage 5) from C57BL mouse embryos were compared with those of human skin fibroblast cells. UDS in the mouse cells was approximately 75% of that in the human cells, although the disappearance of T4 endonuclease-V-susceptible sites and the accumulation of single-strand breaks in the mouse cell DNA indicated that the excision-repair capacity of the mouse cells was 20-35% of that in the human cells. This apparent discrepancy was ascribed to the difference in intracellular dTTP pool size, which was approximately twice as large in the human cells as in the mouse cells. UDS may not be suitable as a quantitative measure of excision repair when comparing the cells from different species.

Animals↗
PubMedDate not supplied

Reduced DNA-repair capacity in cells originating from a progeria patient.

A Chinese boy was identified to be suffering from progeria (Hutchinson-Gilford syndrome), the first case of the disease ever reported in China. Cells originating from the patient had a reduced amount of unscheduled DNA synthesis after irradiation with ultraviolet light (UV). The fractions of the progeria cells surviving against UV irradiation measured by colony-forming ability, and the host-cell reactivation capacity of the progeria cells, measured by the plaque formation of UV-irradiated herpes simplex virus were lower than those measured in normal cells. The progeria cells appear to have a reduced capacity to repair UV excision damage.

Cells, Cultured↗