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Fibroblast cells from two Japanese patients with Bloom's syndrome (BS) and normal donors were studied for the inactivation of colony-forming ability and the induction of sister-chromatid exchanges (SCEs) after N-ethyl-N-nitrosourea (ENU) treatment. The reduction of ENU-induced SCEs as a function of post-treatment incubation time was also compared between BS and normal fibroblasts. BS cells were approximately 4 times more sensitive than normal cells to the lethal effect of ENU and remarkably hypersensitive to the SCE induction by ENU. The post-treatment incubation of ENU-treated normal cells in the fresh medium resulted in a time-dependent decrease of the SCE level until 6 h after which time the SCE level remained the plateau of about 50% of the initial level. In contrast, the ENU-induced SCEs in BS cells decreased much more slowly with post-treatment incubation time and its half life was 24 h. These results collectively support the view that BS cells may be defective in the rapid repair of certain type(s) of DNA damages induced by ENU. 相似文献
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Sister-chromatid exchanges induced by ultraviolet light in Bloom's syndrome fibroblasts 总被引:1,自引:0,他引:1
The relationships between the cytotoxic effect of ultraviolet light and the UV-induced sister-chromatid exchanges (SCEs) were compared among fibroblast cell strains from two unrelated Bloom's syndrome (BS) patients, one xeroderma pigmentosum (XP) patient belonging to complementation group A and two unrelated normal controls. The "net" induced SCEs as a function of UV fluence, obtained by subtracting spontaneous SCEs from observed SCEs, were much higher in both BS cells and XP group A cells than in normal cells. The relative efficiency of induced SCE, defined as the "net" induced SCEs as a function of surviving fraction after UV irradiation, was higher in BS cells than in normal and XP cells, and there was essentially no difference between XP and normal cells. These results imply that in addition to the extremely high frequency of spontaneous SCEs, the increased efficiency in UV induction of SCEs may reflect the intrinsic defect(s) in BS cells. 相似文献
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Biotransformation of 1-nitropyrene and 2-nitrofluorene to novel metabolites, the corresponding formylamino compounds, in animal bodies 总被引:1,自引:0,他引:1
The present study provides the first evidence that nitropolycyclic aromatic hydrocarbons such as 1-nitropyrene and 2-nitrofluorene are metabolized to the corresponding formylamino compounds in animal bodies. The study shows that the formation of such novel metabolites, 1-formylaminopyrene and 2-formylaminofluorene, is due to N-formylation of the nitroreduction products, 1-aminopyrene and 2-aminofluorene, by liver formamidase in the presence of N-formyl-L-kynurenine. 相似文献
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Harringtonine showed cross resistance in adriamycin-resistant murine leukemia P388 (P388/ADM) and human leukemia K562 (K562/ADM) cells. The relative resistance of the P388/ADM and K562/ADM cells to harringtonine was about 7 and 40, respectively. Calcium influx blockers, diltiazem and the biscoclaurine alkaloid cepharanthine enhanced the cytotoxicity of harringtonine in P388/ADM and K562/ADM cells. The extent of enhancement was different for the two drugs, and up to a 9- to 10-fold increase in harringtonine cytotoxicity occurred in P388/ADM cells, and 14- to 22-fold enhancement in K562/ADM cells with diltiazem or cepharanthine. Harringtonine resistance of P388/ADM was circumvented completely, and the resistance of K562/ADM was circumvented partially, by diltiazem or cepharanthine. The mechanism of enhanced cytotoxicity by diltiazem and cepharanthine is probably inhibition of active efflux of harringtonine in P388/ADM and K562/ADM cells. 相似文献
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Tatsumi Nagahama Mitsuru Takata 《Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology》1990,167(1):1-10
1. | Spikes in Aplysia MA1 neurons produced excitatory (EJPs), inhibitory (IJPs), and diphasic inhibitory-excitatory junction potentials in different fibers of the buccal muscles. |
2. | The IJPs following the MA1 spikes were recorded in the muscle fibers innervated by the jaw-closing motoneurons. The depolarization of muscle fibers produced by the motoneurons was largely suppressed by simultaneous MA1 firing, suggesting that the MA1 neurons make a direct connection to a part of the muscle fibers innervated by these motoneurons and inhibit them. |
3. | The excitatory and inhibitory components of the junction potentials produced by MA1 were reversibly blocked by hexamethonium and d-tubocurarine, respectively. In contrast, the EJPs produced by the jaw-closing motoneurons were blocked by an amino acid antagonist, suggesting that the MA1 neurons and the jaw-closing motoneurons use different transmitters in the nerve-muscle junctions. |
4. | The jaw movement produced by the jaw-closing motoneurons was suppressed by simultaneous MA1 firing, and the suppression was released by d-tubocurarine, suggesting that the IJPs produced by MA1 may contribute to the suppression of jaw movement. The firing of MA1 produced the vertical movement of the buccal muscles, which was blocked by hexamethonium, suggesting that the EJPs produced by MA1 may contribute to the vertical movement. |
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Summary One hundred twelve human DNA sequences were analyzed with respect to dinucleotide frequency and amino acid composition. The variation in guanine and cytosine (G+C) content revealed: (1) at 2–3 and 3-1 doublet positions CG discrimination is attenuated at high G+C, but TA disfavor is enhanced, and (2) several amino acids are subject to G+C change. These findings have been reported in part for collections of sequences from various species. The present study confirms that in a single organism-the human-the G+C effects do exist. Aspects of the argument that connects G+C with protein thermal stability are also discussed. 相似文献
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Instability of Mex- phenotype in human lymphoblastoid cell lines 总被引:1,自引:0,他引:1
Three lymphoblastoid cell lines (LCLs) had extremely low activities of O6-alkylguanine-DNA alkyltransferase (O6-AGT), and were classified as Mex-. They were highly sensitive to cell killing by 1-(4-amino-2-methyl-5-pyrimidinyl)-methyl-3-(2-chloroethyl)-3-nitrosoure a hydrochloride (ACNU), whereas NMO2, a Mex+ LCL with a high O6-AGT activity, was resistant to the agent. Small fractions of these Mex- LCLs survived the treatment with 10 micrograms/ml of ACNU for 24 h, and the surviving cells were found to be resistant to subsequent treatments with the agent. In addition, they contained O6-AGT activities comparable to that of NMO2 and were therefore regarded as Mex+. These results suggest that the Mex- phenotype in LCLs is unstable. 相似文献