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Increased constitutional chromosome sensitivity to bleomycin in patients with hereditary non-polyposis colorectal cancer [HNPCC]

100%
Kladny J., Zajaczek S., Lubinski J.
Journal of Applied Genetics
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1996
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tom 37
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nr 4
It has been suggested that mutagen sensitivity is a constitutional factor which may be useful in identification of patients with an increased risk for the development of tumors. In this study, the chromosome sensitivity to bleomycin was measured according to Hsu in patients with hereditary non-polyposis colorectal cancer (HNPCC), sporadic colorectal cancer and in control persons with no tumor history in family. In vitro lymphocytes were exposed to bleomycin according to Hsu and chromosomal damage was quantified by scoring breaks of 100 cells. A significant difference (P < 0.01) in the mean number of breaks per cell (b/c) was found between HNPCC patients (0.59 ± 0.14; n = 12; mean age 55.4 yrs) and control individuals (0.35 ± 0.13: n = 12; mean age 55.8 yrs). In contrast, patients with sporadic colorectal cancer showed a mean b/c value of 0.43 ± 0.14 (n = 14; mean age 63.4 yrs) which was not significantly higher than that in control individuals for this group (0.42 ± 0.15; n = 14; mean age 63.1 yrs). Selenium protected lymphocytes of HNPCC patients against bleomycin activity in vitro.
2

Studies on the nature of genotoxic and cytotoxic effects induced by hydralazine

84%
Marczewska J., Koziorowska J. H.
Acta Biochimica Polonica
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1997
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tom 44
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nr 2
The nature of genotoxic and cytotoxic effects induced by hydralazine was analyzed taking into account possible protection of cells by catalase, superoxide dismutase and dimethyl sulfoxide. For the experiments designed to evaluate the influence of scavengers on the genotoxicity expressed as the SOS induction factor the E. coli PQ37 strain was used. The cytotoxic effects were investigated in V3 cells cultured in vitro. The genotoxicity and cytotoxicity of hydralazine were suppressed by catalase in a dose-dependent manner but they were enhanced by superoxide dismutase. No protective effect of dimethyl sulfoxide was observed. Our results indicate that H2O2 plays an essential role in the genotoxicity and cytotoxicity of hydralazine.
3

Protective action of vitamin C against DNA damage induced by selenium-cisplatin conjugate

84%
Blasiak J., Kowalik J.
Acta Biochimica Polonica
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2001
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tom 48
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nr 1
Genotoxicity of anticancer drugs is of a special interest due to the risk of inducing sec­ondary malignancies. Vitamin C (ascorbic acid) is a recognized antioxidant and, since hu­man diet can be easily supplemented with vitamin C, it seems reasonable to check whether it can protect against DNA-damaging effects of antitumor drugs. In the present work the ability of vitamin C to modulate cytotoxic and genotoxic effects of a cisplatin analog, con­jugate (NH3)2Pt(SeO3), in terms of cell viability, DNA damage and repair in human lym­phocytes was examined using the trypan blue exclusion test and the alkaline comet assay, respectively. The conjugate evoked a concentration-dependent decrease in the cell viabil­ity, reaching nearly 50% at 250 uM. (NH3)2Pt(SeO3) at 1, 10 and 30 uM caused DNA strand breaks, measured as the increase in the comet tail moment of the lymphocytes. The treated cells were able to recover within a 30-min incubation in a drug-free medium at 37°C. Vitamin C at 10 and 50 uM diminished the extent of DNA damage evoked by (NH3)2Pt(SeO3) but had no effect on the kinetics of DNA repair. The vitamin did not di­rectly inactivate the conjugate. Lymphocytes treated with endonuclease III, which recog­nises oxidised pyrimidines, displayed a greater tail moment than those untreated with the enzyme, suggesting that the damages induced by the drug have, at least in part, an oxida- tive origin. Vitamin C can be considered a potential protective agent against side effects of antitumor drugs, but further research with both normal and cancer cells are needed to clarify this point.
4
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Level of DNA damage in lead-exposed workers

67%
Olewinska E., Kasperczyk A., Kapka L., Kozlowska A., Pawlas N., Dobrakowski M., Birkner E., Kasperczyk S.
Annals of Agricultural and Environmental Medicine
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2010
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tom 17
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nr 2
231-236
5

Antimutagenic activity of new analogues of fluphenazine

67%
Gasiorowski K., Malinka W., Swiatek P., Jaszczyszyn A.
Cellular and Molecular Biology Letters
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2003
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tom 08
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nr 4
Fluphenazine (FPh) exhibited antimutagenic activity in lymphocyte cultures, markedly decreasing genotoxic effects of standard mutagenic agents present in cell cultures. However, the strong pharmacological activity of this neuroleptic drug, together with its serious side effects on the central nervous system, limits its use as an antimutagenic compound. In this paper we describe a route of chemical synthesis of FPh analogues that are more hydrophilic than the model compound, thus probably penetrate more weakly through the blood-brain barrier. These new analogues were tested for their antimutagenic and pro-apoptotic activities in human lymphocyte cultures, genotoxically damaged in vitro with benzo[a]pyrene [40 μM, 30 min] and subsequently cultured for 48 h in the presence of the tested compounds. The fluphenazine analogues enhanced apoptosis in genotoxically damaged lymphocytes more strongly than the model compound did. The increase of apoptotic cell frequency was the highest with compound 4a [2-(trifluoromethyl)-10-[3-(diethanolamino)-2-hydroxypropyl] phenothiazine] - a 35% higher effect than that of fluphenazine. The cytotoxicity of derivative 4a was the lowest among the tested compounds; it was 60% lower than that of fluphenazine. The antimutagenic effect of 4a was about 10% stronger than that of fluphenazine. Compund 4a also had the highest hydrophilicity of the new FPh analogues. Compound 4a was chosen for further study as a potentially usable antimutagen that would only weakly penetrate the central nervous system.
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