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  • 1
    Publication Date: 1966-02-01
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Springer Nature
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Molecular genetics and genomics 87 (1956), S. 735-742 
    ISSN: 1617-4623
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary Drosophila males were exposed to a sublethal concentration of cyanide gas prior to the injection of formaldehyde solutions. Compared to the controls which only received formaldehyde the frequency of sex-linked lethals was increased after the cyanide pretreatment in altogether six independent experiments. These results are taken as further proof that formaldehyde exerts at least part of its mutagenic effects via the formation of peroxides. It is suggested that an excessive amount of hydrogen peroxide, due to inhibition of the cytochrome and catalase enzyme systems, favours the formation of a mutagenic, organic peroxide, presumably dihydroxydimethyl peroxide. The fact that formaldehyde exerts an inhibiting effect on catalase in its own right might be of importance for the interpretation of its mutagenic action. It was also observed that after cyanide pretreatment, the mutagenic effectiveness of a mixture of formaldehyde and hydrogen peroxide was lower than that of formaldehyde alone. These findings can be interpreted by assuming that high concentrations of dihydroxydimethyl peroxide or of a combination of cyanide and this peroxide, eliminate selectively germ cells with induced mutations. It is possible that the same explanation applies to the low mutagenic effectiveness of a mixture of formaldehyde and hydrogen peroxide compared with that of formaldehyde alone when both are preceded by cyanide.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature 209 (1966), S. 818-819 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] In their report on tumour chromosomes, Makino et al.1 included tables giving the chromosome complements of single tumours. The chromosome complements of three female gastric carcinomata of the effusion type were recorded in this way. Calculations on the heterogeneity of the complements of each ...
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Somatic cell and molecular genetics 16 (1990), S. 575-581 
    ISSN: 1572-9931
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract It has been shown by genetic complementation analysis that a mitomycin C-sensitive mutant (V-H4) of Chinese hamster V79 cells is the first rodent equivalent of Fanconi anemia (FA) group A. The V-H4 mutant shows many typical characteristics of cells derived from FA patients. V-H4 cells exhibit increased sensitivity towards cross-linking agents as MMC (∼30-fold), cis-DDP (∼10-fold), DEB (∼10-fold), and PUVA (∼1.6-fold), but an only slightly increased sensitivity to monofunctional alkylating agents (EMS and MMS) and actinomycin D. V-H4 cells are also moderately sensitive to adriamycin (1.6-fold), and not sensitive to H2O2. The levels of chromosomal aberrations induced by MMC and cis-DDP treatment are higher (4- to 6-fold) in V-H4 cells than in the wild-type V79 cells. Genetic complementation analysis with other Chinese hamster mutants hypersensitive to MMC (irs1, irs1SF, UV20 and UV41) indicates clearly that V-H4 belongs to a different, new complementation group. This unique mutant is very stable and can serve as a vehicle to isolate the complementing FA-A gene from normal human DNA.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Somatic cell and molecular genetics 8 (1982), S. 307-317 
    ISSN: 1572-9931
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract When mammalian cells are cultured at low concentrations of toxic drugs, they often become phenotypically resistant. We studied whether this phenotypic resistance is due to selection of preexisting variants. The drugs 8-azaguaine (AG) and 6-thioguanine (TG) were used and, as a parameter for resistance, the incorporation of hypoxanthine was determined. Preexisting variation among clones in the uptake of hypoxanthine was found, and this variation has a hereditary component. This transmission of aberrant incorporation of hypoxanthine does not appear a stable trait, and the aberrant cell lines returned gradually to the original steady state. There are indications that within a cell population cells with altered levels of incorporation of hypoxanthine arise continuously and at a high frequency. Treatment with marginally toxic concentrations of AG or TG indicates that, at least for AG, survival is not related to the preexisting variation in hypoxanthine uptake. The observed phenomena could be of importance for the selection of drugs to be used in cancer chemotherapy.
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Somatic cell and molecular genetics 11 (1985), S. 127-134 
    ISSN: 1572-9931
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Clonal variation has been studied in CHO cells. The variant phenotype was an altered morphology of clones in agar: the parental CHO cells give rise to solid clumps of cells (wild-type colonies); occasionally, dispersed colonies arise, and the cells display an invasive growth in agar (INGA-type colonies). The frequency of this altered phenotype can be enhanced by treatment with a variety of mutagens (EMS, ENU, 4NQO, N-Ac-AAF, ultraviolet light, and X-irradiation). Enhancement was not due to a selective killing of wild-type cells or to a side-effect of cytotoxicity, which suggests that DNA damage is the cause of the altered phenotype. The INGA-trait breeds true, but most of the isolated clones have an inherent instability.
    Type of Medium: Electronic Resource
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