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  • 1990-1994  (3)
Source
Material
Years
Year
  • 1
    Electronic Resource
    Electronic Resource
    Degradation of Crystal violet by Nocardia corallina (1993)
    Springer
    Applied microbiology and biotechnology 38 (1993), S. 565-569 
    Details
    ISSN: 1432-0614
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Process Engineering, Biotechnology, Nutrition Technology
    Notes: Abstract Crystal Violet (BV3), a typical triphenylmethane dye, was degraded by growing cells of Nocardia corallina IAM 12121, although their growth was inhibited at the initial stage of incubation. The dye was degraded at a low concentration, below 5 μmol dm−3. The growth of the cells was completely inhibited at a dye concentration of 7 μmol dm−3. A degradation product of BV3 was identified as 4,4′-bis(dimethylamino) benzophenone (Michler's ketone; MK) by gas chromatography-mass spectrometry. The product was obtained in a reasonable yield since it was not further metabolized by N. corallina IAM 12121.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00242956
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Combined oral administration of etoposide and arabinofuranosylcytosine-5′-stearylphosphate enhances the antitumor effect against P388 ascites tumors (1994)
    Springer
    Cancer chemotherapy and pharmacology 33 (1994), S. 281-285 
    Details
    ISSN: 1432-0843
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. We investigated the antitumor effect of oral administration of etoposide and arabinofuranosylcytosine-5′-stearylphosphate (C18PCA) against P388 ascites tumors in B6D2F1 mice. Etoposide (25 mg/kg) and C18PCA (5 mg/kg) were given orally on days 1–5 after tumor inoculation. The median life span of the mice treated with etoposide or C18PCA alone was 19.5 and 18 days, respectively. The combination of both drugs significantly extended the median life span to 33 days. To clarify this enhancement of the increase in median life span, we examined intracellular deoxyribonucleoside triphosphate (dNTP) pools, cell-cycle distribution, DNA fragmentation, and the time course of the plasma drug concentration. Etoposide had no effect on intracellular dNTP pools in this experimental system, whereas treatment of cells with C18PCA or with the combination of both drugs resulted in a significant increase in dTTP pools to values ranging from 1.8- to 2.0-fold higher than the control levels. There was a significant increase in cells in the S+G2/M phase when cells had been treated with both etoposide and C18PCA. Agarose-gel electrophoresis of the extracted DNA revealed that C18PCA enhanced the fragmentation of DNA, with a length of about 180 bp being induced by etoposide. The plasma peak levels of etoposide (1000 nM) and ara-C (50 nM) were observed at 20 and 30 min after the simultaneous administration of both drugs, respectively. The plasma etoposide level gradually decreased to 10% of the peak level at 240 min after administration. On the other hand, the plasma concentration of ara-C was maintained at above 20 nM at 240 min. These observations suggest that C18PCA and etoposide act on P388 murine leukemic cells by accumulating cells in the S+G2/M phase. Even if the plasma concentration of ara-C is low, the repair of DNA damage by etoposide may be hindered in the presence of ara-C following an increase in DNA fragmentation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00685900
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Combined oral administration of etoposide and arabinofuranosylcytosine-5′-stearylphosphate enhances the antitumor effect against P388 ascites tumors (1994)
    Springer
    Cancer chemotherapy and pharmacology 33 (1994), S. 281-285 
    Details
    ISSN: 1432-0843
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We investigated the antitumor effect of oral administration of etoposide and arabinofuranosylcytosine-5′-stearylphosphate (C18PCA) against P388 ascites tumors in B6D2F1 mice. Etoposide (25 mg/kg) and C18PCA (5 mg/kg) were given orally on days 1–5 after tumor inoculation. The median life span of the mice treated with etoposide or C18PCA alone was 19.5 and 18 days, respectively. The combination of both drugs significantly extended the median life span to 33 days. To clarify this enhancement of the increase in median life span, we examined intracellular deoxyribonucleoside triphosphate (dNTP) pools, cell-cycle distribution, DNA fragmentation, and the time course of the plasma drug concentration. Etoposide had no effect on intracellular dNTP pools in this experimental system, whereas treatment of cells with C18PCA or with the combination of both drugs resulted in a significant increase in dTTP pools to values ranging from 1.8-to 2.0-fold higher than the control levels. There was a significant increase in cells in the S+G2/M phase when cells had been treated with both etoposide and C18PCA. Agarose-gel electrophoresis of the extracted DNA revealed that C18PCA enhanced the fragmentation of DNA, with a length of about 180 bp being induced by etoposide. The plasma peak levels of etoposide (100 nM) and ara-C (50 nM) were observed at 20 and 30 min after the simultaneous administration of both drugs, respectively. The plasma etoposide level gradually decreased to 10% of the peak level at 240 min after administration. On the other hand, the plasma concentration of ara-C was maintained at above 20 nM at 240 min. These observations suggest that C18PCA and etoposide act on P388 murine leukemic cells by accumulating cells in the S+G2/M phase. Even if the plasma concentration of ara-C is low, the repair of DNA damage by etoposide may be hindered in the presence of ara-C following an increase in DNA fragmentation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00685900
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
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