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  • 1990-1994  (2)
  • Fructose-1,6-bisphosphatase  (1)
  • Glucose repression  (1)
  • Ifosfamide  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Metabolism and pharmacokinetics of oral and intravenous ifosfamide (1991)
    Springer
    Journal of cancer research and clinical oncology 117 (1991), S. S148 
    Details
    ISSN: 1432-1335
    Keywords: Ifosfamide ; Activated ifosfamide ; Chloroacetaldehyde ; Metabolism ; Pharmacokinetics
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The initial metabolism of ifosfamide (IF) consists of two different pathways: enzymatic hydroxylation at carbon-4 forms the cytostatically active metabolite 4-OH-IF (“activated ifosfamide”) whereas side-chain oxidation results in the liberation of chloroacetaldehyde, a compound with possible neurotoxic properties. The pharmacokinetics of ifosfamide and its activated form were investigated in 12 cancer patients, who received both oral and i.v. treatment in a randomized sequence on days 1 and 3 at a dose of 1 g/m2 (n=7) or 1.5 g/m2 (n=5). In 3 patients the pharmacokinetics of chloroacetaldehyde were also investigated. After oral application, ifosfamide absorption proceeded rapidly, the oral bioavailability was 0.92. Independent of the route of ifosfamide application on day 1, the terminal half-life on day 3 (when the drug was given by the alternative route) was decreased in 6 out of the 12 patients, thus indicating self-induction of hepatic metabolism. 4-OH-IF was already present 20 min after ifosfamide administration. In the individual patient the concentrations of 4-OH-IF were always higher after oral than after i.v. IF application: the mean p.o.:i.v. ratios forc max and the area under the concentration/time curve were 2.3 and 1.7 respectively (P〈0.05). In a first series of 3 patients the chloroacetaldehyde concentrations measured after oral ifosfamide application were about twice as high as those when the drug was given intravenously. These results indicate that (in comparison to the i.v. route) orally administered ifosfamide may be more cancerotoxic but also leads to higher levels of chloroacetaldehyde. This would explain the neurotoxic sideeffects previously seen after oral administration of comparatively low ifosfamide doses.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01613221
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Identification of UAS elements and binding proteins necessary for derepression of Saccharomyces cerevisiae fructose-1,6-bisphosphatase (1992)
    Springer
    Current genetics 22 (1992), S. 363-370 
    Details
    ISSN: 1432-0983
    Keywords: Saccharomyces cerevisiae ; Fructose-1,6-bisphosphatase ; Glucose repression ; Gene activation ; Gluconeogenesis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary Fructose-1,6-bisphosphatase is a key enzyme in gluconeogenesis and the FBP1 gene is not transcribed during growth with glucose. Genetic analysis indicated a positive regulation of FBP1 expression after exhaustion of glucose. By linker-deletion analysis, two upstream activation sites (UAS1 and UAS2) were localized and the respective UAS-binding factors (DAP I and DAP II for derepression activating protein) were identified by gel retardation. UAS1 and UAS2 span about 30 bp each, and are separated by approximately 30 bp. Both UAS sites act synergistically. Although UAS1 showed some similarities to the DNA-binding consensus for the general yeast activator Rap1, competition experiments and DEAE-chromatography proved that DAP I and Rap1 correspond to different proteins. Gel retardation by DAP I depended on carbon sources and did not occur in cells growing logarithmically with glucose, whereas a strong retardation signal was obtained with ethanol-grown cells. The present results suggest that DAP I and DAP II are the final regulatory elements for glucose derepression.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00352437
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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