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  • 1
    Electronic Resource
    Electronic Resource
    Phenobarbital Induction of Aldehyde Dehydrogenase Type 2 mRNA in Mouse Liver: A Candidate Region on Chromosome 7 for a Putative Regulatory Gene (2000)
    Springer
    Biochemical genetics 38 (2000), S. 297-308 
    Details
    ISSN: 1573-4927
    Keywords: liver ; mouse ; phenobarbital ; aldehyde dehydrogenase ; chromosome 7
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Abstract Phenobarbital (PB) strongly induces in the liver the expression of many genes encoding detoxication enzymes, such as the aldehyde dehydrogenase type 2 in the mouse (Aldh2). With the aim of identifying genes involved in this response, we have undertaken an approach based on a genetic analysis in mice. In a previous report, the genetic analysis of both the C57BL/6J (B6) × DBA/2J (D2) F1 and the (F1 × F1) F2 led us to the hypothesis that Aldh2 responsiveness to PB was under the control of one major locus independent of the structural gene. In the present study, the genetic analysis of the inducibility by PB of Aldh2 in the backcross population B6D2F1 × D2 has allowed us to confirm the involvement of a major regulatory gene in this mechanism. By searching for genetic linkage between this locus and a series of microsatellites DNA markers, we obtained indicative evidence for a region on chromosome 7, which may carry this gene.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1002057000788
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  • 2
    Electronic Resource
    Electronic Resource
    Genetic analysis of aflatoxin B1 activation in rat hepatoma cells (1990)
    Springer
    Molecular genetics and genomics 222 (1990), S. 291-296 
    Details
    ISSN: 1617-4623
    Keywords: Aflatoxin B1 ; Cytochrome P450 ; Rat hepatoma cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary We present a strategy to elucidate the rate-limiting steps in activation of carcinogenic compounds by cytochromes P450. The principle was to select Reuber rat hepatoma cells for resistance to a procarcinogen. The hypothesis was that resistant cells should be systematically deficient in the P450 enzyme(s) involved in the activation process. Here we present an example of the use of this approach using aflatoxin B1 (AFB1), a potent hepatocarcinogen, as the selective agent. Parental cells as well as individual and pooled colonies selected for AFB1 resistance from three independent rat hepatoma lines were characterized for their content of 1) mRNA hybridizing to cDNA and/or oligonucleotide probes for cytochromes P450IIB1, P450IIB2 and albumin; and 2) aldrin epoxidase activity. Parental aflatoxin B1-sensitive cells were shown to express P450IIB1 but not P450IIB2. The majority of the aflatoxin B1-resistant clones failed to accumulate cytochrome P450IIB1 mRNA and expressed no or only very low aldrin epoxidase activity. Albumin mRNA levels remained unchanged, demonstrating that loss of expression of cytochrome P450IIB1 was not a consequence of a general dedifferentiation event. A revertant population showing restoration of both cytochrome P450IIB1 mRNA accumulation and aldrin epoxidase activity was fully sensitive to aflatoxin B1. The correlation between expression of cytochrome P450IIB1 and sensitivity to aflatoxin B1 in both parental cells and revertants strongly suggests that cytochrome P450IIB1 is a major contributor to the activation of aflatoxin B1 in rat hepatoma cells. The kind of strategy described here could be applied to other compounds that become cytotoxic for hepatoma cells following activation by cytochromes P450.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00633831
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    Paper (German National Licenses)
    Fulltext
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