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  • American Association for Cancer Research (AACR)  (2)
  • Wakabayashi, Keiji  (2)
  • 2005-2009  (2)
Material
Publisher
  • American Association for Cancer Research (AACR)  (2)
Person/Organisation
Language
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  • 2005-2009  (2)
Year
  • 1
    Online Resource
    Online Resource
    Detection of Aminophenylnorharman, a Possible Endogenous Mutagenic and Carcinogenic Compound, in Human Urine Samples
    American Association for Cancer Research (AACR) ; 2007
    In:  Cancer Epidemiology, Biomarkers & Prevention Vol. 16, No. 1 ( 2007-01-01), p. 151-156
    Details
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 16, No. 1 ( 2007-01-01), p. 151-156
    Abstract: Mutagenic/carcinogenic 9-(4′-aminophenyl)-9H-pyrido[3,4-b]indole [aminophenylnorharman (APNH)] is formed from norharman and aniline in the presence of cytochrome P450 3A4/1A2. Because both precursors are widely distributed in the environment, human exposure is unavoidable. To clarify APNH formation in the human body, amounts of the compound in 24-h human urine collected from smokers and nonsmokers, eating a normal diet, were analyzed by liquid chromatography/electrospray ionization tandem mass spectrometry. In addition, norharman and aniline were also analyzed by high-performance liquid chromatography and gas chromatography, respectively. APNH could be detected in all urine samples at levels 49 to 449 pg for smokers and 21 to 594 pg for nonsmokers per 24-h urine, respectively. The amounts of norharman and aniline were 46 to 185 ng and 0.70 to 8.10 μg for smokers and 52 to 447 ng and 0.49 to 5.72 μg for nonsmokers, respectively, per 24-h urine (none of the levels differing significantly between smokers and nonsmokers). To exclude exogenous exposure to norharman and aniline, we analyzed the levels of APNH, norharman, and aniline in urine samples collected from inpatients receiving parenteral alimentation. Similar to the healthy volunteers, all urine samples contained 12 to 338 pg of APNH, 6 to 75 ng of norharman, and 0.33 to 1.86 μg of aniline per 24-h urine. These results suggest that APNH should be considered as a novel endogenous mutagen/carcinogen; thus, it is very important to determine the biological significance of this carcinogen for human cancer development. (Cancer Epidemiol Biomarkers Prev 2007;16(1):151–6)
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    URL: Article
    DOI: 10.1158/1055-9965.EPI-06-0052
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2007
    detail.hit.zdb_id: 2036781-8
    detail.hit.zdb_id: 1153420-5
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    Online Resource
  • 2
    Online Resource
    Online Resource
    Involvement of the ATR- and ATM-Dependent Checkpoint Responses in Cell Cycle Arrest Evoked by Pierisin-1
    American Association for Cancer Research (AACR) ; 2006
    In:  Molecular Cancer Research Vol. 4, No. 2 ( 2006-02-01), p. 125-133
    Details
    In: Molecular Cancer Research, American Association for Cancer Research (AACR), Vol. 4, No. 2 ( 2006-02-01), p. 125-133
    Abstract: Pierisin-1 identified from the cabbage butterfly, Pieris rapae, is a novel mono-ADP-ribosylating toxin that transfers the ADP-ribose moiety of NAD at N2 of dG in DNA. Resulting mono-ADP-ribosylated DNA adducts cause mutations and the induction of apoptosis. However, little is known about checkpoint responses elicited in mammalian cells by the formation of such bulky DNA adducts. In the present study, it was shown that DNA polymerases were blocked at the specific site of mono-ADP-ribosylated dG, which might lead to the replication stress. Pierisin-1 treatment of HeLa cells was found to induce an intra-S-phase arrest through both ataxia telangiectasia mutated (ATM) and Rad3-related (ATR) and ATM pathways, and ATR pathway also contributes to a G2-M-phase delay. In the colony survival assays, Rad17−/− DT40 cells showed greater sensitivity to pierisin-1-induced cytotoxicity than wild-type and ATM−/− DT40 cells, possibly due to defects of checkpoint responses, such as the Chk1 activation. Furthermore, apoptotic 50-kb DNA fragmentation was observed in the HeLa cells, which was well correlated with occurrence of phosphorylation of Chk2. These results thus suggest that pierisin-1 treatment primarily activates ATR pathway and eventually activates ATM pathway as a result of the induction of apoptosis. From these findings, it is suggested that mono-ADP-ribosylation of DNA causes a specific type of fork blockage that induces checkpoint activation and signaling. (Mol Cancer Res 2006;4(2):125–33)
    Type of Medium: Online Resource
    ISSN: 1541-7786 , 1557-3125
    URL: Article
    DOI: 10.1158/1541-7786.MCR-05-0104
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2006
    detail.hit.zdb_id: 2097884-4
    SSG: 12
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