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  • 1
    Electronic Resource
    Electronic Resource
    DNA single strand break analysis in mononuclear blood cells of petrol pump attendants (1995)
    Springer
    International archives of occupational and environmental health 67 (1995), S. 35-39 
    Details
    ISSN: 1432-1246
    Keywords: Biomonitoring ; DNA damage Benzene ; Cigarette smoking
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract DNA single strand breaks, including DNA adducts that lead to alkali-labile sites, were measured in peripheral mononuclear blood cells of 35 petrol pump attendants by alkaline filter elution. Blood samples from petrol pump attendants were taken on Monday and Friday. Additionally, DNA single strand breaks of smoking and non-smoking control persons were examined. For the smoking (n = 12) and the non-smoking controls (n = 20) a mean normalized elution rate of 1.49 ± 0.52 (mean value ± 95% confidence interval) and 1.32 ± 0.28, respectively, was obtained. The difference between smoking and non-smoking controls was not statistically significant (U test). An increase in DNA single strand breaks from Monday to Friday was detected for non-smoking petrol pump attendants with a daily working time of more than 4 h at the pump station. Their mean normalized elution rate increased from 1.08 on Monday to 1.89 on Friday. This difference was statistically significant (P 〈 0.05; Wilcoxon test for paired data), although the 95% confidence interval was large on Friday (0.43 on Monday; 1.23 on Friday). However, no significant increase was found for non-smoking petrol pump attendants who were on duty for less than 4 h per day at the pump station. No statistically significant increase in DNA single strand breaks could be detected for smoking petrol pump attendants whether they were pumping gasoline for more or for less than 4 h per day.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00383130
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    DNA binding, adduct characterisation and metabolic activation of aflatoxin B1 catalysed by isolated rat liver parenchymal, Kupffer and endothelial cells (1991)
    Springer
    Archives of toxicology 65 (1991), S. 633-639 
    Details
    ISSN: 1432-0738
    Keywords: Aflatoxin B1 ; Parenchymal cells ; Nonparenchymal cells ; Mutagenicity ; DNA binding
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In vitro studies with rat liver parenchymal, Kupffer and endothelial cells isolated from male Sprague-Dawley rats were undertaken to investigate cell-specific bioactivation of aflatoxin B1, DNA binding and adduct formation. In the mutagenicity studies, using homogenates of all three separated liver cell populations (co-incubated with NADP+ and glucose-6-phosphate as cofactors for the cytochrome P-450 monooxygenase system) parenchymal, Kupffer and endothelial cells were able to activate aflatoxin B1 to a metabolite mutagenic to Salmonella typhimurium TA 98. In the case of nonparenchymal cells (i.e. Kupffer and endothelial cells) 10-fold higher concentrations of aflatoxin B1 had to be used to obtain a similar number of revertants to that observed with parenchymal cells. Induction studies with Aroclor 1254 led to a striking decrease in the activation of aflatoxin B1 in parenchymal cells, whereas nonparenchymal cells had a slightly enhanced metabolic activation capacity for aflatoxin B1. Metabolism studies with microsomes from induced and noninduced cells using testosterone as substrate revealed comparable results: after induction with Aroclor 1254, parenchymal cells showed a 60% decrease in the formation rate of 2α-hydroxytestosterone, whereas the formation rate of this metabolite remained unchanged in nonparenchymal cells; 2α-hydroxytestosterone is specifically formed by cytochrome P-450 IIC11, which also catalyses the activation of aflatoxin B1 to its epoxide. When freshly isolated, intact cells were incubated with tritiated aflatoxin B1, a dose-dependent aflatoxin B1 binding to DNA in parenchymal and nonparenchymal cells was observed. HPLC analysis of DNA acid hydrolysates of all three cell types showed the major adduct to be 8,9-dihydro-8-(N7-guanyl)-9-hydroxyaflatoxin B1.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02098028
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    Paper (German National Licenses)
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