Effect of varying the exposure and H-thymidine labeling period upon the outcome of the primary hepatocyte DNA repair assay
Cell Biology and Toxicology, ISSN: 0742-2091, Vol: 4, Issue: 2, Page: 199-209
1988
- 8Citations
- 5Captures
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Article Description
The results presented in this report demonstrate that an 18-20 hour exposure/H-thymidine DNA labeling period is superior to a 4 hour incubation interval for general genotoxicity screening studies in the rat primary hepatocyte DNA repair assay. When DNA damaging agents which give rise to bulky-type DNA base adducts such as 2-acetylaminofluorene, aflatoxin Bi and benzidine were evaluated, little or no difference was observed between the 4 hour or an 18-20 hour exposure/labeling period. Similar results were also noted for the DNA ethylating agent diethylnitrosamine. However, when DNA damaging chemicals which produce a broader spectrum of DNA lesions were studied, differences in the amount of DNA repair as determined by autoradiographic analysis did occur. Methyl methanesulfonate and dimethylnitrosamine induced repairable DNA damage that was detected at lower dose levels with the 18-20 hour exposure/labeling period. Similar results were also observed for the DNA cross-linking agents, mitomycin C and nitrogen mustard. Ethyl methanesulfonate produced only a marginal amount of DNA repair in primary hepatocytes up to a dose level of 10M during the 4 hour incubation period, whereas a substantial amount of DNA repair was detectable at a dose level of 2.5 × 10M when the 18-20 hour exposure/labeling period was employed. The DNA alkylating agent 4-nitroquinoline-1-oxide, which creates DNA base adducts that are slowly removed from mammalian cell DNA, induced no detectable DNA repair in hepatocytes up to a toxic dose level of 2 × 10M with the 4 hour exposure period, whereas a marked DNA repair response was observed at 10M when the 18-20 hour exposure/labeling period was used. © 1988 Princeton Scientific Publishing Co., Inc.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0023700870&origin=inward; http://dx.doi.org/10.1007/bf00119246; http://www.ncbi.nlm.nih.gov/pubmed/3233531; http://link.springer.com/10.1007/BF00119246; http://www.springerlink.com/index/pdf/10.1007/BF00119246; https://dx.doi.org/10.1007/bf00119246; https://link.springer.com/article/10.1007/BF00119246; http://www.springerlink.com/index/10.1007/BF00119246
Springer Nature
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