Role of nucleotide excision repair and p53 in zidovudine (AZT)-induced centrosomal deregulation.
作者： Dariya Momot , Terri A. Nostrand , Kaarthik John , Yvona Ward , Seth M. Steinberg
DOI: 10.1002/EM.21889
关键词:
摘要: The nucleoside reverse transcriptase inhibitor zidovudine (AZT) induces genotoxic damage that includes centrosomal amplification (CA > 2 centrosomes/cell) and micronucleus (MN) formation. Here we explored these end points in mice deficient DNA repair tumor suppressor function to evaluate their effect on AZT-induced damage. We used mesenchymal-derived fibroblasts cultured from C57BL/6J were null wild type (WT) for Xpa, WT, haploinsufficient p53 (6 different genotypes). Dose-responses CA formation, cells exposed 0, 10, 100 μM AZT 24 hr, observed all genotypes except the Xpa(+/+)p53(+/−) cells, which had very low levels of CA, Xpa(−/−)p53(−/−) high CA. For there was a significant three-way interaction between p53, concentration, Xpa(−/−) significantly higher than Xpa(+/+) only p53(+/−) cells. In contrast, MN MN + chromosomes (MN + C) data showed lack dose response. with p53(+/+) or (+/−) genotypes, MN + C corresponding show is major event induced by exposure complicated relationship formation respect gene dosage Xpa p53. loss both genes resulted damage, haploinsufficicency strongly protected Environ. Mol. Mutagen. 55:719–726, 2014. Published This article U.S. Government work public domain USA.
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