Abstract
Bleomycin (BLM) is a glycopeptide antibiotic and anti-tumor agent that targets primarily the furanose rings of DNA and in the presence of ferrous ions produces oxidative damage and DNA strand breaks. Escherichia coli cells growing in broth medium and exposed to low concentrations of BLM contain double-strand breaks and require homologous recombination to survive. To a lesser extent, the cells also require the abasic (AP) endonucleases associated with base excision repair, presumably to repair oxidative damage. As expected, there is strong induction of the SOS system in treated cells. In contrast, E. coli cells growing in glucose or glycerol minimal medium are resistant to the lethal action of BLM and do not require either homologous recombination functions or AP-endonucleases for survival. DNA ligase activity, however, is needed for cells growing in minimal medium to resist the lethal effects of BLM. There is weak SOS induction in such treated cells.
Highlights
Bleomycin (BLM) is a glycopeptide antibiotic and anti-tumor agent isolated from Streptomyces verticillis [1,2] that targets primarily the furanose rings of DNA
There is no dose-dependent accumulation of low molecular weight DNA in either the wildtype or recBCD cells (Fig. 6B). These results indicate that, after BLM exposure, double-strand breaks (DSBs) are detectable in cells growing in broth but not in cells growing in glucose minimal medium
DNA breaks in BLM-exposed cells growing in broth For E. coli cells growing in broth, exposure to BLM results in the formation of DSBs
Summary
Bleomycin (BLM) is a glycopeptide antibiotic and anti-tumor agent isolated from Streptomyces verticillis [1,2] that targets primarily the furanose rings of DNA. Degradation by BLM is initiated by generating a free radical, in the presence of ferrous ion, in the deoxyribose resulting in two different types of DNA damage [3,4]. At low oxygen tension, oxidized abasic (AP) sites are favored while at high oxygen tension single-and double-strand breaks (DSBs) predominate. These alternative pathways lead to a mix of abasic sites and strand breaks which occur at a 1:1 ratio [5]. Up to one-third of BLM-induced lesions are double-strand breaks which consist of either two identical breaks in opposite strands or arise from an abasic site with a closely opposed strand break [6]
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