Peroxiredoxin and catalase genes were induced by Amp and the thioredoxin gene was highly Sulfamethazine upregulated by Km and Tc, whereas the redox-sensing regulatory gene soxR was induced by all antibiotics. Antibiotic induced oxidative stress upregulated glyoxylate-bypass genes. The expression levels of isocitrate lyase and malate synthase genes, which are link to glyoxylate bypass, were increased substantially in response to Amp and Nor, but not Tc and Km. These results suggest that distinct Bismuth Subsalicylate classes of antibiotics elicit different responses to oxidative stress by dissimilarly affecting the expression of genes associated with ROS defense and glyoxylate bypass. Unexpectedly, only Nor treatment substantially upregulated the expression of these SOS response-related genes and DNA-repair genes. The SOS response is a global response to DNA damage in bacteria that is induced by a variety of environmental factors such as UV radiation, chemicals, and antimicrobial compounds. The RecA protein and LexA repressor play central roles in SOS response, but a LexA-like transcriptional repressor has been studied only poorly in Acinetobacter species. DNA damage increases the frequency of mutations when MMC is used, which indirectly confirms the presence of the SOS response. Previously, MMC-induced mutation frequency was monitored by measuring the increase of colonies resistant to rifampicin. MMC treatment increased the rifampicin-resistance mutation frequency 47-fold in DR1. When E. coli GC4468 and A. baumannii ATCC17978 were used as reference strains, the mutation frequency was determined to be increased 22- and 37fold in E. coli and A. baumannii, respectively. Our results reveal that crucial features of the canonical SOS response exist in the genome of DR1 cells. When we measured antibiotic induced SOS response, we determined that rifampicin-resistance mutation frequency was strongly induced only by Nor. Agreeing with these data, our reporter strains carrying GFP fused to the recA promoter region showed that Nor treatment induced the SOS response. The fluorescence of these reporter cells depended on the concentration of Nor, although a high concentration of Amp increased recA expression.