The product of the sulA gene, a key component of the SOS response that leads to cell elongation by binding to FtsZ or DpiAB in a two-component system, induces cell filamentation. In the cell walls of most bacteria, peptidoglycans play an essential role in antimicrobial resistance; peptidoglycans determine cell shape, and their biosynthesis is critical for antibiotics resistance. We measured the change in membrane Azlocillin sodium salt permeability by using ANS, a neutral, hydrophobic fluorescent probe; in membrane damaged cells, fluorescence is increased because the enhanced permeability leads to ANS uptake. The fluorescence-intensity values measured were divided by the OD600 values for normalizing the measurements, and the results showed that distinct antibiotic treatments altered membrane permeability to different degrees. The membrane-permeability properties have a major impact on the susceptibility of microorganisms to antibiotics. Membrane permeability was increased substantially after Km treatment, whereas only a slight increase of membrane permeability was induced by Amp and Tc, which might explain the sensitive response of DR1 cells to Km. Porins are considered to be permanently open pores, and lowering porin expression reduces outer-membrane permeability; thus, porin-mediated permeability is a critical aspect of anti-biotic resistance mechanisms. The DR1 genome contains several porin encoding genes. The expression of omp C, which encodes an outer-membrane porin protein, increased 1.5-fold under Km treatment, but decreased in response to Amp and Nor and did not change after Tc treatment. Antibiotics have been widely reported to induce the production of reactive oxygen species, which causes oxidative stress damage. We used the fluorescent probe DHR 123 and flow cytometry to monitor ROS generation following treatment with the 4 antibiotics: under the Orbifloxacin tested conditions, treatment with Amp, Km, and Nor, but not Tc, potently induced ROS generation. Interestingly, the expression profiles of oxidative stress related genes were distinct following treatment with these antibiotics of different classes, based on which we suggest that distinct mechanisms exist that are used by bacteria for coping with disparate types and levels of oxidative stress induced by various antibiotics.