E. coli exposure to ciprofloxacin disturbs cysteine homeostasis; an increase in the intracellular concentration of cysteine is dangerous due to its ability to enhance ROS generation. Unlike wild-type bacteria, in which the cysteine content did not exceed the control level, cells of the gshA mutant lacking glutathione are characterized by increased concentration of intracellular cysteine in proportion to the concentrations of the antibiotic, despite the intensive export of cysteine into the medium. At low concentrations of ciprofloxacin, the mutant strain formed half as many colonies as the parent strain in the survival test. These findings attest to the important role of the incorporation of excess cysteine into glutathione as one of the mechanisms of cysteine homeostasis during the stress response to antibiotic.
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