Endogenous HS has been proposed to be a universal defense mechanism against different antibiotics. Here, we studied the role of HS transiently generated during ciprofloxacin (CF) treatment in M9 minimal medium with sulfate or produced by E. coli when fed with cystine.
View Article and Find Full Text PDFCysteine and its derivatives, including HS, can influence bacterial virulence and sensitivity to antibiotics. In minimal sulfate media, HS is generated under stress to prevent excess cysteine and, together with incorporation into glutathione and export into the medium, is a mechanism of cysteine homeostasis. Here, we studied the features of cysteine homeostasis in LB medium, where the main source of sulfur is cystine, whose import can create excess cysteine inside cells.
View Article and Find Full Text PDFThe ability of hydrogen sulfide (HS) to protect bacteria from bactericidal antibiotics has previously been described. The main source of HS is the desulfurization of cysteine, which is either synthesized by cells from sulfate or transported from the medium, depending on its composition. Applying electrochemical sensors and a complex of biochemical and microbiological methods, changes in growth, respiration, membrane potential, SOS response, HS production and bacterial survival under the action of bactericidal ciprofloxacin and bacteriostatic chloramphenicol in commonly used media were studied.
View Article and Find Full Text PDFChanges in the redox balance in the medium and in Escherichia coli cells significantly affect the ability of bacteria to form biofilms. An increase in the level of aeration in the culture of wild-type bacteria led to a 3-fold decrease in the mass of biofilms. Mutants lacking components of the glutathione and thioredoxin redox systems, as well as transporters involved in the transmembrane cycling of glutathione, demonstrated increased biofilm formation ability.
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