Publications by authors named "L V Sutormina"
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.
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- Extracts from certain fodder grasses have been shown to inhibit growth and biofilm formation in avian pathogenic strains, both individually and alongside antibiotics.
- The research found that the extracts could enhance the effectiveness of multiple antibiotics against both biofilms and free-floating bacteria, including antibiotic-resistant strains.
- The extracts exhibited low prooxidant activity, which might change how certain biological processes work, leading to stronger effects when used with antibiotics.
Article Synopsis
- In Gram-negative bacteria, stress-induced growth arrest leads to the release of hydrogen sulfide, which comes from the breakdown of intracellular cysteine to prevent toxic accumulation.
- Research using electrochemical sensors showed that both Gram-positive and Gram-negative bacteria produce sulfide during growth arrests caused by low nutrients or antibiotics, with notable changes in physiological parameters.
- Differences in sulfide production between the two types of bacteria are attributed to the absence of glutathione in Gram-positive bacteria, suggesting that this process may represent a previously unknown natural source of hydrogen sulfide.
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.
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.
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