Role of Secondary Oxidative Stress in the Bactericidal Action of Antibiotics
Tóm tắt
Exposure to β-lactam, fluoroquinolone, and aminoglycoside antibiotics caused an increase in the production of hydrogen peroxide and the expression of OxyR-regulon of the oxidative stress response in Escherichia coli cells. Under the conditions of microaeration, the attenuation of secondary oxidative stress due to the addition of the antioxidant thiourea influenced the antibacterial effect of fluoroquinolones. Thiourea potentiated the effect of sublethal (not decreasing the number of colony-forming units below 103/mL) doses of the antibiotic and increased the viability of cells exposed to lethal doses. The addition of thiourea reduced the expression of OxyR-regulon activated by the sublethal action of the antibiotic to the level of antibiotic-free culture. When exposed to lethal doses, a decrease in the antibiotic-mediated expression of oxidative stress response genes in the presence of thiourea was also observed; however, the expression level remained higher compared to antibiotic-free culture. This may indicate the dual role of ROS under antibiotic treatment as the damaging agents contributing to cell death and as signal molecules activating stress responses.
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