Oxygen Limitation Suppresses Reactive Oxygen Species Formation by Norfloxacin

Content Provider	Semantic Scholar
Author	Lee, Sherry D. Lin, Bryan Tang, Yi Wang, Taixiang
Copyright Year	2013
Abstract	Previous research showed that the formation of reactive oxygen species (ROS) serves as a common mechanism of bactericidal antibiotics induced cell death. The purpose of this study was to better understand the mechanism of oxygen radicals formation by assessing the effect of oxygen limitation on the production of ROS when two strains of Escherichia coli, BW25113 and JW0419, were treated with the quinolone antibiotic Norfloxacin under aerobic or anaerobic conditions. JW0419 strain is deficient in the cyoD gene, a subunit of the cytochrome bo terminal oxidase, an aerobic respiratory enzyme predominantly expressed under high oxygen levels. This strain served to assess the ability of cytochrome bo to produce oxygen species. Aerobic and anaerobic condition did not affect the minimal inhibitory concentration of norfloxacin for either strain. High concentration of norfloxacin treatment resulted in an increase in ROS formation after one hour of treatment under aerobic conditions for both strains but decreased to a plateau at 2 hours. Anaerobically treated cultures showed a lower steady increase in ROS formation before reaching a plateau at 2 hours. Our data suggests that oxygen was required for norfloxacin induced increase in the formation of oxygen radicals, in a mechanism which is likely independent of cytochrome bo activity.
File Format	PDF HTM / HTML
Alternate Webpage(s)	https://www.microbiology.ubc.ca/sites/default/files/roles/drupal_ungrad/JEMI/17/13.3G.pdf
Language	English
Access Restriction	Open
Content Type	Text
Resource Type	Article