Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 625, Issue -, Pages 134-139Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2022.07.102
Keywords
Escherichia coli; Fe3+; Gentamicin; Antibiotic resistance
Categories
Funding
- National Natural Science Foundation of China [31902414, 42076095]
- Natural Science Foundation of Guangdong Province [2019A1515012211]
- Science and Technology Planning Project of Guangzhou City [202102021206]
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This study explores the combined effection of metal ions and antibiotics on the drug resistance of Escherichia coli. The results showed that exogenous Fe3+ could decrease intracellular gentamicin concentration and reduce reactive oxygen species (ROS) production, leading to the restoration of gentamicin-mediated killing by Fe3+.
Kinds of antibiotics are used to prevent and control bacteria infections, unfortunately, the overuse and misuse of antibiotic have promoted the emergence and spread of antibiotic-resistant bacteria. Therefore, understanding the mechanism of antibiotic resistance is very important. This study explores the combined effection of metal ions and antibiotic to the drug resistance of Escherichia coli. Our results found that the minimum inhibitory concentration (MIC) increased as the ammonium ferric citrate concentration increased, especially for gentamicin antibiotic. When the Fe3+ concentration reached 300 mu M, the survival of E. coli was stably restored with the increased gentamicin concentration. Exogenous Fe3+ could decrease intracellular gentamicin concentration. On the other hand, Fe3+ treatment together with gentamicin could reduce reactive oxygen species (ROS) production, characterized by decreased levels of NADH and ATP. Furthermore, ROS-scavenging enzymes of superoxide dismutase (SOD) and catalase (CAT) were up-regulated and H2O2 plus gentamicin-mediated killing was restored by Fe3+. These results may have significant implications in understanding bacterial antibiotic-resistant mechanisms based on the external Fe3+ concentration. (C) 2022 The Authors. Published by Elsevier Inc.
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