Bactericidal antibiotics induce programmed metabolic toxicity

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Bactericidal antibiotics induce programmed metabolic toxicity

The misuse of antibiotics has led to the development and spread of antibiotic resistance in clinically important pathogens. These resistant infections are having a significant impact on treatment outcomes and contribute to approximately 25,000 deaths in the U.S. annually. If additional therapeutic options are not identified, the number of annual deaths is predicted to rise to 317,000 in North A...

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Bactericidal Antibiotics Induce Toxic Metabolic Perturbations that Lead to Cellular Damage.

Understanding how antibiotics impact bacterial metabolism may provide insight into their mechanisms of action and could lead to enhanced therapeutic methodologies. Here, we profiled the metabolome of Escherichia coli after treatment with three different classes of bactericidal antibiotics (?-lactams, aminoglycosides, quinolones). These treatments induced a similar set of metabolic changes after...

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Bactericidal antibiotics induce mitochondrial dysfunction and oxidative damage in Mammalian cells.

Prolonged antibiotic treatment can lead to detrimental side effects in patients, including ototoxicity, nephrotoxicity, and tendinopathy, yet the mechanisms underlying the effects of antibiotics in mammalian systems remain unclear. It has been suggested that bactericidal antibiotics induce the formation of toxic reactive oxygen species (ROS) in bacteria. We show that clinically relevant doses o...

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Staphylococcus aureus persisters tolerant to bactericidal antibiotics.

Bacterial persister cells are non- or slow-growing reversible phenotypic variants of the wild type, tolerant to bactericidal antibiotics. We analyzed here Staphylococcus aureus persister levels by monitoring colony-forming unit counts of planktonically grown cells treated with six different antimicrobials over time. The model laboratory strains HG001-HG003, SA113 and the small colony variant (S...

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ژورنال

عنوان ژورنال: Microbial Cell

سال: 2016

ISSN: 2311-2638

DOI: 10.15698/mic2016.04.493