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pretomanid, article, pubmed, methylglyoxal, treatment, accumulation, google, scholar, nature, metabolite, mass, metabolites, analysis, action, smegmatis, pathway, cas, mycobacterium, bacterial, samples, data, tuberculosis, mode, metabolic, metabolism, fig, antibiotics, phosphate, glucosephosphate, central, growth, cell, metabolomics, drug, spectrometry, pentose, significant, fructosephosphate, antibiotic, metabolomic, acn, bacteria, activity, gctofms, min, content, mechanisms, mycobacteria, fiehrms, identification,

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nature portfolio privacy policy nature communications 1 advertising 10 μl n-methyl-n-trimethylsilyltrifluoride nitroimidazo-oxazine-specific protein involved 8888/hrmet/index nature 405 nature f420-dependent glucose-6-phosphate dehydrogenase social media tb drug development reprints aba-regulated gene expression cw-cell wall synthesis author information authors promising anti-tubercular drug rational development mycobacteria-induced macrophage apoptosis clear multi-target profile full size image mid-exponential growth phase cross-validated p-values permissions thermo-scientific author correspondence original author anti-tuberculosis agent pa-824 flight mass spectrometry flight mass spectrometry tandem mass spectrometry deazaflavin dependent nitroreductase deazaflavin-dependent nitroreductase diverse nutrient conditions mycobacterium tuberculosis involved bacterial growth conditions anti-tubercular molecules access principal component analysis glucose-6-phosphate dehydrogenase intracellular accumulation glucose-6-phosphate fie-ms data untargeted metabolomics reveals accela uhplc system privacy tb therapeutic candidates published maps des-nitroimidazole derivative ps-protein synthesis esi source parameters

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• Bacterial production of methylglyoxal: a survival strategy or death by misadventure?

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         headline:Untargeted metabolomics reveals a new mode of action of pretomanid (PA-824)
         description:Pretomanid is a promising anti-tubercular drug currently at clinical phase III, but its mechanisms of action are currently unclear. This study aimed to: (i) reveal the metabolome of Mycobacterium smegmatis under pretomanid treatment; (ii) compare major sources of metabolite variation in bacteria treated with pretomanid treatment and other antibiotics; and (iii) to target metabolites responsible for the killing activity of pretomanid in mycobacteria. Untargeted high-resolution metabolite profiling was carried out using flow infusion electrospray ion high resolution mass spectrometry (FIE-HRMS) to identify and quantify metabolites. The identification of key metabolites was independently confirmed by gas-chromatography time-of flight mass spectrometry (GC-tofMS) in comparison to standards. Pretomanid treatments generated a unique distinctive metabolite profile when compared to ampicillin, ethambutol, ethionamide, isoniazid, kanamycin, linezolid, rifampicin and streptomycin. Metabolites which differed significantly only with pretomanid treatment were identified and mapped on to bacterial metabolic pathways. This targeted the pentose phosphate pathway with significant accumulation seen with fructose-6-phosphate, ribose-5-phosphate and glyceraldehyde-3-phosphate. These effects were linked to the accumulation of a toxic metabolite methylglyoxal. This compound showed significant antimicrobial activity (MIC 0.65 mM) against M. smegmatis.
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