Evidence map›Paper›PMID 35975988›Full record

ArticleAntimicrobial agents and chemotherapy2022

Moxifloxacin-Mediated Killing of Mycobacterium tuberculosis Involves Respiratory Downshift, Reductive Stress, and Accumulation of Reactive Oxygen Species.

Somnath Shee, Samsher Singh, Ashutosh Tripathi, Chandrani Thakur, Anand Kumar T, Mayashree Das, Vikas Yadav, Sakshi Kohli, Raju S Rajmani, Nagasuma Chandra and 3 more

Open access · greenAbstract read
In one paragraph

Article in Antimicrobial agents and chemotherapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
6.6field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

39 citing papers in PubMed, 75 citations in OpenAlex.

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  18. Reactive Oxygen Detoxification Contributes tobioRxiv : the preprint server for biology · 2025
    Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 3 institutions in 2 countries.

Somnath Shee *Department of Microbiology and Cell Biology, Indian Institute of Science, Bangalore, Karnataka, India.
Samsher Singh *Department of Microbiology and Cell Biology, Indian Institute of Science, Bangalore, Karnataka, India.ORCID 0000-0001-7075-931X
Ashutosh TripathiDepartment of Microbiology and Cell Biology, Indian Institute of Science, Bangalore, Karnataka, India.
Chandrani ThakurDepartment of Biochemistry, Indian Institute of Science, Bangalore, Karnataka, India.
Anand Kumar TDepartment of Chemistry, Indian Institute of Science Education and Research Punegrid.417959.7, Pune, Maharashtra, India.
Mayashree DasDepartment of Microbiology and Cell Biology, Indian Institute of Science, Bangalore, Karnataka, India.
Vikas YadavDepartment of Microbiology and Cell Biology, Indian Institute of Science, Bangalore, Karnataka, India.
Sakshi KohliDepartment of Microbiology and Cell Biology, Indian Institute of Science, Bangalore, Karnataka, India.
Raju S RajmaniCentre for Infectious Disease Research, Indian Institute of Science, Bangalore, Karnataka, India.
Nagasuma ChandraDepartment of Biochemistry, Indian Institute of Science, Bangalore, Karnataka, India.ORCID 0000-0002-9939-8439
Harinath ChakrapaniDepartment of Chemistry, Indian Institute of Science Education and Research Punegrid.417959.7, Pune, Maharashtra, India.
Karl DrlicaPublic Health Research Institute and Department of Microbiology, Biochemistry & Molecular Genetics, New Jersey Medical School, Rutgers Biomedical and Health Sciences, Rutgers University, Newark, New Jersey, USA.
Amit SinghDepartment of Microbiology and Cell Biology, Indian Institute of Science, Bangalore, Karnataka, India.ORCID 0000-0001-6761-1664
Indian Institute of Science Bangalore · INIndian Institute of Science Education and Research Pune · INRutgers, The State University of New Jersey · US

Funding

Wellcome Trust
6 · The paper itself

Abstract

Moxifloxacin is central to treatment of multidrug-resistant tuberculosis. Effects of moxifloxacin on the Mycobacterium tuberculosis redox state were explored to identify strategies for increasing lethality and reducing the prevalence of extensively resistant tuberculosis. A noninvasive redox biosensor and a reactive oxygen species (ROS)-sensitive dye revealed that moxifloxacin induces oxidative stress correlated with M. tuberculosis death. Moxifloxacin lethality was mitigated by supplementing bacterial cultures with an ROS scavenger (thiourea), an iron chelator (bipyridyl), and, after drug removal, an antioxidant enzyme (catalase). Lethality was also reduced by hypoxia and nutrient starvation. Moxifloxacin increased the expression of genes involved in the oxidative stress response, iron-sulfur cluster biogenesis, and DNA repair. Surprisingly, and in contrast with Escherichia coli studies, moxifloxacin decreased expression of genes involved in respiration, suppressed oxygen consumption, increased the NADH/NAD

Indexed as

Mycobacterium tuberculosisTuberculosis2,2'-DipyridylAnimalsAntioxidantsCatalaseCysteineIronIron Chelating AgentsMiceMoxifloxacinNADReactive Oxygen SpeciesSulfurThiourea2,2'-DipyridylAntioxidantsCatalaseCysteineIronIron Chelating AgentsMoxifloxacinNADReactive Oxygen SpeciesSulfurThioureaantimycobacterialfluoroquinolonemoxifloxacinN-acetyl cysteineNADHoxidative stressredox biosensorreductive stressresistancerespirationROS

Identifiers

PMID35975988
PMCPMC9487606
OpenAlexW4292262965

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.