Evidence map›Paper›PMID 23695675›Full record

ArticleNature communications2013

Mycobacterium tuberculosis is extraordinarily sensitive to killing by a vitamin C-induced Fenton reaction.

Catherine Vilchèze, Travis Hartman, Brian Weinrick, William R Jacobs

Open access · bronzeAbstract read
In one paragraph

Article in Nature communications, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 152 papers.

0numbers the graph read from it
0cells of the map it votes in
152citing papers in PubMed
15.5field-weighted citation impact, top 1% 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

152 citing papers in PubMed, 329 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Protective role of VitC, Glutathione and Sodium Pyruvate against antibiotic-induced oxidative damage in Escherichia coli.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2026
    Article
  5. Inhibition of ascorbic acid on Pseudomonas bubulae under super-chilled storage.World journal of microbiology & biotechnology · 2026
    Article
  6. Metabolic perturbation reduces antibiotic tolerance inMicrobiology (Reading, England) · 2026
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

92 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 1 country.

Catherine VilchèzeDepartment of Microbiology and Immunology, Howard Hughes Medical Institute, Albert Einstein College of Medicine, 1301 Morris Park Avenue, Bronx, New York 10461, USA.
Travis Hartman
Brian Weinrick
William R Jacobs
Albert Einstein College of Medicine · USHoward Hughes Medical Institute · US

Funding

Immunology/Pathology CoreP30AI051519 · NIAID · YESHIVA UNIVERSITY · PI GOLDSTEIN, HARRIS · 2003 to 2013
$18.6M
Molecular Genetic Analysis of Mycobacterium TuberculosisR37AI026170 · NIAID · ALBERT EINSTEIN COL OF MED YESHIVA UNIV · PI WILLIAM Robert JACOBS · 2004 to 2026
$7.7M
MOLECULAR GENETIC ANALYSIS OF MYCOBACTERIUM TUBERCULOSISR01AI026170 · NIAID · YESHIVA UNIVERSITY · PI JACOBS, WILLIAM ROBERT · 1989 to 2022
$7.1M
Metabolomic Analysis of Redox control in Mycobacterium tuberculosis persistersR21AI090473 · NIAID · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI JACOBS, WILLIAM ROBERT, WU, PENG · 2010 to 2011
$427k
MOLECULAR GENETIC ANALYSIS OF MYCOBACTERIUM TUBERCULOSISR22AI026170 · NIAID · YESHIVA UNIVERSITY · PI JACOBS, WILLIAM ROBERT · 1989 to 1991
–
NIAID NIH HHS AI-051519NIAID NIH HHS AI26170NIAID NIH HHS AI90473NIAID NIH HHS P30 AI051519NIAID NIH HHS R01 AI026170NIAID NIH HHS R37 AI026170
6 · The paper itself

Abstract

Drugs that kill tuberculosis more quickly could shorten chemotherapy significantly. In Escherichia coli, a common mechanism of cell death by bactericidal antibiotics involves the generation of highly reactive hydroxyl radicals via the Fenton reaction. Here we show that vitamin C, a compound known to drive the Fenton reaction, sterilizes cultures of drug-susceptible and drug-resistant Mycobacterium tuberculosis, the causative agent of tuberculosis. While M. tuberculosis is highly susceptible to killing by vitamin C, other Gram-positive and Gram-negative pathogens are not. The bactericidal activity of vitamin C against M. tuberculosis is dependent on high ferrous ion levels and reactive oxygen species production, and causes a pleiotropic effect affecting several biological processes. This study enlightens the possible benefits of adding vitamin C to an anti-tuberculosis regimen and suggests that the development of drugs that generate high oxidative burst could be of great use in tuberculosis treatment.

Indexed as

Antitubercular AgentsAscorbic AcidCysteineDNA DamageDrug Resistance, BacterialGlycopeptidesHydrogen PeroxideInositolIronLipidsMicrobial Sensitivity TestsMicrobial ViabilityModels, BiologicalMycobacterium tuberculosisOxidantsReactive Oxygen SpeciesAntitubercular AgentsAscorbic AcidCysteineFenton's reagentGlycopeptidesHydrogen PeroxideInositolIronLipidsmycothiolOxidantsReactive Oxygen Species

Identifiers

PMID23695675
PMCPMC3698613
OpenAlexW2140867711

What OpenQuestion holds

Textmetadata
LicenceTDM
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.