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

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

Research output: Contribution to journalArticle

134 Citations (Scopus)

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.

Original languageEnglish (US)
Article number1881
JournalNature communications
Volume4
DOIs
StatePublished - Jun 12 2013

Fingerprint

tuberculosis
ascorbic acid
Mycobacterium tuberculosis
Ascorbic Acid
Tuberculosis
Pharmaceutical Preparations
drugs
Biological Phenomena
Multidrug-Resistant Tuberculosis
Chemotherapy
Respiratory Burst
Pathogens
Cell death
Hydroxyl Radical
Escherichia coli
Reactive Oxygen Species
Cell Death
Ions
Anti-Bacterial Agents
pathogens

ASJC Scopus subject areas

  • Chemistry(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Physics and Astronomy(all)

Cite this

Mycobacterium tuberculosis is extraordinarily sensitive to killing by a vitamin C-induced Fenton reaction. / Vilchèze, Catherine; Hartman, Travis; Weinrick, Brian; Jacobs, William R.

In: Nature communications, Vol. 4, 1881, 12.06.2013.

Research output: Contribution to journalArticle

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