Evidence map›Paper›PMID 8655566›Full record

ArticleJournal of bacteriology1996

Oxidative stress response and its role in sensitivity to isoniazid in mycobacteria: characterization and inducibility of ahpC by peroxides in Mycobacterium smegmatis and lack of expression in M. aurum and M. tuberculosis.

S Dhandayuthapani, Y Zhang, M H Mudd, V Deretic

Open access · greenAbstract readComparative Study
In one paragraph

Article in Journal of bacteriology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
11.1field-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

47 citing papers in PubMed, 120 citations in OpenAlex.

  1. Article
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  4. TheAntimicrobial agents and chemotherapy · 2025
    Article
  5. Article
  6. Review
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  8. Arginine-deprivation-induced oxidative damage sterilizesProceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  9. Article
  10. Article
  11. Investigations into Isoniazid TreatedJournal of pathogens · 2018
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
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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 1 institution in 1 country.

S DhandayuthapaniDepartment of Microbiology, University of Texas Health Science Center at San Antonio 78284-7758, USA.
Y Zhang
M H Mudd
V Deretic
The University of Texas Health Science Center at San Antonio · US

Funding

SIGNAL TRANSDUCTION AND CONTROL OF M TB VIRULENCER01AI035217 · NIAID · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI DERETIC, VOJO P · 1993 to 1997
–
NIAID NIH HHS AI35217
6 · The paper itself

Abstract

Mycobacterium tuberculosis is a natural mutant with inactivated oxidative stress regulatory gene oxyR. This characteristic has been linked to the exquisite sensitivity of M. tuberculosis to isonicotinic acid hydrazide (INH). In the majority of mycobacteria tested, including M. tuberculosis, oxyR is divergently transcribed from ahpC, a gene encoding a homolog of the subunit of alkyl hydroperoxide reductase that carries out substrate peroxide reduction. Here we compared ahpC expression in Mycobacterium smegmatis, a mycobacterium less sensitive to INH, with that in two highly INH sensitive species, M. tuberculosis and Mycobacterium aurum. The ahpC gene of M. smegmatis was cloned and characterized, and the 5' ends of ahpC mRNA were mapped by S1 nuclease protection analysis. M. smegmatis AhpC and eight other polypeptides were inducible by exposure to H2O2 or organic peroxides, as determined by metabolic labeling and Western blot (immunoblot) analysis. In contrast, M. aurum displayed differential induction of only one 18-kDa polypeptide when exposed to organic peroxides. AhpC could not be detected in this organism by immunological means. AhpC was also below detection levels in M. tuberculosis H37Rv. These observations are consistent with the interpretation that ahpC expression and INH sensitivity are inversely correlated in the mycobacterial species tested. In further support of this conclusion, the presence of plasmid-borne ahpC reduced M. smegmatis susceptibility to INH. Interestingly, mutations in the intergenic region between oxyR and ahpC were identified and increased ahpC expression observed in deltakatG M. tuberculosis and Mycobacterium bovis INH(r) strains. We propose that mutations activating ahpC expression may contribute to the emergence of INH(r) strains.

Indexed as

Oxidative StressPeroxidasesAmino Acid SequenceBase SequenceDrug Resistance, MicrobialEnzyme InductionGene Expression Regulation, BacterialGene Expression Regulation, EnzymologicGenes, BacterialIsoniazidMolecular Sequence DataMycobacteriumMycobacterium tuberculosisOxidation-ReductionOxidoreductasesPeroxidesIsoniazidOxidoreductasesPeroxidasesPeroxidesPeroxiredoxinsRNA, Messenger

Identifiers

PMID8655566
PMCPMC178138
OpenAlexW2138084570

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.