Enhancement of fludioxonil fungicidal activity by disrupting cellular glutathione homeostasis with 2,5-dihydroxybenzoic acid

Jong H. Kim, Bruce C. Campbell, Noreen Mahoney, Kathleen L. Chan, Russell J. Molyneux, Gregory S. May

Research output: Contribution to journalArticlepeer-review

33 Scopus citations

Abstract

The activity of fludioxonil, a phenylpyrrole fungicide, is elevated by coapplication of the aspirin/salicylic acid metabolite, 2,5-dihydroxybenzoic acid (2,5-DHBA). Fludioxonil activity is potentiated through a mitogen-activated protein kinase (MAPK) pathway that regulates osmotic/oxidative stress-responses. 2,5-DHBA disrupts cellular GSH (reduced glutathione)/GSSG (oxidized glutathione) homeostasis, further stressing the oxidative stress-response system. This stress enhances fludioxonil activity. 2,5-DHBA treatment also prevents tolerance of MAPK mutants resistant to fludioxonil.

Original languageEnglish (US)
Pages (from-to)284-290
Number of pages7
JournalFEMS Microbiology Letters
Volume270
Issue number2
DOIs
StatePublished - May 2007

Keywords

  • 2,5-dihydroxybenzoic acid
  • Antioxidative stress system
  • Aspergillus
  • Fludioxonil
  • Saccharomyces cerevisiae

ASJC Scopus subject areas

  • Microbiology
  • Molecular Biology
  • Genetics

Fingerprint

Dive into the research topics of 'Enhancement of fludioxonil fungicidal activity by disrupting cellular glutathione homeostasis with 2,5-dihydroxybenzoic acid'. Together they form a unique fingerprint.

Cite this