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Induction of oxidative stress as a possible mechanism of the antifungal action of three phenylpropanoids.

Authors
  • Khan, Amber
  • Ahmad, Aijaz
  • Akhtar, Feroz
  • Yousuf, Snowber
  • Xess, Immaculata
  • Khan, Luqman Ahmad
  • Manzoor, Nikhat
Type
Published Article
Journal
FEMS Yeast Research
Publisher
Oxford University Press
Publication Date
Feb 01, 2011
Volume
11
Issue
1
Pages
114–122
Identifiers
DOI: 10.1111/j.1567-1364.2010.00697.x
PMID: 21114624
Source
Medline
License
Unknown

Abstract

The increasing incidence of hospital-acquired infections caused by drug-resistant pathogens, host toxicity, the poor efficacy of drugs and high treatment costs has drawn attention to the potential of natural products as antifungals in mucocutaneous infections and combinational therapies. Moreover, cellular and subcellular targets for these compounds may provide better options for the development of novel antifungal therapies. Eugenol, methyl eugenol and estragole are phenylpropanoids found in essential oil. They are known to possess pharmacological properties including antimicrobial activity. Induction of oxidative stress characterized by elevated levels of free radicals and an impaired antioxidant defence system is implicated as a possible mechanism of cell death. An insight into the mechanism of action was gained by propidium iodide cell sorting and oxidative stress response to test compounds in Candida albicans. The extent of lipid peroxidation (LPO) of cytoplasmic membranes was estimated to confirm a state of oxidative stress. Activity levels of primary defence enzymes and glutathione were thus further determined. Whereas these compounds cause fungal cell death by disrupting membrane integrity at minimum inhibitory concentrations (MIC), sub-MIC doses of these compounds significantly impair the defence system in C. albicans. The study has implications for understanding microbial cell death caused by essential oil components eliciting oxidative stress in Candida. The formation of membrane lesions by these phenylpropanoids thus appears to be the result of free radical cascade-mediated LPO.

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