Document Detail

Glutathione Modulates the Toxicity of, but is not a Biologically Relevant Reductant for, the Pseudomonas aeruginosa Redox Toxin Pyocyanin.
MedLine Citation:
PMID:  21255639     Owner:  NLM     Status:  Publisher    
Pyocyanin is an important redox toxin produced by the common human pathogen Pseudomonas aeruginosa. It generates reactive oxygen species (ROS) that alter intracellular redox status and cell function. Reducing equivalents for pyocyanin are provided by intracellular NAD(P)H and, it has been reported, glutathione (GSH). Cellular GSH levels are at least 1-2 orders of magnitude greater than NAD(P)H therefore GSH should represent the major reductant for pyocyanin and potentiate its toxicity. Paradoxically, GSH has been found to inhibit pyocyanin toxicity in cellular models. This study was undertaken to evaluate the potential of GSH as a biologically relevant reductant for pyocyanin. Using spectrophotometry, under aerobic conditions pyocyanin readily oxidized NADPH while oxidation of GSH could not be detected. Under anaerobic conditions pyocyanin was reduced by NADPH while reduction by GSH could not be detected. Reduction of molecular oxygen and the formation of ROS readily proceeded in the presence of pyocyanin and NADPH while GSH was without effect. Finally, exposure of normal human dermal fibroblasts to sub-cytotoxic concentrations of pyocyanin did not lead to depletion of endogenous GSH while exogenous GSH provided protection against the senescence-inducing effects of the toxin. In summary, GSH does not reduce pyocyanin under physiologically relevant conditions or contribute to pyocyanin toxicity. However, GSH does provide protection against the deleterious effects of this important bacterial toxin towards mammalian cells.
Michael Muller
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2011-1-18
Journal Detail:
Title:  Free radical biology & medicine     Volume:  -     ISSN:  1873-4596     ISO Abbreviation:  -     Publication Date:  2011 Jan 
Date Detail:
Created Date:  2011-1-24     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8709159     Medline TA:  Free Radic Biol Med     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2010. Published by Elsevier Inc.
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