2009
DOI: 10.1128/jb.00164-09
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Abstract: In this report we provide evidence that the antimicrobial action of stannous salts and a gold drug, auranofin, against Treponema denticola is mediated through inhibition of the metabolism of selenium for synthesis of selenoproteins.

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Cited by 38 publications
(29 citation statements)
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“…Jackson-Rosario et al demonstrated that auranofin binds selenium, a catalyst in energy metabolism that affects redox balance [9,11]. Investigation of microbial inhibition by auranofin has provided evidence that the drug binds to hydrogen selenide, blocking selenium utilization by bacteria, preventing selenoprotein synthesis [9].…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…Jackson-Rosario et al demonstrated that auranofin binds selenium, a catalyst in energy metabolism that affects redox balance [9,11]. Investigation of microbial inhibition by auranofin has provided evidence that the drug binds to hydrogen selenide, blocking selenium utilization by bacteria, preventing selenoprotein synthesis [9].…”
Section: Discussionmentioning
confidence: 99%
“…As an anti-inflammatory compound, auranofin has been used to treat arthritic conditions and previous groups indicate that auranofin can exhibit antimicrobial activities. Bacterial pathogens found to be susceptible to auranofin include Clostridium difficile, Treponema denticola and Pseudomonas putida [9][10][11]. Both C. difficile and T. denticola had a reduction in selenoproteins, as a result of auranofin exposure and investigation of microbial inhibition by auranofin has provided evidence that the drug binds to hydrogen selenide, blocking selenium utilization by bacteria, preventing selenoprotein synthesis [9].…”
mentioning
confidence: 99%
“…Auranofin has been reported for its activity against some bacteria, cancer cell lineages and parasites (Kean et al, 1997;Lobanov et al, 2006;Kuntz et al, 2007;Sannella et al, 2008;Jackson-Rosario et al, 2009;Jackson-Rosario and Self, 2009;Chen et al, 2009;Angelucci et al, 2009;Martínez-González et al, 2010) including very recently to Leishmania cells (Sharlow et al, 2013). The mechanism of action of this drug has been proposed to be a result of the interaction of Gold with the Cys residues of Thioredoxin-Glutathione Reductase (TGR) and likely the interaction of Gold and the catalytically active selenium-containing Sec residue of TGR selenoprotein (Angelucci et al, 2009).…”
Section: Discussionmentioning
confidence: 98%
“…Indeed, tungstate did inhibit biofilm formation, suggesting that inactivation of the biosynthesis of the Mo cofactor does lead to the inability of the cell to form a biofilm. We have recently shown that the rheumatoid drug auranofin can block the metabolism of selenium to selenophosphate by forming an adduct to hydrogen selenide in Clostridium difficile, E. coli, and Treponema denticola (31,32). Exposure of E. faecalis to auranofin also inhibited biofilm formation, suggesting strongly that selenium is required for biofilm formation in this organism.…”
Section: Vol 193 2011 Sdmh Contributes To Biofilm Formation In E Fmentioning
confidence: 99%