OBJECTIVES: To assess the effect of triclosan on fatty acid synthesis and to relate the inhibition of enoyl reductase to bacterial viability. METHODS: The effect of triclosan on fatty acid synthesis in a triclosan-resistant Escherichia coli and its sensitive counterpart and in Pseudomonas aeruginosa was investigated by measuring acetate incorporation into total lipid followed by analysis of fatty acid methyl esters by gas chromatography. Concurrently, the bactericidal effect of triclosan against these bacterial strains was assessed. RESULTS: Triclosan inhibited fatty acid biosynthesis in all the strains tested. However, for triclosan-resistant E. coli (MIC > 1000 mg/L) the concentration required to achieve inhibition was higher than that required for the susceptible counterpart. These concentrations did not significantly affect cell survival in any of the strains tested. CONCLUSIONS: This study shows that the inhibition of fatty acid biosynthesis by the bisphenol might be involved in its growth-inhibitory action and that other mechanisms are involved in its lethal effect. In addition, although microorganisms with a high triclosan MIC were still susceptible to the inhibitory effect of the bisphenol on fatty acid biosynthesis, a higher concentration of the compound was required. This suggested that triclosan bioavailability was different in these strains.
OBJECTIVES: To assess the effect of triclosan on fatty acid synthesis and to relate the inhibition of enoyl reductase to bacterial viability. METHODS: The effect of triclosan on fatty acid synthesis in a triclosan-resistant Escherichia coli and its sensitive counterpart and in Pseudomonas aeruginosa was investigated by measuring acetate incorporation into total lipid followed by analysis of fatty acid methyl esters by gas chromatography. Concurrently, the bactericidal effect of triclosan against these bacterial strains was assessed. RESULTS:Triclosan inhibited fatty acid biosynthesis in all the strains tested. However, for triclosan-resistant E. coli (MIC > 1000 mg/L) the concentration required to achieve inhibition was higher than that required for the susceptible counterpart. These concentrations did not significantly affect cell survival in any of the strains tested. CONCLUSIONS: This study shows that the inhibition of fatty acid biosynthesis by the bisphenol might be involved in its growth-inhibitory action and that other mechanisms are involved in its lethal effect. In addition, although microorganisms with a high triclosan MIC were still susceptible to the inhibitory effect of the bisphenol on fatty acid biosynthesis, a higher concentration of the compound was required. This suggested that triclosan bioavailability was different in these strains.
Authors: Nicola L Cowley; Sarah Forbes; Alejandro Amézquita; Peter McClure; Gavin J Humphreys; Andrew J McBain Journal: Appl Environ Microbiol Date: 2015-08-07 Impact factor: 4.792
Authors: Laura Knapp; Alejandro Amézquita; Peter McClure; Sara Stewart; Jean-Yves Maillard Journal: Appl Environ Microbiol Date: 2015-01-30 Impact factor: 4.792
Authors: Gilles Bedoux; Benoit Roig; Olivier Thomas; Virginie Dupont; Barbara Le Bot Journal: Environ Sci Pollut Res Int Date: 2011-11-05 Impact factor: 4.223
Authors: Suresh K Tipparaju; Debbie C Mulhearn; Gary M Klein; Yufeng Chen; Subhasish Tapadar; Molly H Bishop; Shuo Yang; Juan Chen; Mahmood Ghassemi; Bernard D Santarsiero; James L Cook; Mary Johlfs; Andrew D Mesecar; Michael E Johnson; Alan P Kozikowski Journal: ChemMedChem Date: 2008-08 Impact factor: 3.466