Inhibitory action of a non-metabolizable fatty acid on the growth of Escherichia coli: role of metabolism and outer membrane integrity

Abstract

The inhibitory action of decanoic acid on both Escherichia coli K-12/154 (normal lipopolysaccharide) and E. coli RC59 (defective lipopolysaccharide) was studied. A correlation was found between the doubling time of E. coli 154 growing in different media and the lethal effect of 0.4% decanoic acid on this bacterium. Decanoic acid (0.4%) exerted a lytic action on glucose-starved and NaN 1-inhibited cells of E. coli 154 and RC59. Exponentially growing cultures of both strains were not affected by the addition of 0.4% methyldecanoate, but cells of E. coli RC59 reaching the stationary phase were attacked by that compound. A bactericidal action of 0.4% methyldecanoate on exponential E. coli 154 and RC59 was observed when sodium azide was also present in the media. Concentrations lower than 0.01% methyldecanoate had a lytic effect on spheroplasts from E. coli 154 and RC59. These results indicate that the inhibitory action of a non-metabolizable fatty acid on E. coli depends on the cellular metabolic activity and the outer membrane integrity. We previously reported that the extent of growth inhibition by fatty acids in Escherichia coli K-12 and other E. coli strains was dependent on many variables, including the chain length and fatty acid concentration, as well as the growth phase and culture medium in which the bacteria were grown (8). These latter facts suggest that in addition to the mechanisms of

Identification of β-oxidation and thioesterase activities in Staphylococcus carnosus 833 strain

“…The growth of S. carnosus 833 was largely independent of the chain length of the methyl ester (3.5 mM) with only a small increase in the growth rate (W) in the presence of methyl decanoate, methyl laurate and methyl oleate and a small decrease for methyl palmitate (Table 1). These results are consistent with those obtained in Escherichia coli for which methyl decanoate (23.2 mM) had no e¡ect on growth [10,11]. Those authors reported an inhibitory e¡ect of free decanoic acid.…”

Chemostat‐based proteomic analysis of toluene‐affected Pseudomonas putida S12

“…Two phenomena that lower the energy status of the cell could account for these effects. Firstly, the presence of toxic levels of toluene severely perturbs the membrane, bringing about the passive flux of protons across the membrane (Fay and Farias, 1977; Leao and Van Uden, 1984; Cartwright et al ., 1986; Sikkema et al ., 1994), thus dissipating the PMF (Cartwright et al ., 1986; Sikkema et al ., 1994). Secondly, toluene induces expression of the solvent‐resistance pump SrpABC (Kieboom et al ., 1998a,b), which is a proton‐dependent solvent‐efflux system (Isken and de Bont, 1996; Isken et al ., 1999).…”

Arachidonic acid and other unsaturated fatty acids and some of their metabolites function as endogenous antimicrobial molecules: A review

“…Human fecal lipids contain a mixture of long chain free fatty acids such as C16:0, C I8:1, C18:2, and C 20 or more, which are bactericidal for gonococci [24] . The mechanism of the antimicrobial action of AA seems to be by inducing leakage and even lysis of bacterial cell membranes [25] , [26] as well as various cellular metabolic effects, including but not limited to inhibition of respiratory activity, effects on transportation of amino acids, and uncoupling of oxidative phosphorylation [27] , [28] , [29] , [30] .…”