Furthermore, sodium lactate exacerbated growth inhibition by LA,

Furthermore, sodium selleck compound lactate exacerbated growth inhibition by LA, in a similar manner to that observed with B. proteoclasticus [23], but had no similar effect on the influence of LA on cell integrity of B. fibrisolvens. A similar conclusion was reached by Maia et al. [17] when comparing the toxic effects of fatty acids on growth and cell integrity in different species of ruminal bacteria. Thus, although a toxic mechanism involving disruption of the extraordinarily thin cell envelope of B. fibrisolvens Salubrinal cell line [35] seems an attractive

and logical possibility, the evidence suggests that the primary effect of PUFA lies elsewhere. An alternative possibility is that the ready diffusion of the free fatty acid across the membrane causes chemiosmotic difficulties, perhaps uncoupling the proton-motive force [36], dissipating the membrane potential by facilitating ion leakage [37] or decoupling intramembrane pathways [38, 39]. While this remains a possibility, the different

effects on acyl CoA and ATP pools on PUFA toxicity suggest a metabolic effect, specifically in acyl CoA metabolism. Measurement of CoA metabolic pools in bacteria is relatively rare. Here, acetyl CoA and butyryl CoA were present at highest concentration and the butyrate pathway intermediates at much lower concentrations, as found also in Clostridium acetobutylicum [40]. All acyl CoAs except acetoacetyl CoA were diminished by PRN1371 molecular weight >96% when LA was added to the medium. In contrast, the ATP pool was affected later than acyl CoA pools, and remained at about one-third of the control values, presumably due to the contribution of glycolysis. The toxicity of PUFA in different species of ruminal bacteria was found to be related partly to whether the bacteria produced www.selleck.co.jp/products/Neratinib(HKI-272).html butyrate; cellulolytic bacteria were the other most sensitive species [17]. Within the Butyrivibrio phylogenetic group, the most sensitive species were those that formed butyrate via the butyrate kinase mechanism rather than acyl CoA transferase [16].

Thus, there seems to be a connection between PUFA toxicity and butyrate formation. A metabonomic analysis [41] might help to identify precisely where the PUFA act. It may also be instructive to determine why trans-11, cis-15-18:2, a product of LNA metabolism, appeared to permit growth while the other dienoic acid investigated here did not. The influence of sodium lactate in lengthening the lag phase indicates that lactate potentiates the toxic effects of PUFA in B. fibrisolvens, as shown previously with B. proteoclasticus [22]. Such a high concentration of lactate (70 mM) would only occur in animals suffering acidosis [42]. The toxicity may be an osmotic effect, or due to a leakage of ions across the membrane, or may even be a metabolic effect. Lactate is a major product of glucose metabolism in B.

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