Concentrations Of Caprylic Acid Research Articles

In Vitro Inactivation of Salmonella Enteritidis in Autoclaved Chicken Cecal Contents by Caprylic Acid

Contamination of poultry and poultry products by Salmonella Enteritidis is a serious problem worldwide. The effects of caprylic acid (50 and 100 mM) on S. Enteritidis in autoclaved chicken cecal contents and tryptic soy broth at 40°C was studied. Both concentrations of caprylic acid reduced the population of S. Enteritidis by ~5.0 log10 cfu/mL within 1 min, with complete inactivation of the pathogen at 24 h. Results of the study revealed that caprylic acid was highly effective in killing S. Enteritidis in autoclaved chicken cecal contents in a rapid time frame.

In vitro effect of C2-C18 fatty acids on Salmonellas.

The susceptibility of Salmonella spp. to 15 fatty acids was determined in vitro in cultures grown on glucose. Antimicrobial activity was expressed as IC50 (a concentration at which only 50% of the initial glucose in cultures was utilized). Caprylic acid was the only acid inhibiting glucose utilization. In cultures of S. enteritidis, S. infantis and S. typhimurium, IC50 of caprylic acid ranged from 0.75 to 1.17 mg/mL. A moderate adaptation effect was observed as these values increased 1.5-1.8 times when bacteria were subcultured 10 times in media containing a low concentration of caprylic acid (1/3 IC50). No effect of calcium ions added in excess on antimicrobial activity of caprylic acid was observed. Incubation of salmonellas with caprylic acid (1 mg/mL; 30 min) at pH 5.2-5.3 led to a reduction in the concentration of viable cells below the detection limit; 2-6% of Salmonella cells survived at pH 6.3-6.6.

Death Kinetics for Escherichia coli Cells Heated in the Presence of Short- and Medium-Chain Fatty Acids.

We investigated the death kinetics for Escherichia coli K12 cells heated at different temperatures in the presence of saturated fatty acids having short and medium alkyl-chain lengths at various concentrations. Apparent first-order death kinetics were observed with cells heated in the presence of caproic acid, caprylic acid, capric acid, or lauric acid. Values of activation enthalpy and activation entropy of the death reaction decreased with an increase in the concentration of caprylic acid, capric acid, and lauric acid, but did not decrease much for caproic acid. Also, the value of dilution coefficient decreased with increasing heating temperature for the former three fatty acids but was not noticeably temperature dependent for caproic acid. These results suggest that there are two distinct modes for the death reaction of E. coli cells heated in the presence of fatty acids and that the hydrophobicity based on the alkyl-chain length of fatty acid molecule is responsible for such a difference in the death kinetics.

Caprylic acid fractionation of hyperimmune horse plasma: Description of a simple procedure for antivenom production

G. Rojas, J. M. Jiménez and J. M. Gutiérrez. Caprylic acid fractionation of hyperimmune horse plasma: description of a simple procedure for antivenom production. Toxicon 32, 351–363, 1994.—A simple methodology for hyperimmune horse plasma fractionation, based on caprylic acid precipitation, is described. Optimal conditions for fractionation were studied; the method gives best results when concentrated caprylic acid was added to plasma, whose pH had been adjusted to 5.8, until a final caprylic acid concentration of 5% was reached. The mixture was vigorously stirred during caprylic acid addition and then for 60 min; afterwards the mixture was filtered. Non-immunoglobulin proteins precipitated in these conditions, whereas a highly enriched immunoglobulin preparation was obtained in the filtrate, which was then dialysed to remove caprylic acid before the addition of NaCl and phenol. Thus, antivenom was produced after a single precipitation step followed by dialysis. In order to compare this methodology with that based on ammonium sulfate fractionation, a sample of hyperimmune plasma was divided into two aliquots which were fractionated in parallel by both methods. It was found that caprylic acid-fractionated antivenom was superior in terms of yield, production time, albumin/globulin ratio, turbidity, protein aggregates, electrophoretic pattern and neutralizing potency against several activities of Bothrops asper venom. Owing to its efficacy and simplicity, this method could be of great value in antivenom and antitoxin production laboratories.

Cellular mechanism of caprylic acid-induced growth hormone suppression

To determine the dynamic secretory pattern of growth hormone (GH) in the presence of free fatty acids (FFA), we studied the effect of caprylic acid on basal and rGRF(1-29)NH 2 (GRF)-induced GH secretion in acutely dispersed and perifused rat pituitary cells. At a concentration of 3.0 mmol/L, caprylic acid inhibited both basal ( P < .05) and GRF-stimulated GH secretions ( P < .01), except when the maximal (near the EC 100) GRF concentration of 100 pmol/L was used. Lower concentrations of caprylic acid such as 0.3 and 1.0 mmol/L significantly inhibited, in a concentration-dependent manner, GH secretion induced by a 6.25-pmol/L GRF. However, at a GRF concentration of 25 pmol/L, this inhibitory effect was abolished. The time-course of GH response to GRF was similar in both control and caprylic acid-treated cells. To elucidate the mechanism(s) of action of the caprylic acid-induced blockade of GH secretion, we studied, in 3-day cultured rat pituitary cells, the effect of caprylic acid on basal and GRF-stimulated GH and 3′,5′-cyclic adenosine monophosphate (cAMP) release. We also tested its effect on the Ca 2+ ionophore, A23187-induced GH release. Caprylic acid (0.3 to 3.0 mmol/L) significantly inhibited basal GH release and GRF- or A23187-induced GH secretion. Furthermore, it decreased both basal and GRF-stimulated cAMP release ( P < .05). In addition, the effect of caprylic acid on rGRF(1-29)NH 2 affinity to GRF pituitary binding sites was determined using [ 125I-Tyr 10]hGRF(1-44)NH 2 as radioligand. This affinity was markedly diminished at 3 mmol/L caprylic acid, shifting IC 50 of competition curves performed with increasing rGRF(1-29)NH 2 concentrations (0 to 2.4 μmol/L) from 0.87 ± 0.14 nmol/L to 3.05 ± 0.65 nM ( P < .02). Finally, basal prolactin (PRL) secretion was not altered at a low caprylic acid concentration (0.3 mmol/L), while it was significantly decreased in the presence of 3.0 mmol/L caprylic acid ( P < .001). In summary, this study demonstrates that caprylic acid affects GH release by interfering with GRF receptors and altering adenylate cyclase-cAMP and calcium channel systems.

Effects of exogenous fatty acids on calcium uptake by brush-border membrane vesicles from rabbit small intestine

The uptake of a variety of fatty acids by isolated brush-border membranes from rabbit small intestine was studied. This uptake increased with acyl chain-length and was not diminished by washing of the lipid-treated membranes with 0.25 M CsBr. The binding of fatty acid was not accompanied by a decrease in endogenous acyl groups or of cholesterol and therefore corresponded to a net uptake accountable qualitatively and quantitatively by the fatty acid added to the membranes. The uptake of Ca 2+ was stimulated by treatment of the membranes with low concentrations of unsaturated fatty acids (0.05 mM) as well as with various concentrations of caprylic acid (0.10–3.00 mM) and inhibited by treatment with higher concentrations of unsaturated fatty acids (0.20–0.60 mM). Saturated fatty acids had no marked effects on Ca 2+ uptake. The stimulatory concentrations of unsaturated fatty acids did not change the Ca 2+-binding characteristics of the membranes, whereas the higher concentrations decreased equilibrium binding of Ca 2+ and very probably the number of high-affinity binding sites. The results of this study are assessed in terms of the effects of normal fatty acids found in the diet on the absorptive properties of the brush-border membranes.