Acanthamoeba is found in seawater, fresh water, and soil and is an opportunistic pathogen that causes a potentially blinding corneal infection known as Acanthamoeba keratitis. The antiamoeba activity of 9 fatty acid salts potassium butyrate C4K , caproate C6K , caprylate C8K , caprate C10K , laurate C12K , myristate C14K , oleate C18:1K , linoleate C18:2K , and linolenate C18:3K was tested on Acanthamoeba castellanii ATCC 30010 trophozoites and cysts . Fatty acid salts 350 mM and pH 10.5 were prepared by mixing fatty acids with the appropriate amount of KOH. C8K, C10K, and C12K showed growth reduction of 4 log-units 99.99% suppression in A. castellanii upon 180 min incubation at 175 mM, whereas the pH-adjusted control solution showed no effect. After the amoeba suspension was mixed with C10K or C12K, cell membrane destruction was observed. The minimum inhibitory concentration of C10K and C12K was also determined to be 2.7 mM. Confirmation tests were conducted using contact lenses to evaluate the effectiveness of C10K and C12K as multi-purpose solutions. Experiments using increasing concentrations showed reduced numbers of living cells in C10K 5.5 mM, 10.9 mM and in C12K 5.5 mM, 10.9 mM . These results demonstrate the inhibitory activity of C10K and C12K against A. castellanii and indicate their potential as anti-amoeba agents.

In this study, we investigated the relationship between MgSO(4) and luminescence in Vibrio fischeri under nutrient-starved conditions. When V. fischeri was cultured in an artificial seawater medium, the luminescence intensity was low relative to that observed under normal growth conditions. It decreased during the initial 14 h, and then increased slightly at 24 h. This regulation of luminescence was not dependent on the quorum-sensing mechanism, because the cell densities had not reached a critical threshold concentration. Under MgSO(4)-starved conditions, luminescence was not fully induced at 14 h, and decreased at 24 h. In contrast, induction of luminescence occurred under MgSO(4)-supplemented conditions, but MgSO(4) alone was insufficient to induce luminescence, and required NaHCO(3) or KCl. These results suggest that the luminescence of V. fischeri is controlled by an exogenous sulfur source under nutrient-starved conditions. In addition, they indicate that the induction of sulfur-dependent luminescence is regulated by the NaHCO(3) or KCl concentration.

The antifungal activity of nine fatty acid salts (butyrate, caproate, capr ylate, caprate, laurate, myristate, oleate, linoleate, and linolenate) was tested on the spores of Penicillium pinophilum NBRC 6345 and Penicillium digitatum NBRC 9651. Potassium caprate showed the strongest antifungal activity at 4 log-units. At incubation times of 180 min, potassium capr ylate and potassium laurate showed antifungal activities of 2 log-units against P. pinophilum NBRC 6345. These results suggest medium-chain fatty acid salts showed the highest antifungal activity. The minimum inhibitor y concentration of potassium caprate against P. pinophilum NBRC 6345 was 175 mM, and >175 mM for other fatty acid salts. When mixed with short-chain fatty acid salts (potassium butyrate, potassium caproate) or medium-chain fatty acid salts (potassium capr ylate or potassium laurate), potassium caprate caused a 4 log-unit reduction in fungal growth; however, when mixed with long-chain fatty acid salts (potassium myristate, potassium oleate, potassium linoleate, or potassium linolenate) it had no antifungal effect. Thus, long-chain fatty acid salts inhibited antifungal activity of C10K. We also evaluated the ability of C10K to inhibit fungal growth on orange rind. C10K effectively inhibited P. pinophilum NBRC 6345 growth on orange rind. Thus, C10K shows promise as an antifungal agent.

Fatty acid salts are a type of surfactant known to have potent antibacterial activity. We therefore examined the antibacterial activities of fatty acid salts against Streptococcus mutans. Potassium caprylate (C10K), potassium laurate (C12K), potassium myristate (C14K), potassium oleate （C18:1K), potassium linoleate (C18:2K), and potassium linolenate (C18:3K), used at a concentration of 175 mM, resulted in a 7 log-unit reduction of S. mutans after a 10-min incubation. The minimum inhibitory concentration (MIC) of C18:2K and C18:3K was 5.5 mM. C12K also demonstrated high antibacterial activity (MIC of 21.9 mM). These results indicate that C12K, C18:2K, and C18:3K have high antibacterial activity against S. mutans, and possess great potential as antibacterial agents.

In spite of its central importance in research efforts, the relationship between seawater compounds and bacterial luminescence has not previously been investigated in detail. Thus, in this study, we investigated the effect of cations (Na(+) , K(+) , NH(4) (+) , Mg(2+) , and Ca(2+) ) and anions (Cl(-) , HCO(3) (-) , CO(3) (2-) , and NO(3) (-) ) on the induction of both inorganic (sulfate, sulfite, and thiosulfate) and organic (L-cysteine and L-cystine) sulfur-dependent luminescence in Vibrio fischeri. We found that HCO(3) (-) (bicarbonate) and CO(3) (2-) (carbonate), in the form of various compounds, had a stimulatory effect on sulfur-dependent luminescence. The luminescence induced by bicarbonate was further promoted by the addition of magnesium. Potassium also increased sulfur-dependent luminescence when sulfate or thiosulfate was supplied as the sole sulfur source, but not when sulfite, L-cysteine, or L-cystine was supplied. The positive effect of potassium was accelerated by the addition of magnesium and/or calcium. Furthermore, the additional supply of magnesium improved the induction of sulfite- or L-cysteine-dependent luminescence, but not the l-cystine-dependent type. These results suggest that sulfur-dependent luminescence of V. fischeri under nutrient-starved conditions is mainly controlled by bicarbonate, carbonate, and potassium. In addition, our results indicate that an additional supply of magnesium is effective for increasing V. fischeri luminescence.