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Lactobacillus sakei subsp. sakei 2a is a bacteriocinogenic lactic acid bacteria isolated from a Brazilian meat product, capable to inhibit Listeria monocytogenes in vitro and in foods. In this study, bacteriocin produced by this strain were encapsulated in phosphatidylcholine (FC) and 1,2-dioleoyloxy-3-trimethylammonium-propane (DOTAP) liposomes, separately and in combination, were characterized and evaluated for activity against L. monocytogenes in vitro and in experimentally contaminated UHT goat milk, during storage at 7 °C for 14 days and 30 °C for 24 h. The FC and DOTAP/FC (3:1) nanovesicles containing bacteriocins (12.800 AU mL −1 ) presented zeta potential of −1.54 and + 38.13 mV, Entrapment Efficiency of 80.0% and 94.1%, and diameter of 91.19 and 81.49 nm, respectively. DOTAP/FC nanovesicle presented excellent stability, and maintained the same physicochemical characteristics over 28 days. Both free and encapsulated bacteriocins controlled L. monocytogenes growth in BHI medium and goat milk stored at 30 °C for at least 8 h, in a similar pattern. After 24 h in BHI medium, bacteriocins encapsulated in FC nanovesicles were more effective ( p < 0.05 ) than free bacteriocins. However, in goat milk, no significant differences ( p ≥ 0.05 ) were observed for the two types of nanovesicles. At 7 °C, both free and encapsulated bacteriocins retarded the L. monocytogenes growth, and after 5 days, counts were 5 log lower than in the controls, both in BHI and in goat milk. Encapsulation of bacteriocin in FC and DOTAP/FC nanovesicles did not affect the antimicrobial activity, but the advantages of their application for control of L. monocytogenes in goat milk based dairy products, when compared to free bacteriocins, remain unclear and more studies are needed. [ABSTRACT FROM AUTHOR]

Nitric oxide (NO)-releasing nonsteroidal anti-inflammatory drugs (NSAIDs) have been developed to overcome the gastrointestinal and cardiovascular toxicity of NSAIDs, by chemically associating a NO-releasing moiety with commercial NSAIDs. Since increasing evidence supports that NSAIDs toxicity is related to their topical actions in membrane lipids, this work aims to evaluate the impact of adding a NO-releasing moiety to parent NSAIDs regarding their effect on lipid bilayers. Thus, the interactions of NO-indomethacin and indomethacin (parent drug) with 1,2-dimyristoyl- sn -glycero-3-phosphocholine (DMPC) bilayers were described herein at pH 3.0 and 7.4. Diverse experimental techniques were combined to characterize the partitioning and location of drugs in DMPC bilayers, and to analyze their effect on the lipid phase transition and the bilayer structure and dynamics. The partitioning of NO-indomethacin into DMPC bilayers was similar to that of charged indomethacin and smaller than that of neutral indomethacin. Both drugs were found to insert the DMPC bilayer and the membrane location of indomethacin was pH-dependent. NO-indomethacin and indomethacin induced a decrease of the main phase transition temperature of DMPC. The effect of these drugs on the bilayer structure and dynamics was dependent on diverse factors, namely drug ionization state, drug:lipid molar ratio, temperature and lipid phase. It is noteworthy that NO-indomethacin induced more pronounced alterations in the biophysical properties of DMPC bilayers than indomethacin, considering equivalent membrane concentrations. Such modifications may have in vivo implications, particularly in the gastric mucosa, where NO-NSAIDs-induced changes in the protective properties of phospholipid layers may contribute to the occurrence of adverse effects. [ABSTRACT FROM AUTHOR]

Abstract: DD K is an antimicrobial peptide previously isolated from the skin of the amphibian Phyllomedusa distincta. The effect of cholesterol on synthetic DD K binding to egg lecithin liposomes was investigated by intrinsic fluorescence of tryptophan residue, measurements of kinetics of 5(6)-carboxyfluorescein (CF) leakage, dynamic light scattering and isothermal titration microcalorimetry. An 8nm blue shift of tryptophan maximum emission fluorescence was observed when DD K was in the presence of lecithin liposomes compared to the value observed for liposomes containing 43mol% cholesterol. The rate and the extent of CF release were also significantly reduced by the presence of cholesterol. Dynamic light scattering showed that lecithin liposome size increase from 115 to 140nm when titrated with DD K but addition of cholesterol reduces the liposome size increments. Isothermal titration microcalorimetry studies showed that DD K binding both to liposomes containing cholesterol as to liposomes devoid of it is more entropically than enthalpically favored. Nevertheless, the peptide concentration necessary to furnish an adjustable titration curve is much higher for liposomes containing cholesterol at 43mol% (2mmolL−1) than in its absence (93μmolL−1). Apparent binding constant values were 2160 and 10,000Lmol−1, respectively. The whole data indicate that DD K binding to phosphatidylcholine liposomes is significantly affected by cholesterol, which contributes to explain the low hemolytic activity of the peptide. [Copyright &y& Elsevier]