Food Preservatives: Substances capable of inhibiting, retarding or arresting the process of fermentation, acidification or other deterioration of foods.Sorbic Acid: Mold and yeast inhibitor. Used as a fungistatic agent for foods, especially cheeses.Preservatives, Pharmaceutical: Substances added to pharmaceutical preparations to protect them from chemical change or microbial action. They include ANTI-BACTERIAL AGENTS and antioxidants.Nisin: A 34-amino acid polypeptide antibiotic produced by Streptococcus lactis. It has been used as a food preservative in canned fruits and vegetables, and cheese.Benzoic Acid: A fungistatic compound that is widely used as a food preservative. It is conjugated to GLYCINE in the liver and excreted as hippuric acid.Bacteriocins: Substances elaborated by specific strains of bacteria that are lethal against other strains of the same or related species. They are protein or lipopolysaccharide-protein complexes used in taxonomy studies of bacteria.Pharmaceutic Aids: Substances which are of little or no therapeutic value, but are necessary in the manufacture, compounding, storage, etc., of pharmaceutical preparations or drug dosage forms. They include SOLVENTS, diluting agents, and suspending agents, and emulsifying agents. Also, ANTIOXIDANTS; PRESERVATIVES, PHARMACEUTICAL; COLORING AGENTS; FLAVORING AGENTS; VEHICLES; EXCIPIENTS; OINTMENT BASES.Benzalkonium Compounds: A mixture of alkylbenzyldimethylammonium compounds. It is a bactericidal quaternary ammonium detergent used topically in medicaments, deodorants, mouthwashes, as a surgical antiseptic, and as a as preservative and emulsifier in drugs and cosmetics.Parabens: Methyl, propyl, butyl, and ethyl esters of p-hydroxybenzoic acid. They have been approved by the FDA as antimicrobial agents for foods and pharmaceuticals. (From Hawley's Condensed Chemical Dictionary, 11th ed, p872)Food: Any substances taken in by the body that provide nourishment.Chlorobutanol: A colorless to white crystalline compound with a camphoraceous odor and taste. It is a widely used preservative in various pharmaceutical solutions, especially injectables. Also, it is an active ingredient in certain oral sedatives and topical anesthetics.Thimerosal: An ethylmercury-sulfidobenzoate that has been used as a preservative in VACCINES; ANTIVENINS; and OINTMENTS. It was formerly used as a topical antiseptic. It degrades to ethylmercury and thiosalicylate.Benzethonium: Bactericidal cationic quaternary ammonium surfactant used as a topical anti-infective agent. It is an ingredient in medicaments, deodorants, mouthwashes, etc., and is used to disinfect apparatus, etc., in the food processing and pharmaceutical industries, in surgery, and also as a preservative. The compound is toxic orally as a result of neuromuscular blockade.
Preservative: A preservative is a substance that is added to products such as foods, pharmaceuticals, paints, biological samples, wood, beverages etc. to prevent decomposition by microbial growth or by undesirable chemical changes.Sodium sorbate: Sodium sorbate is the sodium salt of sorbic acid.Biocidal Products DirectiveNisinBacteriocin: Bacteriocins are proteinaceous toxins produced by bacteria to inhibit the growth of similar or closely related bacterial strain(s). They are phenomenologically analogous to yeast and paramecium killing factors, and are structurally, functionally, and ecologically diverse.Fenclozic acidRoccal-D: Roccal-D is a disinfectant manufactured by Pfizer that is used in many animal care facilities and some biological laboratories. It is effective against bacteria including Mycoplasma, Streptococcus, Staphylococcus, E.ButylparabenBanquet Foods: Banquet Foods is a subsidiary of ConAgra Foods that sells various food products, including frozen pre-made entrées, meals, and desserts.ChlorobutanolJoint Committee on Vaccination and Immunisation: The Joint Committee on Vaccination and Immunisation (JCVI) is an independent expert advisory committee of the United Kingdom Department of Health. JCVI was established, in 1963, "To advise the Secretaries of State for Health, Scotland, Wales and Northern Ireland on matters relating to communicable diseases, preventable and potentially preventable through immunisation.Quaternary ammonium cation: Quaternary ammonium cations, also known as quats, are positively charged polyatomic ions of the structure NR4+, R being an alkyl group or an aryl group. Unlike the ammonium ion (NH4+) and the primary, secondary, or tertiary ammonium cations, the quaternary ammonium cations are permanently charged, independent of the pH of their solution.
(1/138) Ubiquinol:cytochrome c oxidoreductase. Effects of inhibitors on reverse electron transfer from the iron-sulfur protein to cytochrome b.
The effects of inhibitors on the reduction of the bis-heme cytochrome b of ubiquinol: cytochrome c oxidoreductase (complex III, bc1 complex) has been studied in bovine heart submitochondrial particles (SMP) when cytochrome b was reduced by NADH and succinate via the ubiquinone (Q) pool or by ascorbate plus N,N,N', N'-tetramethyl-p-phenylenediamine via cytochrome c1 and the iron-sulfur protein of complex III (ISP). The inhibitors used were antimycin (an N-side inhibitor), beta-methoxyacrylate derivatives, stigmatellin (P-side inhibitors), and ethoxyformic anhydride, which modifies essential histidyl residues in ISP. In agreement with our previous findings, the following results were obtained: (i) When ISP/cytochrome c1 were prereduced or SMP were treated with a P-side inhibitor, the high potential heme bH was fully and rapidly reduced by NADH or succinate, whereas the low potential heme bL was only partially reduced. (ii) Reverse electron transfer from ISP/c1 to cytochrome b was inhibited more by antimycin than by the P-side inhibitors. This reverse electron transfer was unaffected when, instead of normal SMP, Q-extracted SMP containing 200-fold less Q (0. 06 mol Q/mol cytochrome b or c1) were used. (iii) The cytochrome b reduced by reverse electron transfer through the leak of a P-side inhibitor was rapidly oxidized upon subsequent addition of antimycin. This antimycin-induced reoxidation did not happen when Q-extracted SMP were used. The implications of these results on the path of electrons in complex III, on oxidant-induced extra cytochrome b reduction, and on the inhibition of forward electron transfer to cytochrome b by a P-side plus an N-side inhibitor have been discussed. (+info)
(2/138) Nisin promotes the formation of non-lamellar inverted phases in unsaturated phosphatidylethanolamines.
Nisin, a peptide used as a food preservative, is shown, by 31P-nuclear magnetic resonance and infrared spectroscopy, to perturb the structure of membranes formed of unsaturated phosphatidylethanolamine (PE) and to induce the formation of inverted non-lamellar phases. In the case of dioleoyl-sn-glycero-3-phosphatidylethanolamine (DOPE), nisin promotes the formation of inverted hexagonal phase. Similarly, the peptide induces the formation of an isotropic phase, most likely a cubic phase, with 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphatidylethanolamine (POPE). It is proposed that the insertion of the peptide in the bilayer shifts the amphiphilic balance by increasing the hydrophobic contribution and is at the origin of the changes in the polymorphic propensities of PE. This is supported by the fact that the presence of cholesterol in the PE bilayer inhibits the power of nisin to perturb the membrane structure, most likely because the peptide insertion is difficult in the fluid ordered phase. This finding provides insight into possible antibacterial mechanisms of nisin. (+info)
(3/138) Characterization of permeability and morphological perturbations induced by nisin on phosphatidylcholine membranes.
Nisin is an antimicrobial peptide used as food preservative. To gain some insights into the hypothesis that its bactericidal activity is due to the perturbation of the lipid fraction of the bacterial plasmic membrane, we have investigated the effect of nisin on model phosphatidylcholine (PC) membranes. We show that nisin affects the PC membrane permeability, and this perturbation is modulated by the lipid composition. Nisin-induced leakage from PC vesicles is inhibited by the presence of cholesterol. This inhibition is associated with the formation of a liquid ordered phase in the presence of cholesterol, which most likely reduces nisin affinity for the membrane. Conversely, phosphatidylglycerol (PG), an anionic lipid, promotes nisin-induced leakage, and this promotion is associated with an increased affinity of the peptide for the bilayer because nisin is a cationic peptide. When the electrostatic interactions are encouraged by the presence of 70 mol% PG in PC, the inhibitory effect of cholesterol is not observed anymore. Nisin drastically modifies the morphology of the dipalmitoyl-sn-glycero-3-phosphatidylcholine (DPPC) multilamellar dispersion without causing a significant change in the gel-to-liquid crystalline phase transition of the lipid. The morphological changes are observed from (31)P and (2)H NMR and cryo-electron microscopy. From the NMR point of view, the interactions giving rise to a broad signal (quadrupolar interactions and chemical shift anisotropy for (2)H NMR and (31)P NMR, respectively) are partly averaged out in the presence of nisin. This phenomenon is interpreted by the formation of curved lipid planes that lead to the lipid lateral diffusion occurring in the intermediate motional regime. By cryo-electron microscopy, large amorphous aggregates containing small dense globular particles are observed for samples quenched from 25 and 50 degrees C. Long thread-like structures are also observed in the fluid phase. A structural description of DPPC/nisin complex, consistent with the experimental observation, is proposed. The presence of 30 mol% cholesterol in DPPC completely inhibits the morphological changes induced by nisin. Therefore, it is concluded that nisin can significantly perturb PC bilayers from both the permeability and the structural points of view, and these perturbations are modulated by the lipidic species in the bilayer. (+info)
(4/138) A nisin bioassay based on bioluminescence.
A Lactococcus lactis subsp. lactis strain that can sense the bacteriocin nisin and transduce the signal into bioluminescence was constructed. By using this strain, a bioassay based on bioluminescence was developed for quantification of nisin, for detection of nisin in milk, and for identification of nisin-producing strains. As little as 0.0125 ng of nisin per ml was detected within 3 h by this bioluminescence assay. This detection limit was lower than in previously described methods. (+info)
(5/138) Computational study of nisin interaction with model membrane.
Nisin is a 34-residue lantibiotic widely used as food preservative. Its mode of action on the bacterial cytoplasmic membrane is unclear. It should form ion channels but a molecular description of the interaction between nisin and phospholipids is lacking. The interactions between nisin and a membrane and the influence of phospholipids are here analysed by molecular modelling. The NMR structures of nisin in a micellar environment were previously determined (Van den Hooven et al., Eur. J. Biochem. 235 (1996) 382-393) Those structures were used to start with. They were refined by running a Monte Carlo procedure at a model lipid/water interface. It was shown that nisin is adsorbing onto the interface, with its N-terminal moiety more deeply inserted in lipids than the C-end, indicating distinct hydrophobic properties of the N- and C-domains. Therefore, we suggest that the N-terminal part is implied in the insertion of nisin in lipids, while the C-terminal moiety could be involved in the initial interaction with the membrane surface. Modelling the interaction of nisin with different neutral or anionic phospholipids shows that it disturbs the lipid organisation. The disturbance is maximal with phosphatidylglycerol. In this system, nisin curves the surface of phosphatidylglycerol layer round suggesting it could induce micelle formation. This could be a preliminary step to pore formation. It suggests that phosphatidylglycerol could have a direct action on nisin insertion and on ion channel formation. Appearance of a curvature also agrees with the 'wedge model' proposed in the literature for the nisin pore formation. (+info)
(6/138) Synergistic actions of nisin, sublethal ultrahigh pressure, and reduced temperature on bacteria and yeast.
Nisin in combination with ultrahigh-pressure treatment (UHP) showed strong synergistic effects against Lactobacillus plantarum and Escherichia coli at reduced temperatures (<15 degrees C). The strongest inactivation effects were observed when nisin was present during pressure treatment and in the recovery medium. Elimination (>6-log reductions) of L. plantarum was achieved at 10 degrees C with synergistic combinations of 0.5 microg of nisin per ml at 150 MPa and 0.1 microg of nisin per ml at 200 MPa for 10 min. Additive effects of nisin and UHP accounted for only 1.2- and 3.7-log reductions, respectively. Elimination was also achieved for E. coli at 10 degrees C with nisin present at 2 microg/ml, and 10 min of pressure at 200 MPa, whereas the additive effect accounted for only 2.6-log reductions. Slight effects were observed even against the yeast Saccharomyces cerevisiae with nisin present at 5 microg/ml and with 200 MPa of pressure. Combining nisin, UHP, and lowered temperature may allow considerable reduction in time and/or pressure of UHP treatments. Kill can be complete without the frequently encountered survival tails in UHP processing. The slightly enhanced synergistic kill with UHP at reduced temperatures was also observed for other antimicrobials, the synthetic peptides MB21 and histatin 5. The postulated mode of action was that the reduced temperature and the binding of peptides to the membrane increased the efficacy of UHP treatment. The increases in fatty acid saturation or diphosphatidylglycerol content and the lysylphosphatidyl content of the cytoplasm membrane of L. plantarum were correlated with increased susceptibility to UHP and nisin, respectively. (+info)
(7/138) Antimicrobial actions of degraded and native chitosan against spoilage organisms in laboratory media and foods.
The objective of this study was to determine whether chitosan (poly-beta-1,4-glucosamine) and hydrolysates of chitosan can be used as novel preservatives in foods. Chitosan was hydrolyzed by using oxidative-reductive degradation, crude papaya latex, and lysozyme. Mild hydrolysis of chitosan resulted in improved microbial inactivation in saline and greater inhibition of growth of several spoilage yeasts in laboratory media, but highly degraded products of chitosan exhibited no antimicrobial activity. In pasteurized apple-elderflower juice stored at 7 degrees C, addition of 0.3 g of chitosan per liter eliminated yeasts entirely for the duration of the experiment (13 days), while the total counts and the lactic acid bacterial counts increased at a slower rate than they increased in the control. Addition of 0.3 or 1.0 g of chitosan per kg had no effect on the microbial flora of hummus, a chickpea dip; in the presence of 5.0 g of chitosan per kg, bacterial growth but not yeast growth was substantially reduced compared with growth in control dip stored at 7 degrees C for 6 days. Improved antimicrobial potency of chitosan hydrolysates like that observed in the saline and laboratory medium experiments was not observed in juice and dip experiments. We concluded that native chitosan has potential for use as a preservative in certain types of food but that the increase in antimicrobial activity that occurs following partial hydrolysis is too small to justify the extra processing involved. (+info)
(8/138) Lack of specificity of trans,trans-muconic acid as a benzene biomarker after ingestion of sorbic acid-preserved foods.
The benzene metabolite, trans,trans-muconic acid (MA), has been shown to be a sensitive and specific biomarker for ambient benzene exposure levels as low as approximately 0.5 ppm. However, at lower exposure levels, the use of MA as a benzene biomarker is complicated by the fact that it is also a metabolite of the food preservative, sorbic acid. To better assess the extent of this interference, MA was measured in sequential spot urine samples over a 2-day study period from eight volunteers (four adults and two parent-children pairs) who consumed two sorbic acid-preserved foods. Large increases in MA concentration were seen after ingestion of both foods. Individual peaks ranged as high as 1673.7 ng/ml (705.3 ng/mg creatinine) in adults and 1752.1 ng/mg creatinine (1221.3 ng/ml) in children. Ratios of peak to baseline values varied from 2.5 to 60. The average peak in the seven subjects who showed an increase in MA after ingestion of the first sorbic acid-containing food was 531.1 ng/ml (693.2 ng/mg creatinine). The average in the seven participants who ingested the second food was 1102.1 ng/ml (795.3 ng/mg creatinine). Twenty-four-hour personal air benzene levels were all low (< or = 5.6 ppb). Substantial variation in MA results were seen in some males related to creatinine adjustment. These data indicate that sorbic acid-preserved foods have the potential to cause substantial interference with MA as a biomarker for both occupational and environmental benzene exposure in populations, such as in the United States, where consumption of preserved foods is common. Development of methods to minimize and/or assess sorbic acid interference will improve MA specificity in such populations. (+info)