The Lowdown on Lauric Arginate

As more and more food products are produced on a large industrial scale and distributed over extensive geographic areas, the concerns regarding quality and food safety throughout the shelf life of the product have become more and more critical. Effective control of bacterial growth is a constant concern due to the risk of spoilage and food-borne disease. The federal government continually estimates that 76 million cases of foodborne illnesses occur each year in the U.S. alone, resulting in 300,000 hospitalizations and 5,000 deaths annually. The populations most at risk are the very young, those who have a chronic illness, and those with damaged immune systems. Bacterial pathogens are the most commonly identified cause of food-borne illness. Some of these pathogens include Campylobacter, Salmonella, Clostridium, Escherichia and Staphylococus. Deaths have occurred due to bacterial pathogens, with Salmonella and Listeria topping the list. Lauric arginate is a novel antimicrobial compound derivative of lauric acid, L-arginine and ethanol, all naturally occurring substances. The molecule was first synthesized by the CSIC (Higher Council of Scientific Research) in Barcelona in 1984. It was then patented and commercialized by the Vedeqsa Lamirsa Group and distributed in the U.S. through A&B Ingredients. Its most notable features are: . Broad spectrum of antimicrobial efficacy; . High partition coefficient (>10), means the product concentrates in the water phase of products, where most bacterial action occurs; . Activity over a wide pH range (3 to 7); . Safe ingredient: LAE is hydrolyzed in the human body by chemical and metabolic pathways, which quickly break the molecule into its natural components; . GRAS Status: Granted by a panel of FDA experts in the U.S. through scientific procedures set forth under 21 CFR §170.30(b).

Antimicrobial Activity

Its low toxicity in conjunction with its remarkable antimicrobial properties, make LAE a valuable tool for the food industry for improved safety and product quality. The following tables (p. 58) show the minimal inhibitory concentrations of LAE versus different types of microorganisms, mostly pathogens, which give insight into compound potency and activity range. These results were obtained by an independent laboratory from the faculty of pharmacy and biology at the University of Barcelona.

Action Mechanism

The antimicrobial properties of LAE are derived from its action on the cytoplasmic membranes of microorganisms. LAE causes a disruption/instability of plasma membrane lipid bilayer, altering the metabolic process and detaining the cellular cycle. No cellular lysis has been observed in any case in bacteria cells exposed to usual doses of LAE. The effect of LAE on gram-negative microorganisms (Salmonella typhimur-ium ATCC 14028) and gram-positive (Staphylococcus aureus ATCC 6538) was studied at inhibition concentrations of 32 y 8 ºg/mL respectively, by the pharmacy faculty at the University of Barcelona and recently published in the Journal of Applied Microbiology. By means of electronic transmitting microscopy the alterations caused by LAE on the bacteria cytoplasmic membrane were studied and can be seen clearly in figures 1, 2 and 3. The action level on bacterial populations was analyzed by means of fluorescence microscopy and flux citometry, based on nucleic acid staining with two fluorescent pigments: first SYTO-13 (green), marking all cells, and then propidium iodide (red) which replaces the previous one only in damaged cells. LAE was able to act on 91 percent of the cell population of S. typhimurium and 45 percent of S. aureus population after 30 minutes of contact and 96 percent and 55 percent, respectively, after three hours of contact. Finally, potassium and proton trans-membrane ionic flux was determined after 30 minute contact showing a potassium flux increment for S. aureus and S. typhimurium, as well as a decrease in the proton flux. Both experiments indicate a clear alteration of the membrane potential as a direct consequence of the structural modification induced by LAE on the bacterial membrane.