L-asparaginase (L-asnase) is an amino hydrolase that has been used in the last decades for leukemia treatment, which boosted scientific studies on production, purification and immobilization of this enzyme. More recently, L-asnase has called food industry attention because of its effect on acrylamide formation in fried and baked foods. Several studies have been carried out in order to evaluate the effect of L-asnase in reducing acrylamide formation in different food models. This review brings up an overview in L-asnase kinetic parameters from different sources, immobilization methods, its therapeutic use in leukemia treatment and food processing applications. This review also discusses acrylamide formation in fried and baked foods. Commercial L-asnase is produced by two microorganisms, Escherichia coli and Erwinia sp. However, studies using different microorganisms have shown the possibility of producing this enzyme from different sources, obtaining enzymes with interesting kinetic properties. Immobilization strategies have provided enzymes with greater activity and stability, which could contribute to maintain L-asnase activity in the body for longer periods. Researches applying L-asnase in food products have shown significant reduction in acrylamide production, above 90% in some cases. For this purpose, during enzyme application some variables must be taken into account, as enzyme dose, food matrix, pretreatment, processing time and temperature. Medical and food applications make L-asnase a multipurpose enzyme. Reducing prices, improving enzyme stability and reducing co-lateral effects in leukemia treatment are still challenges to overcome.
Ethanol abuse is a risk factor for the development of pneumonia caused by Streptococcus pneumoniae, a critical pathogen for public health. The aim of this article was to investigate the inflammatory mechanisms involved in pneumococcal pneumonia that may be associated with chronic ethanol exposure. Male C57BL6/J-Unib mice were exposed to 20% (v/v) ethanol for twelve weeks and intranasally infected with 5x104 CFU of S. pneumoniae. Twenty-four hours after infection, lungs, bronchoalveolar lavage and blood samples were obtained to assess the consequences of chronic ethanol exposure during infection. Alcohol-fed mice showed increased production of nitric oxide and CXCL1 in alveoli and plasma during pneumococcal pneumonia. Beside this, ethanol-treated mice exhibited a decrease in leukocyte infiltration into the alveoli and reduced frequency of severe lung inflammation, which was associated with an increase in bacterial load. Curiously, no changes were observed in survival after infection. Taken together, these results demonstrate that chronic ethanol exposure alters the inflammatory response during S. pneumoniae lung infection in mice with a reduction in the inflammatory infiltrate even in the presence of higher levels of the chemoattractant CXCL1.
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