Acrylamide in Foods: Data and More Questions
The presence of acrylamide in foods was first reported in April 2002. Because the chemical has been classified as "probably carcinogenic" to humans, and following confirmation of these initial findings, this immediately became a worldwide problem. Acrylamide occurs in many foods common to diets globally. It is formed during the heat preparation of carbohydrate-rich foods containing the reducing sugars glucose and fructose and the amino acid asparagine, which are common to the plant ingredients used in the preparation of many foods. It is not present naturally, nor is it added. It is formed in many common foods during the Maillard browning reaction, which produces their color, flavor, and aroma during the heating process. In the years since then, the extent of formation in foods, the mechanisms by which it is formed, the exposure in human populations, and many continuing investigations into methods for reducing its contents in foods have occurred. The central issue of concern is whether there is a potential adverse health implication for consumers from the amounts of acrylamide consumed in common diets. Data are still not sufficient to fully answer this, so there are no current recommendations regarding changes in dietary intake. Current dietary advice advocates following dietary guidelines to eat a variety of foods, prepared in a variety of ways, and to focus on reducing saturated fat and salt and eating adequate amounts of fruits, vegetables, and whole grains. This review updates the current status of the issues of acrylamide in foods including the data available and the questions still existing
Available from: V. Bartkevics
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ABSTRACT: a b s t r a c t This study mainly focuses on a strategy for reducing of acrylamide in cereal products, predominantly in bakery products. The effect of mesophilic lactic acid bacteria (LAB) strains as well as a novel fermentation media on the bases of extruded rye wholemeal on the acrylamide formation in mixed rye bread of different weight of loaf was studied. The LCeMS/MS method for acrylamide determination in bread crumb has been applied. Addition of 15% low pH (pH 3.4e4.3) fermented product to bread dough, which were produced by using commercial strain Lactobacillus casei and bacteriocin-like inhibitory substances (BLIS) producing strains Lactobacillus sakei KTU05-6, Pediococcus acidilactici KTU05-7 and Pediococcus pentosaceus KTU05-8 separately, caused significant reduction of acrylamide in mixed rye bread. All bread loafs of 1000 g contained less by 27% acrylamide concentrations versus loafs of 500 g. Acrylamide formation was affected (r 2 ¼ 0.7193) by total reducing sugar content in bread and slightly correlated (r 2 ¼ 0.5587) with reducing sugar content in sourdough. The treatment of extruded rye wholemeal with Aspergillus niger glucoamylase as compared to the control sample was found to have a positive effect on the acidification process lowering the acrylamide formation on an average by 59.4% and 40% in 500 g and 1000 g loafs of bread, respectively. This study demonstrates that acrylamide content could be reduced by using LAB excreting lower amylolytic activity in the medium, while the higher proteolytic activity is preferred.
Available from: Jian xin Shi
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ABSTRACT: Acrylamide (AA) was firstly detected in food in 2002, and since then, studies on AA analysis, occurrence, formation, toxicity, risk assessment and mitigation have been extensively carried out, which have greatly advanced understanding of this particular biohazard at both academic and industrial levels. There is considerable variation in the levels of AA in different foods and different brands of the same food; therefore, so far, a general upper limit for AA in food is not available. In addition, the link of dietary AA to human cancer is still under debate, although AA has been known as a potential cause of various toxic effects including carcinogenic effects in experimental animals. Furthermore, the oxidized metabolite of AA, glycidamide (GA), is more toxic than AA. Both AA and GA can form adducts with protein, DNA, and hemoglobin, and some of those adducts can serve as biomarkers for AA exposure; their potential roles in the linking of AA to human cancer, reproductive defects or other diseases, however, are unclear. This review addresses the state-of-the-art understanding of AA, focusing on risk assessment, mechanism of formation and strategies of mitigation in foods. The potential application of omics to AA risk assessment is also discussed.
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