Antioxidant properties of kilned and roasted malts

Compounds possessing antioxidant activity play a crucial role in delaying or preventing lipid oxidation in foods and beverages during processing and storage. Such reactions lead to loss of product quality, especially as a consequence of off-flavor formation. The aim of this study was to determine the antioxidant activity of kilned (standard) and roasted (speciality) malts in relation to phenolic compounds, sugars, amino acids, and color [assessed as European Brewing Convention units (degrees EBC) and absorbance at 420 nm]. The concentrations of sugars and amino acids decreased with the intensity of the applied heat treatment, and this was attributed to the extent of the Maillard reaction, as well as sugar caramelization, in the highly roasted malts. Proline, followed by glutamine, was the most abundant free amino/imino acid in the malt samples, except those that were highly roasted, and maltose was the most abundant sugar in all malts. Levels of total phenolic compounds decreased with heat treatment. Catechin and ferulic acid were the most abundant phenolic compounds in the majority of the malts, and amounts were highest in the kilned samples. In highly roasted malts, degradation products of ferulic acid were identified. Antioxidant activity increased with the intensity of heating, in parallel with color formation, and was significantly higher for roasted malts compared to kilned malts. In kilned malts, phenolic compounds were the main identified contributors to antioxidant activity, with Maillard reaction products also playing a role. In roasted malts, Maillard reaction products were responsible for the majority of the antioxidant activity.

Fermentation of heated gluten systems by gut microflora

The Maillard reaction causes changes to protein structure and occurs in foods mainly during thermal treatment. Melanoidins, the final products of the Maillard reaction, may enter the gastrointestinal tract, which is populated by different species of bacteria. In this study, melanoidins were prepared from gluten and glucose. Their effect on the growth of faecal bacteria was determined in culture with genotype and phenotype probes to identify the different species involved. Analysis of peptic and tryptic digests showed that low molecular mass products are formed from the degradation of melanoidins. Results showed a change in the growth of bacteria. This in vitro study demonstrated that melanoidins, prepared from gluten and glucose, affect the growth of the gut microflora.

Effect of cultivar and storage time on the volatile flavor components of baked potato

Tubers of five cultivars of potato were stored at 4 degreesC for 2 3 and 8 months and baked in a conventional oven The flavor compounds from the baked potato flesh were isolated by headspace adsorption onto Tenax and analyzed by gas chromatography-mass spectrometry On a quantitative basis compounds derived from lipid and Maillard reaction/sugar degradation dominated the flavor isolates with sulfur compounds, methoxypyrazines, and terpenes making smaller contributions Levels of 37 of the > 150 detected compounds were monitored in each cultivar with time of storage Many significant differences were found in levels of individual compounds compound classes and total monitored compounds for the individual effects of cultivar and storage time and for their two way interaction Differences may be explained by variations in levels of flavor precursors and activities of enzymes mediating flavor compound formation among cultivars and storage times In addition differences in agronomic conditions may partly account for variations among cultivars Overall of the compounds monitored those most likely having the greatest flavor impact were 2-isopropyl 3 methyoxypyrazine 2 isobutyl 3-methoxypyrazine dimethyl trisulfide, decanal and 3 methylbutanal, with methylpropanal, 2 methylbutanal methional, and nonanal also being probable important contributors to flavor.

Comparison of the volatile components of two cultivars of potato cooked by boiling, conventional baking and microwave baking

Tubers of two cultivars (Estima and Maris Piper) of potato were cooked by three different procedures, ie boiling, conventional baking and microwave baking. Peeled and sliced tubers were boiled, while intact potatoes were baked in their skins. Flavour components from the boiled slices and the flesh of the baked tubers were isolated by headspace adsorption onto Tenax and analysed by gas chromatography-mass spectrometry (GC-MS). For all cooking procedures, Estima gave stronger isolates than Maris Piper. The two main sources of flavour compounds (regardless of cooking procedure) were lipid degradation and the Maillard reaction and/or sugar degradation. The ratio (yield derived from lipid)/(yield derived from Maillard reaction and/or sugar) decreased from 8.5-9.1 (boiling) to 2.7-3.4 (microwave baking) and to 0.4-1.1 (conventional baking). Quantitative and qualitative differences among the cooking procedures are explained in terms of the variations in heat and mass transfer processes that occurred. Each cooking procedure resulted in a unique profile of flavour compounds. (C) 2002 Society of Chemical Industry.

Comparison of the volatile components of eight cultivars of potato after microwave baking

Eight cultivars of potato were baked in a microwave oven. The flavour components of the flesh were isolated by headspace trapping onto Tenax and analysed by gas chromatography-mass spectrometry. Lipid degradation and the Maillard reaction and/or sugar degradation were the main sources of the 80 flavour components identified. It is suggested that total levels of compounds and variations among their profiles may be attributed to differences in activities of lipid enzymes and levels of flavour precursors in the range of cultivars investigated. (C) 2002 Elsevier Science Ltd.

Volatile flavour components of baked potato flesh. A comparison of eleven potato cultivars

Tubers of eleven cultivars of potato were baked and the flavour compounds from the flesh were isolated by headspace adsorption onto Tenax and analysed by gas chromatography-mass spectrometry (GC-MS). Lipid degradation and the Maillard reaction were the main sources of flavour compounds, accounting for 22-69% and 28-77%, respectively, of the total yields. Various sulfur compounds, methoxypyrazines and terpenes were also identified at lower levels. Relative aroma impact values (RAVs) were calculated by dividing compound yields by the odour threshold value. Compounds contributing most to aroma (RAV > 10000 in at least one cultivar) were 2-isobutyl-3-methoxypyrazine, 2-isopropyl-3-methoxypyrazine, beta -damascenone, dimethyl trisulfide, decanal and 3-methylbutanal. The observed differences in yields and RAVs for compounds among cultivars would be expected to result in differences in perceived flavour.

Lipoxidation products as biomarkers of oxidative damage to proteins during lipid peroxidation reactions

Oxidative stress is implicated in the pathogenesis of numerous disease processes including diabetes mellitus, atherosclerosis, ischaemia reperfusion injury and rheumatoid arthritis. Chemical modification of amino acids in protein during lipid peroxidation results in the formation of lipoxidation products which may serve as indicators of oxidative stress in vivo. The focus of the studies described here was initially to identify chemical modifications of protein derived exclusively from lipids in order to assess the role of lipid peroxidative damage in the pathogenesis of disease. Malondialdehye (MDA) and 4-hydroxynonenal (HNE) are well characterized oxidation products of polyunsaturated fatty acids on low-density lipoprotein (LDL) and adducts of these compounds have been detected by immunological means in atherosclerotic plaque. Thus, we first developed gas chromatography-mass spectrometry assays for the Schiff base adduct of MDA to lysine, the lysine-MDA-lysine diimine cross-link and the Michael addition product of HNE to lysine. Using these assays, we showed that the concentrations of all three compounds increased significantly in LDL during metal-catalysed oxidation in vitro. The concentration of the advanced glycation end-product N epsilon-(carboxymethyl)lysine (CML) also increased during LDL oxidation, while that of its putative carbohydrate precursor the Amadori compound N epsilon-(1-deoxyfructose-1-yl)lysine did not change, demonstrating that CML is a marker of both glycoxidation and lipoxidation reactions. These results suggest that MDA and HNE adducts to lysine residues should serve as biomarkers of lipid modification resulting from lipid peroxidation reactions, while CML may serve as a biomarker of general oxidative stress resulting from both carbohydrate and lipid oxidation reactions.

Decrease in skin collagen glycation with improved glycemic control in patients with insulin-dependent diabetes mellitus

Glycation, oxidation, and nonenzymatic browning of protein have all been implicated in the development of diabetic complications. The initial product of glycation of protein, fructoselysine (FL), undergoes further reactions, yielding a complex mixture of browning products, including the fluorescent lysine-arginine cross-link, pentosidine. Alternatively, FL may be cleaved oxidatively to form N(epsilon)-(carboxymethyl)lysine (CML), while glycated hydroxylysine, an amino-acid unique to collagen, may yield N(epsilon)-(carboxymethyl)hydroxylysine (CMhL). We have measured FL, pentosidine, fluorescence (excitation = 328 nm, emission = 378 nm), CML, and CMhL in insoluble skin collagen from 14 insulin-dependent diabetic patients before and after a 4-mo period of intensive therapy to improve glycemic control. Mean home blood glucose fell from 8.7 +/- 2.5 (mean +/- 1 SD) to 6.8 +/- 1.4 mM (P less than 0.005), and mean glycated hemoglobin (HbA1) from 11.6 +/- 2.3% to 8.3 +/- 1.1% (P less than 0.001). These changes were accompanied by a significant decrease in glycation of skin collagen, from 13.2 +/- 4.3 to 10.6 +/- 2.3 mmol FL/mol lysine (P less than 0.002). However, levels of browning and oxidation products (pentosidine, CML, and CMhL) and fluorescence were unchanged. These results show that the glycation of long-lived proteins can be decreased by improved glycemic control, but suggest that once cumulative damage to collagen by browning and oxidation reactions has occurred, it may not be readily reversed. Thus, in diabetic patients, institution and maintenance of good glycemic control at any time could potentially limit the extent of subsequent long-term damage to proteins by glycation and oxidation reactions.

Glycation, oxidation, and lipoxidation in the development of the complications of diabetes: a carbonyl stress hypothesis

Modifications of extant plasma proteins, structural proteins,and other macromolecules are enhanced in diabetes because of increased glycation (secondary to increased glucose concentrations) and perhaps because of increased oxidative stress, Increased glycation is present from the time of onset of diabetes, but the relation between diabetes and oxidative stress is less clear: increased oxidative stress may occur later in the course of disease, as vascular damage becomes established, or it may be a feature of uncomplicated diabetes, The combined effects of protein modification by glycation and oxidation may contribute to the development of accelerated atherosclerosis in diabetes and to the development of microvascular complications, Thus, even if not increased by diabetes, variations in oxidative stress may modulate the consequences of hyperglycemia in individual diabetic patients, In this review, the close interaction between glycation and oxidative processes is discussed, and the theme is developed that the most significant modifications of proteins are the result of interactions with reactive carbonyl groups, While glucose itself contains a carbonyl group that is involved in the initial glycation reaction, the most important and reactive carbonyls are formed by free radical-oxidation reactions damaging either carbohydrates (including glucose itself) or lipids, The resulting carbonyl-containing intermediate products then modify proteins, yielding "glycoxidation" and "lipoxidation" products, respectively, This common pathway for glucose and lipid-mediated stress, which may contribute to diabetic complications, is the basis for the carbonyl stress hypothesis for the development of diabetic complications.

Quantum Discord Bounds the Amount of Distributed Entanglement

The ability to distribute quantum entanglement is a prerequisite for many fundamental tests of quantum theory and numerous quantum information protocols. Two distant parties can increase the amount of entanglement between them by means of quantum communication encoded in a carrier that is sent from one party to the other. Intriguingly, entanglement can be increased even when the exchanged carrier is not entangled with the parties. However, in light of the defining property of entanglement stating that it cannot increase under classical communication, the carrier must be quantum. Here we show that, in general, the increase of relative entropy of entanglement between two remote parties is bounded by the amount of nonclassical correlations of the carrier with the parties as quantified by the relative entropy of discord. We study implications of this bound, provide new examples of entanglement distribution via unentangled states, and put further limits on this phenomenon.

Defining the role of common variation in the genomic and biological architecture of adult human height

Using genome-wide data from 253,288 individuals, we identified 697 variants at genome-wide significance that together explained one-fifth of the heritability for adult height. By testing different numbers of variants in independent studies, we show that the most strongly associated 1/42,000, 1/43,700 and 1/49,500 SNPs explained 1/421%, 1/424% and 1/429% of phenotypic variance. Furthermore, all common variants together captured 60% of heritability. The 697 variants clustered in 423 loci were enriched for genes, pathways and tissue types known to be involved in growth and together implicated genes and pathways not highlighted in earlier efforts, such as signaling by fibroblast growth factors, WNT/I 2-catenin and chondroitin sulfate-related genes. We identified several genes and pathways not previously connected with human skeletal growth, including mTOR, osteoglycin and binding of hyaluronic acid. Our results indicate a genetic architecture for human height that is characterized by a very large but finite number (thousands) of causal variants.