Degradation of N‐(1‐Deoxy‐d‐xylulos‐1‐yl)glycine and N‐(1‐Deoxy‐d‐xylulos‐1‐yl)proline using thermal treatment

The formation and degradation of N‐(1‐Deoxy‐d ‐xylulos‐1‐yl)glycine and N‐(1‐Deoxy‐d ‐xylulos‐1‐yl)proline, derived from the secondary amine Maillard reaction in xylose‐amino acid model solutions, were detailed in this study. The identification and quantitative analysis of N‐(1‐Deoxy‐d‐ xylulos‐1‐yl)glycine and N‐(1‐Deoxy‐d‐ xylulos‐1‐yl)proline were carried out using high‐performance anion‐exchange chromatography and high‐performance liquid chromatography. The formation of intermediate and advanced products derived from N‐(1‐Deoxy‐d‐ xylulos‐1‐yl)glycine and N‐(1‐Deoxy‐d‐ xylulos‐1‐yl)proline was also tested using an UV‐Vis spectrophotometer to gain a better comparing of the degradation process of the two important Maillard reaction products using thermal treatment. Results showed that the degradation of N‐(1‐Deoxy‐d‐ xylulos‐1‐yl)glycine was more significant than N‐(1‐Deoxy‐d‐ xylulos‐1‐yl)proline. Moreover, xylose was tested in the degradation products of both N‐(1‐Deoxy‐d‐ xylulos‐1‐yl)glycine and N‐(1‐Deoxy‐d‐ xylulos‐1‐yl)proline, which indicated that the degradation of N‐substituted 1‐amino‐1‐deoxyketoses was a reversible reaction to form reducing sugar.     

Absorption and twenty‐four‐hour metabolism time‐course of quercetin‐3‐O‐glucoside in rats,in vivo

Rats were meal‐fed a semi‐synthetic diet, with or without quercetin 3‐O‐glucoside (Q3G; 100 mg per meal) and groups of three were killed either fasting, or at 2, 5 and 24 post‐feeding. Flavonoids and their metabolites in the diet, stomach contents, small intestinal lumen and mucosa, caecal contents and plasma were determined by LC/MS. Q3G was not hydrolysed in the stomach, but deglycosylation and further metabolism occurred in the small intestinal mucosa. At least 17 flavonoid glucuronides were identified in the lumen and mucosa, with evidence of time‐dependent changes such as de‐ and re‐glucuronidation. Quercetin mono‐sulphate was also detected in the small intestinal contents. Metabolites were still present in tissue and plasma 24 h after feeding. There was also evidence of complex microbial processing of Q3G in the caecal lumen with the appearance of at least one methylquercetin‐mono‐glucuronide, mono‐sulphate unique to this site in the gut, together with phenolic acid derivatives. Intestinal flavonoid metabolism is thus a very complex process in mammals, involving both enterocytes and bacteria. Copyright © 2004 Society of Chemical Industry     

Glycyrrhetic Acid 3‐O‐Mono‐β‐d‐glucuronide (GAMG): An Innovative High‐Potency Sweetener with Improved Biological Activities

Glycyrrhetic acid 3‐O‐mono‐β‐d ‐glucuronide (GAMG) is an important derivative of glycyrrhizin (GL) and has attracted considerable attention, especially in the food and pharmaceutical industries, due to its natural high sweetness and strong biological activities. The biotransformation process is becoming an efficient route for GAMG production with the advantages of mild reaction conditions, environmentally friendly process, and high production efficiency. Recent studies showed that several β‐glucuronidases (β‐GUS) are key GAMG‐producing enzymes, displaying a high potential to convert GL directly into the more valuable GAMG and providing new insights into the generation of high‐value compounds. This review provides details of the structural properties, health benefits, and potential applications of GAMG. The progress in the development of the biotransformation processes and fermentation strategies to improve the yield of GAMG is also discussed. This work further summarizes recent advances in the enzymatic synthesis of GAMG using β‐GUS with emphasis on the physicochemical and biological properties, molecular modifications, and enzymatic strategies to improve β‐GUS biocatalytic efficiencies. This information contributes to a better framework to explore production and application of bioactive GAMG.     

Formation of protein adducts of 2‐amino‐1‐methyl‐6‐phenylimidazo[4,5‐b]pyridine in cooked foods

Heterocyclic amines (HCAs) are mutagenic and carcinogenic compounds found in cooked meat and fish. Although HCAs are known to form adducts with protein after metabolic activation, adduct formation during cooking has not been elucidated. In this study, we showed that 2‐amino‐1‐methyl‐6‐phenylimidazo[4,5‐b]pyridine (PhIP) is released from high molecular weight compounds by acid or enzymatic hydrolysis of cooked foods. Formation of free and protein adduct forms of PhIP was dependent on cooking temperature and time, and PhIP–protein adducts were estimated to form after formation of free PhIP. We also demonstrated that PhIP–protein adduct is formed by heating of PhIP and albumin as a model protein. A new adduct peak including [M+H]⁺ (m/z=225) of PhIP as a fragment ion was detected in the high molecular weight fraction of heat‐treated protein by LC–MS analysis. From model experiments by heating of PhIP and amino acids, the adduct was estimated to be produced by condensation of the amino group of PhIP and the carboxyl group of protein. PhIP–protein adducts were detected in several cooked meat and fish at ng/g food level as PhIP content. These results suggest that food‐borne protein adducts of HCAs may influence human HCA exposure and carcinogenic risk.     

In vitro anti‐HSV‐2 activity and mechanism of action of proanthocyanidin A‐1 from Vaccinium vitis‐idaea

The aim of this study was to investigate the in vitro anti‐HSV‐2 activity and mechanism of action of proanthocyanidin A‐1, a compound isolated from Vaccinium vitis‐idaea Linn (Ericaceae). The results demonstrated that proanthocyanidin A‐1 exhibited anti‐HSV‐2 activity. The IC₅₀ value for the XTT assay was 73.3 ± 14.5 µM and the IC₅₀ and IC₉₀ values for the plaque reduction assay were 41.9 ± 2.0 and 62.8 ± 6.3 µM respectively. Proanthocyanidin A‐1 showed no cell cytotoxic effect at concentrations that blocked HSV‐2 infection, with a CC₅₀ value of 282.1 ± 27.5 µM . The mechanism studies demonstrated that proanthocyanidin A‐1 did not reduce viral infectivity but inhibited viral attachment and penetration and affected the late stage(s) of HSV‐2 infection. It was concluded that proanthocyanidin A‐1 suppressed HSV‐2 infection through many modes of action and thus merits further investigation. Copyright © 2004 Society of Chemical Industry