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David D Kitts - One of the best experts on this subject based on the ideXlab platform.
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detection of Maillard Reaction Product 5 5 6 dihydro 4h pyridin 3 ylidenemethyl furan 2 yl methanol f3 a in breads and demonstration of bioavailability in caco 2 intestinal cells
Journal of Agricultural and Food Chemistry, 2016Co-Authors: Xiumin Chen, David D KittsAbstract:[5-(5,6-Dihydro-4H-pyridin-3-ylidenemethyl)furan-2-yl]methanol, also called F3-A, has been isolated from hexose–lysine Maillard Reaction (MR) models. Here we report on optimized conditions for the recovery of F3-A and concentrations found in bread. Recovery of F3-A was best achieved when samples were extracted with dichloromethane (DCM) at a solvent to sample ratio of 2:1 (v/v) after adjustment of the pH to 12. The amount of F3-A in whole wheat bread was significantly (P < 0.05) higher than that in white bread; bread crust contained a significantly (P < 0.05) higher amount of F3-A (0.9–7.8 μg/100 g) than the bread crumb (not detectable–3.5 μg/100 g); and toasting increased F3-A concentration with a range of not detectable to 6.0 μg/100 g in the control bread and 4.0 and 17.7 μg/100 g in the dark-toasted white sandwich bread and 100% whole wheat sandwich bread, respectively. The in vitro permeability of F3-A was measured using Caco-2 cell monolayer. The apparent permeability coefficient (Papp) of F3-A is (...
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evidence for inhibition of nitric oxide and inducible nitric oxide synthase in caco 2 and raw 264 7 cells by a Maillard Reaction Product 5 5 6 dihydro 4h pyridin 3 ylidenemethyl furan 2 yl methanol
Molecular and Cellular Biochemistry, 2015Co-Authors: Xiumin Chen, David D KittsAbstract:We have recently isolated and characterized the chemical structure of a bioactive Maillard Reaction Product, [5-(5,6-dihydro-4H-pyridin-3-ylidenemethyl)furan-2-yl]-methanol (F3-A), from an aqueous glucose (Glc) and lysine (Lys) Maillard Reaction (MR) model system. Here, we investigate further the mechanisms for anti-inflammatory effects of this Product in Caco-2 and RAW 264.7 cells. The anti-inflammatory capacity of F3-A recovered from Glc–Lys MR mixture and a synthesized Product were compared with those of the specific inducible nitric oxide synthase (iNOS) inhibitor, aminoguanidine (AG), and the nuclear factor-kappa B (NF-κB) inhibitor, pyrrolidine dithiocarbamate (PDTC). F3-A produced a dose-dependent inhibition of extracellular nitric oxide (NO) Production and iNOS translation in Caco-2 cells induced with interferon gamma (IFN-γ) and phorbol 12-myristate 13-acetate (PMA), and these effects were more potent than those obtained with AG. Moreover, a combination of F3-A and AG to attenuate intestinal inflammation was additive. However, F3-A inhibited only intracellular NO Production in RAW 264.7 cells and did not inhibit COX-2 or NF-κB in either cell line. We conclude that the anti-inflammatory properties of F3-A are cell specific, working through different mechanism between macrophages and intestinal cells.
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elucidation of the chemical structure and determination of the Production conditions for a bioactive Maillard Reaction Product 5 5 6 dihydro 4h pyridin 3 ylidenemethyl furan 2 yl methanol isolated from a glucose lysine heated mixture
Journal of Agricultural and Food Chemistry, 2015Co-Authors: Xiumin Chen, Gang Chen, Hongwen Chen, Yilin Zhang, David D KittsAbstract:We previously isolated a bioactive molecule, named F3-A, from an aqueous glucose (Glc) and lysine (Lys) Maillard Reaction (MR) model system. Herein, F3-A was verified as [5-(5,6-dihydro-4H-pyridin-3-ylidenemethyl)furan-2-yl]methanol (5) and was subsequently synthesized for confirmation of bioactivity. Using Taguchi and factorial designs, we determined that the conditions which best increased the yield of F3-A were at pH 6 with a sugar:amino acid ratio of 2:1 and heating time of 12 h at 100 °C. The MR mixtures containing glucose produced highest yield, compared to fructose, lactose, and sucrose. Both the F3-A recovered from Glc-Lys MR mixture and the synthesized Product exhibited significant (P < 0.05), dose dependent, nitric oxide (NO) inhibitory activity in Caco-2 cells that was comparable to aminoguanidine (AG) and pyrrolidine dithiocarbamate (PDTC), respectively. Finally, an additional inhibitory effect of F3-A was determined when coincubated with AG in cytokine-induced Caco-2 cells. This bioactivity p...
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comparison of physicochemical and antioxidant properties of egg white proteins and fructose and inulin Maillard Reaction Products
Food and Bioprocess Technology, 2011Co-Authors: Hao Jing, Melissa Yap, Peter Y.y. Wong, David D KittsAbstract:The Maillard Reaction (MR), involving the condensation of a carbonyl group of reducing sugar and an amino group of protein, can change functional properties of proteins. In this study, chemical characteristics and functional properties of glycosylated albumin, ovomucoid, and lysozyme (egg proteins) and casein with fructose or inulin through the MR were evaluated. The protein and sugar mixtures were heated at 60 °C and 79% relative humidity for 3 days. Chemical characteristics of the egg protein–sugar Maillard Reaction Product (MRP) mixtures were evaluated by fluorescence development, absorbance intensity (at 420 nm), and color change. Functional properties of the protein–sugar MRP mixtures were also evaluated, including emulsifying activity, emulsion stability, and antioxidant activity. The protein–sugar conjugates were found to have significant (p < 0.05) changes compared to the controls (unheated protein–sugar samples) in color, fluorescence, and absorbance intensity. All protein–sugar MR models exhibited a change in emulsifying activity, with Csn–Fru MRP displaying the greatest significant (p < 0.05) improvement. In addition, all protein–sugar MR models exhibited changes in emulsion stability, with Ovo/Inu MRP displaying the greatest significant (p < 0.05) change. All protein–sugar MR models exhibited great scavenging activity towards 1,1-diphenyl-2-picryl-hydrazyl radical at MRP concentrations of 0.2, 0.5, and 1.0 mg/mL. With the exception of the 0.2 mg/mL MRP concentration, there was a significant difference (p < 0.05) between the heated protein–fructose and the heated protein–inulin MRPs.
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effect of glucose lysine Maillard Reaction Product fractions on tissue xenobiotic enzyme systems
Journal of Agricultural and Food Chemistry, 1993Co-Authors: David D Kitts, C H Wu, W D PowrieAbstract:Maillard Reaction Product (MRP) fractions were prepared from a glucose-lysine (gluc-lys) browning model system by heating 1.0 M solutions of glucose and lysine at 121 o C for 4 h. MRP systems were fractionated into a melanoidin precipitate and a supernatant by the addition of absolute ethanol to a level of 90% volume. The fractions were freeze-dried and called freeze-dried supernatant (FDS) and freeze-dried melanoidin precipitate (FDMP). Chronic animal feeding studies were conducted with the addition of FDS and FDMP to experimental synthetic diets at a 2% level in mice, either B[a]P treated or untreated
Xiumin Chen - One of the best experts on this subject based on the ideXlab platform.
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detection of Maillard Reaction Product 5 5 6 dihydro 4h pyridin 3 ylidenemethyl furan 2 yl methanol f3 a in breads and demonstration of bioavailability in caco 2 intestinal cells
Journal of Agricultural and Food Chemistry, 2016Co-Authors: Xiumin Chen, David D KittsAbstract:[5-(5,6-Dihydro-4H-pyridin-3-ylidenemethyl)furan-2-yl]methanol, also called F3-A, has been isolated from hexose–lysine Maillard Reaction (MR) models. Here we report on optimized conditions for the recovery of F3-A and concentrations found in bread. Recovery of F3-A was best achieved when samples were extracted with dichloromethane (DCM) at a solvent to sample ratio of 2:1 (v/v) after adjustment of the pH to 12. The amount of F3-A in whole wheat bread was significantly (P < 0.05) higher than that in white bread; bread crust contained a significantly (P < 0.05) higher amount of F3-A (0.9–7.8 μg/100 g) than the bread crumb (not detectable–3.5 μg/100 g); and toasting increased F3-A concentration with a range of not detectable to 6.0 μg/100 g in the control bread and 4.0 and 17.7 μg/100 g in the dark-toasted white sandwich bread and 100% whole wheat sandwich bread, respectively. The in vitro permeability of F3-A was measured using Caco-2 cell monolayer. The apparent permeability coefficient (Papp) of F3-A is (...
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evidence for inhibition of nitric oxide and inducible nitric oxide synthase in caco 2 and raw 264 7 cells by a Maillard Reaction Product 5 5 6 dihydro 4h pyridin 3 ylidenemethyl furan 2 yl methanol
Molecular and Cellular Biochemistry, 2015Co-Authors: Xiumin Chen, David D KittsAbstract:We have recently isolated and characterized the chemical structure of a bioactive Maillard Reaction Product, [5-(5,6-dihydro-4H-pyridin-3-ylidenemethyl)furan-2-yl]-methanol (F3-A), from an aqueous glucose (Glc) and lysine (Lys) Maillard Reaction (MR) model system. Here, we investigate further the mechanisms for anti-inflammatory effects of this Product in Caco-2 and RAW 264.7 cells. The anti-inflammatory capacity of F3-A recovered from Glc–Lys MR mixture and a synthesized Product were compared with those of the specific inducible nitric oxide synthase (iNOS) inhibitor, aminoguanidine (AG), and the nuclear factor-kappa B (NF-κB) inhibitor, pyrrolidine dithiocarbamate (PDTC). F3-A produced a dose-dependent inhibition of extracellular nitric oxide (NO) Production and iNOS translation in Caco-2 cells induced with interferon gamma (IFN-γ) and phorbol 12-myristate 13-acetate (PMA), and these effects were more potent than those obtained with AG. Moreover, a combination of F3-A and AG to attenuate intestinal inflammation was additive. However, F3-A inhibited only intracellular NO Production in RAW 264.7 cells and did not inhibit COX-2 or NF-κB in either cell line. We conclude that the anti-inflammatory properties of F3-A are cell specific, working through different mechanism between macrophages and intestinal cells.
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elucidation of the chemical structure and determination of the Production conditions for a bioactive Maillard Reaction Product 5 5 6 dihydro 4h pyridin 3 ylidenemethyl furan 2 yl methanol isolated from a glucose lysine heated mixture
Journal of Agricultural and Food Chemistry, 2015Co-Authors: Xiumin Chen, Gang Chen, Hongwen Chen, Yilin Zhang, David D KittsAbstract:We previously isolated a bioactive molecule, named F3-A, from an aqueous glucose (Glc) and lysine (Lys) Maillard Reaction (MR) model system. Herein, F3-A was verified as [5-(5,6-dihydro-4H-pyridin-3-ylidenemethyl)furan-2-yl]methanol (5) and was subsequently synthesized for confirmation of bioactivity. Using Taguchi and factorial designs, we determined that the conditions which best increased the yield of F3-A were at pH 6 with a sugar:amino acid ratio of 2:1 and heating time of 12 h at 100 °C. The MR mixtures containing glucose produced highest yield, compared to fructose, lactose, and sucrose. Both the F3-A recovered from Glc-Lys MR mixture and the synthesized Product exhibited significant (P < 0.05), dose dependent, nitric oxide (NO) inhibitory activity in Caco-2 cells that was comparable to aminoguanidine (AG) and pyrrolidine dithiocarbamate (PDTC), respectively. Finally, an additional inhibitory effect of F3-A was determined when coincubated with AG in cytokine-induced Caco-2 cells. This bioactivity p...
Chaujong Wang - One of the best experts on this subject based on the ideXlab platform.
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tumor promotion of n nitroso n 3 keto 1 2 butanediol 3 nitrotyramine derived from nitrosation of Maillard Reaction Product in cd 1 mice
Toxicology and Applied Pharmacology, 2000Co-Authors: Wencheng Chang, Changche Chen, Tsuihwa Tseng, Hweipei Huang, Chaujong WangAbstract:Abstract N -Nitroso- N -(3-keto-1,2-butanediol)-3′-nitrotyramine (NO-NTA) is a Product of a model browning system generated in the presence of sodium nitrite. Our previous study showed that NO-NTA had genotoxicity and proved to be an initiator and promoter on mouse C3H10T1/2 cells. In this study, a two-stage skin carcinogenesis protocol was used to promote CD-1 mouse skin carcinogenesis using NO-NTA. Twice weekly, for 38 weeks, topical application of NO-NTA at the concentration of 250 nmol to mice previously initiated with benzo( a )pyrene (B a P) caused 90% tumor incidence. However, no tumors were observed in mice treated with B a P or treated with NO-NTA alone. The NO-NTA-promoted tumors that were observed histologically in mice showed well-differentiated squamous cell carcinoma with invasion into the subscutaneous region. Application of the same amount of NO-NTA not only caused significant induction of hyperplasia but also epidermal ornithine decarboxylase (ODC) activity. Treatment of mouse skin (1 cm 2 ) with various amounts of NO-NTA (10, 50, or 250 nmol) caused Production of hydrogen peroxide by 1.63-, 1.91-, and 2.38-fold, respectively, and marked induction of myeloperoxidase (MPO) by 21-, 39-, and 61-fold. These results indicate that NO-NTA is a new tumor promoter and may induce tumor promotion by oxidant stress in CD-1 mouse skin.
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tumor promoting effect of n nitroso n 2 hexanonyl 3 nitrotyramine a nitrosated Maillard Reaction Product in benzo a pyrene initiated mouse skin carcinogenesis
Chemico-Biological Interactions, 1998Co-Authors: Tsuihwa Tseng, Mingcheng Chang, Chaujong WangAbstract:Abstract N-nitroso-N-(2-hexanonyl)-3′-nitrotyramine (NO-HNTA) is a Product generated in a model browning system in the presence of sodium nitrite. The chemical structure of this compound has been confirmed by UV, mass, nuclear magnetic resonance and infrared spectroscopy in our study. Twenty weeks, twice weekly, topical application of NO-HNTA at the concentration of 10, 50 and 250 μmol to mice previously initiated with benzo(a)pyrene (B[a]P) increased their tumor formaiton by 3.2-, 4.6- and 5.8-fold respectively. Application of the same amount of NO-HNTA not only caused significant induction of hyperplasia but also the activity of epidermal ornithine decarboxylase (ODC). Treatment of mouse skin with various amounts of NO-HNTA (10, 50 and 250 μmol) caused Production of hydrogen peroxide by 1.38-, 1.95- and 3.26-fold respectively, and induction myeloperoxidase (MPO) by 24-, 63- and 102-fold. These results indicate that the formation of NO-HNTA or its derivatives derived from the Reaction of tyrosine and glucose in the presence of sodium nitrite has the potential as a tumor promoter.
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promotional effect of n nitroso n 3 keto 1 2 butanediol 3 nitrotyramine a nitrosated Maillard Reaction Product in mouse fibroblast cells
Food and Chemical Toxicology, 1998Co-Authors: Chaujong Wang, H P Huang, Wei Chiao ChangAbstract:Abstract N -Nitroso- N -(3-keto-1,2-butanediol)-3′-nitrotyramine (NO-NTA) is a Product of model browning system generated in the presence of sodium nitrite. The chemical structure of this compound has been confirmed by UV, mass and nuclear magnetic resonance, and infrared spectroscopy in our previous study. A two-stage transformation protocol was used to chemically transform the mouse embryo fibroblasts C3H10T1/2 cells. To initiate transformation, the cells were treated with benzo[ a ]pyrene (BaP) (0.1 mg/ml), and NO-NTA (0.01, 0.1 and 1 mg/ml) was employed subsequently to complete the transformation process. Malignant transformed foci were formed in BaP-initiated and NO-NTA promoted C3H10T1/2 cells after 8 wk. Cells treated with NO-NTA alone failed to induce transformation. However, cells initiated with BaP and promoted by cells initiated with BaP and promoted by NO-NTA demonstrated oncogenic properties. Cell lines transformed with NO-NTA-transformed colonies exhibited enhanced growth rate, anchorage independence and tumorigenicity in animals relative to parent cells. These results indicate that NO-NTA is a new tumour promoter and may induce tumour promotion by two-stage oncogenesis. Further studies on the mechanism of action of NO-NTA are now in progress.
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hepatotoxicity of l 3 5 trinitro 2 acetyl pyrrole derived from nitrosation of Maillard Reaction Product in balb c mouse
Toxicology Letters, 1996Co-Authors: T H Tseng, Chaujong WangAbstract:Abstract 1,3,5-Trinitro-2-acetyl pyrrole (TNAP) is a Product derived from the Reaction of 2-acetyl pyrrole with nitrite in the model of Maillard browning systems. This compound is moderately mutagenic to the Salmonella strains TA98 and TA100 and is markedly cytotoxic to mouse C3H10T1/2 cells. Experiments are performed to investigate the effects of TNAP on the hepatic toxicity in mouse. Male BALB/C mice were subjected to a dose of 7.2 mg/kg body weight twice a week by i.p. injection for 24 weeks, then followed by a feeding diet for 21 weeks. TNAP-treated mice showed an increase in mortality and time-dependent appearance of lesions in the liver. TNAP is hepatotoxic as demonstrated by a marked increase in the activities of serum alanine transaminase (ALT) and aspartic transaminase (AST). TNAP-related lesions observed histologically in mice, included hapatic atrophy, mild fatty metamorphosis with multilocular cysts in the liver. In conclusion, TNAP was considered to be a toxic compound in mice as evidenced by increased incidences of mortality, and lesions of liver.
Thomas Hofmann - One of the best experts on this subject based on the ideXlab platform.
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renal effects of oral Maillard Reaction Product load in the form of bread crusts in healthy and subtotally nephrectomized rats
Annals of the New York Academy of Sciences, 2005Co-Authors: Katarina Sebekova, Ol'ga Ulicná, Helmut F Erbersdobler, August Heidland, Peter Boor, Thomas Hofmann, John W. Baynes, Suzanne R. Thorpe, Veronika SomozaAbstract:The biological consequences of chronic consumption of Maillard Reaction Products (MRPs) on renal function in health and renal disease are still incompletely understood. We investigated the metabolic and renal effects of a diet with varying MRP content in healthy and subtotally nephrectomized rats. Male Wistar rats were subjected to sham operation (control, C, n = 12), or to 5/6 nephrectomy (5/6NX, n = 12). Both groups were randomized into subgroups and pair-fed with either a MRP-poor or -rich diet for six weeks. The diet was prepared by replacing 5{%} or 25{%} of wheat starch by bread crust (BC). In spite of pair-feeding, the rats on the 25{%} BC diet gained more body weight (C: 183 +/- 6 g; C + 5{%} BC: 197 +/- 7 g; C + 25{%} BC: 229 +/- 6 g [P {\textless} 0.05]; 5/6NX: 165 +/- 10 g; 5/6NX + 5{%} BC: 202 +/- 3 g; 5/6NX + 25{%} BC: 209 +/- 8 g [P {\textless} 0.05]) and had a higher organ weight (heart, liver, lung, kidney/remnant kidney). Bread crust-enriched diet induced proteinuria (C: 15 +/- 5 mg/24 h; C + 5{%} BC: 19 +/- 4; C + 25{%} BC: 26 +/- 3 [P {\textless} 0.05]; 5/6NX: 30 +/- 7 mg/24 h; 5/6NX + 5{%} BC: 47 +/- 9; 5/6NX + 25{%} BC: 87 +/- 19 [P {\textless} 0.01]) and a rise in urinary transforming growth factor beta(1) excretion (C: 0.4 +/- 0.1 ng/24 h; C + 5{%} BC: 0.6 +/- 0.1; C + 25{%} BC: 1.2 +/- 0.3; 5/6NX: 0.5 +/- 0.1 ng/24 h; 5/6NX + 5{%} BC: 0.9 +/- 0.1; 5/6NX + 25{%} BC: 1.6 +/- 0.2 [P {\textless} 0.01]). Plasma creatinine or creatinine clearance were not affected significantly. In conclusion, our data suggests that long-term consumption of a diet rich in MRPs may lead to damage of the kidneys.
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Renal effects of oral Maillard Reaction Product load in the form of bread crusts in healthy and subtotally nephrectomized rats
Annals of the New York Academy of Sciences, 2005Co-Authors: Katarina Sebekova, Ol'ga Ulicná, Helmut F Erbersdobler, August Heidland, Peter Boor, Thomas Hofmann, John W. Baynes, Suzanne R. Thorpe, Veronika SomozaAbstract:The biological consequences of chronic consumption of Maillard Reaction Products (MRPs) on renal function in health and renal disease are still incompletely understood. We investigated the metabolic and renal effects of a diet with varying MRP content in healthy and subtotally nephrectomized rats. Male Wistar rats were subjected to sham operation (control, C, n = 12), or to 5/6 nephrectomy (5/6NX, n = 12). Both groups were randomized into subgroups and pair-fed with either a MRP-poor or -rich diet for six weeks. The diet was prepared by replacing 5% or 25% of wheat starch by bread crust (BC). In spite of pair-feeding, the rats on the 25% BC diet gained more body weight (C: 183 ± 6 g; C + 5% BC: 197 ± 7 g; C + 25% BC: 229 ± 6 g [P < 0.05]; 5/6NX: 165 ± 10 g; 5/6NX + 5% BC: 202 ± 3 g; 5/6NX + 25% BC: 209 ± 8 g [P < 0.05]) and had a higher organ weight (heart, liver, lung, kidney/remnant kidney). Bread crust-enriched diet induced proteinuria (C: 15 ± 5 mg/24 h; C + 5% BC: 19 ± 4; C + 25% BC: 26 ± 3 [P < 0.05]; 5/6NX: 30 ± 7 mg/24 h; 5/6NX + 5% BC: 47 ± 9; 5/6NX + 25% BC: 87 ± 19 [P < 0.01]) and a rise in urinary transforming growth factor ?1 excretion (C: 0.4 ± 0.1 ng/24 h; C + 5% BC: 0.6 ± 0.1; C + 25% BC: 1.2 ± 0.3; 5/6NX: 0.5 ± 0.1 ng/24 h; 5/6NX + 5% BC: 0.9 ± 0.1; 5/6NX + 25% BC: 1.6 ± 0.2 [P < 0.01]). Plasma creatinine or creatinine clearance were not affected significantly. In conclusion, our data suggests that long-term consumption of a diet rich in MRPs may lead to damage of the kidneys. © 2005 New York Academy of Sciences.
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studies on the inhibition of tumor cell growth and microtubule assembly by 3 hydroxy 4 e 2 furyl methylidene methyl 3 cyclopentene 1 2 dione an intensively coloured Maillard Reaction Product
Food and Chemical Toxicology, 2002Co-Authors: Doris Marko, M Kemeny, E Bernady, Michael Habermeyer, U Weyand, S Meiers, Oliver Frank, Thomas HofmannAbstract:Abstract Very recently, 3-hydroxy-4-[(E)-(2-furyl)methylidene]methyl-3-cyclopentene-1,2-dione (1) has been successfully identified as an intensively coloured Maillard Product formed from glucose and l -proline upon thermal food processing. Using a biomimetic synthetic strategy, reference material of compound 1 was prepared and purified, and then used to study its effect on the growth of human tumor cells. Compound 1 was found to potently inhibit the growth of human tumor cells in vitro. Using a reporter gene assay we could show that in growth inhibitory concentrations compound 1 effectively inhibits the phosphorylation of the transcription factor Elk-1. In addition, 1 was found to affect the microtubule skeleton. The human mammary carcinoma cell line MCF-7 exhibits a decrease of the microtubule organisation when treated for 24 h with 1 (⩾20 μ m ). At concentrations of 30 μ m and above a loss of microtubule integrity is observed after 1 h incubation. In vitro studies demonstrated that the polymerisation and, to a minor extent, also the depolymerisation of tubulin, isolated and purified from bovine brain, is inhibited in a dose-dependent manner at concentrations of 30 μ m and above. This is the first time that a non-enzymatically formed browning compound of known structure was reported to effectively inhibit tumor cell growth and microtubule assembly.
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Influence of L-cysteine on the formation of bitter-tasting aminohexose reductones from glucose and L-proline: Identification of a novel furo[2,3- b]thiazine
Journal of Agricultural and Food Chemistry, 1999Co-Authors: Thomas HofmannAbstract:Thermal treatment of a 1 + 1 mixture of glucose and L-proline led to the development of an intense bitter taste being reflected in high amounts of the bitter-tasting bispyrrolidino- (1) and pyrrolidinohexose reductones (2) formed. Heating the Reaction mixture in the presence of L-cysteine drastically reduced the amounts of these aminohexose reductones and, thereby, the intensity of the bitter taste. Studies on the mechanism of the cysteine-induced reduction of the bitter taste revealed that the precursor of the aminohexose reductones, the hexose-derived acetylformoin (3), reacted more easily with L-cysteine to form the 7-hydroxy-4a,6-dimethyl-2H,3H,4aH-furo[2,3-b]thiazine (4), a previousely unknown Maillard Reaction Product, than with L-proline to the aminohexose reductones 1 and 2, thereby blocking the formation of bitter-tasting compounds.
Veronika Somoza - One of the best experts on this subject based on the ideXlab platform.
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n e carboxymethyllysine cml a Maillard Reaction Product stimulates serotonin release and activates the receptor for advanced glycation end Products rage in sh sy5y cells
Food & Function, 2013Co-Authors: Annkatrin Holik, Barbara Rohm, Mark M Somoza, Veronika SomozaAbstract:Maillard Reaction Products, which are formed in highly thermally treated foods, are commonly consumed in a Western diet. In this study, we investigated the impact of Ne-carboxymethyllysine (CML), a well-characterized Product of the Maillard Reaction, on the gene regulation of the human neuroblastoma cell line SH-SY5Y. Pathway analysis of data generated from customized DNA microarrays revealed 3 h incubation with 50 μM and 500 μM CML to affect serotonin receptor expression. Further experiments employing qRT-PCR showed an up-regulation of serotonin receptors 2A, 1A and 1B after 0.25 h and 3 h. In addition, 500 μM CML increased serotonin release, thus showing effects of CML not only at a genetic, but also at a functional level. Intracellular calcium mobilization, which mediates serotonin release, was increased by CML at concentrations of 0.05–500 μM. Since calcium mobilization has been linked to the activation of the receptor for advanced glycation end Products (RAGE), we further investigated the effects of CML on RAGE expression. RAGE was found to be up-regulated after incubation with 500 μM CML for 0.25 h. Co-incubation with the calcium blocker neomycin for 0.25 h blocked the up-regulation of RAGE and the serotonin receptors 2A, 1A and 1B. These results indicate a possible link between a CML-induced calcium-mediated serotonin release and RAGE.
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Maillard Reaction Product rich food impair cell proliferation and induce cell death in vitro
Signal Transduction, 2005Co-Authors: Babett Bartling, Veronika Somoza, Grit Rehbein, Rolfedgar Silber, Andreas SimmAbstract:Maillard Reaction Products (MRPs) and advanced glycation end-Products (AGEs) correspond to modified protein derivatives that are initially generated by non-enzymatic glycation between amino acids and reducing sugars in heat-treated foods and in vivo, respectively. Because lung tissue highly expresses the receptor for advanced glycation end-Products (RAGE), we studied the impact of MRP/AGE-rich foods like bread crust (BC) and coffee extract (CE) on the proliferation and cell death induction using lung epithelial (H358) cells. Here, we showed that CE impairs the proliferation and viability of H358 cells at much higher extent than BC does. Particularly cell death induced by CE showed a concentration-dependent shift from apoptotic to necrotic features as estimated by caspase activation, phosphatidylserine exposure, leakage of the outer membrane, mitochondrial dysfunction and stress kinase activation. Moreover, CE at higher dose triggered the generation of reactive oxygen species thereby mediating caspase inhibition. Non-toxic concentrations of both foods only impaired the proliferation associated with an increased amount of cells in the S/G2 phase of the cell cycle, which did not depend on the over-expression of RAGE. From our data we conclude that MRP/AGE-rich foods mediate antiproliferative effects at moderate concentrations that might be important in physiological conditions like cancer prevention but contributes to cell death at higher levels in vitro.
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renal effects of oral Maillard Reaction Product load in the form of bread crusts in healthy and subtotally nephrectomized rats
Annals of the New York Academy of Sciences, 2005Co-Authors: Katarina Sebekova, Ol'ga Ulicná, Helmut F Erbersdobler, August Heidland, Peter Boor, Thomas Hofmann, John W. Baynes, Suzanne R. Thorpe, Veronika SomozaAbstract:The biological consequences of chronic consumption of Maillard Reaction Products (MRPs) on renal function in health and renal disease are still incompletely understood. We investigated the metabolic and renal effects of a diet with varying MRP content in healthy and subtotally nephrectomized rats. Male Wistar rats were subjected to sham operation (control, C, n = 12), or to 5/6 nephrectomy (5/6NX, n = 12). Both groups were randomized into subgroups and pair-fed with either a MRP-poor or -rich diet for six weeks. The diet was prepared by replacing 5{%} or 25{%} of wheat starch by bread crust (BC). In spite of pair-feeding, the rats on the 25{%} BC diet gained more body weight (C: 183 +/- 6 g; C + 5{%} BC: 197 +/- 7 g; C + 25{%} BC: 229 +/- 6 g [P {\textless} 0.05]; 5/6NX: 165 +/- 10 g; 5/6NX + 5{%} BC: 202 +/- 3 g; 5/6NX + 25{%} BC: 209 +/- 8 g [P {\textless} 0.05]) and had a higher organ weight (heart, liver, lung, kidney/remnant kidney). Bread crust-enriched diet induced proteinuria (C: 15 +/- 5 mg/24 h; C + 5{%} BC: 19 +/- 4; C + 25{%} BC: 26 +/- 3 [P {\textless} 0.05]; 5/6NX: 30 +/- 7 mg/24 h; 5/6NX + 5{%} BC: 47 +/- 9; 5/6NX + 25{%} BC: 87 +/- 19 [P {\textless} 0.01]) and a rise in urinary transforming growth factor beta(1) excretion (C: 0.4 +/- 0.1 ng/24 h; C + 5{%} BC: 0.6 +/- 0.1; C + 25{%} BC: 1.2 +/- 0.3; 5/6NX: 0.5 +/- 0.1 ng/24 h; 5/6NX + 5{%} BC: 0.9 +/- 0.1; 5/6NX + 25{%} BC: 1.6 +/- 0.2 [P {\textless} 0.01]). Plasma creatinine or creatinine clearance were not affected significantly. In conclusion, our data suggests that long-term consumption of a diet rich in MRPs may lead to damage of the kidneys.
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Renal effects of oral Maillard Reaction Product load in the form of bread crusts in healthy and subtotally nephrectomized rats
Annals of the New York Academy of Sciences, 2005Co-Authors: Katarina Sebekova, Ol'ga Ulicná, Helmut F Erbersdobler, August Heidland, Peter Boor, Thomas Hofmann, John W. Baynes, Suzanne R. Thorpe, Veronika SomozaAbstract:The biological consequences of chronic consumption of Maillard Reaction Products (MRPs) on renal function in health and renal disease are still incompletely understood. We investigated the metabolic and renal effects of a diet with varying MRP content in healthy and subtotally nephrectomized rats. Male Wistar rats were subjected to sham operation (control, C, n = 12), or to 5/6 nephrectomy (5/6NX, n = 12). Both groups were randomized into subgroups and pair-fed with either a MRP-poor or -rich diet for six weeks. The diet was prepared by replacing 5% or 25% of wheat starch by bread crust (BC). In spite of pair-feeding, the rats on the 25% BC diet gained more body weight (C: 183 ± 6 g; C + 5% BC: 197 ± 7 g; C + 25% BC: 229 ± 6 g [P < 0.05]; 5/6NX: 165 ± 10 g; 5/6NX + 5% BC: 202 ± 3 g; 5/6NX + 25% BC: 209 ± 8 g [P < 0.05]) and had a higher organ weight (heart, liver, lung, kidney/remnant kidney). Bread crust-enriched diet induced proteinuria (C: 15 ± 5 mg/24 h; C + 5% BC: 19 ± 4; C + 25% BC: 26 ± 3 [P < 0.05]; 5/6NX: 30 ± 7 mg/24 h; 5/6NX + 5% BC: 47 ± 9; 5/6NX + 25% BC: 87 ± 19 [P < 0.01]) and a rise in urinary transforming growth factor ?1 excretion (C: 0.4 ± 0.1 ng/24 h; C + 5% BC: 0.6 ± 0.1; C + 25% BC: 1.2 ± 0.3; 5/6NX: 0.5 ± 0.1 ng/24 h; 5/6NX + 5% BC: 0.9 ± 0.1; 5/6NX + 25% BC: 1.6 ± 0.2 [P < 0.01]). Plasma creatinine or creatinine clearance were not affected significantly. In conclusion, our data suggests that long-term consumption of a diet rich in MRPs may lead to damage of the kidneys. © 2005 New York Academy of Sciences.
