The Experts below are selected from a list of 819 Experts worldwide ranked by ideXlab platform
Michael Murkovic - One of the best experts on this subject based on the ideXlab platform.
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analysis of 5 hydroxymethyl 2 Furoic Acid hmfa the main metabolite of alimentary 5 hydroxymethyl 2 furfural hmf with hplc and gc in urine
Food Chemistry, 2010Co-Authors: Daniela Jobstl, Trine Husoy, Jan Alexander, Thomas Bjellaas, Erich Leitner, Michael MurkovicAbstract:Abstract A liquid chromatographic method with UV detection was developed to analyse 5-hydroxymethyl-2-furfural and its main metabolite 5-hydroxymethyl-2-Furoic Acid in urine. For the analysis on a reversed phase column was used with 5% methanol in water and 5 mM tetramethylammoniumhydrogen sulphate as ion-pair reagent as eluent. The detection was done at the UV absorption maximum of HMFA at 255 nm. The limit of quantification for HMFA was 7 mg/L with a recovery of 89%. For sample preparation the urine was centrifuged and the supernatant diluted with water. Three hundred samples of human urine were analysed. The concentration of HMFA was in the range of 0–100 mg/L with most of the samples around 10 mg/L.
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dietary exposure to 5 hydroxymethylfurfural from norwegian food and correlations with urine metabolites of short term exposure
Food and Chemical Toxicology, 2008Co-Authors: Trine Husoy, Michael Murkovic, Thomas Bjellaas, Margaretha Haugen, D Jobstl, Linn Helene Stolen, C Ronningborg, Hansruedi Glatt, Jan AlexanderAbstract:5-Hydroxymethylfurfural (HMF) is formed in carbohydrate-rich food during Acid-catalysed dehydration and in the Maillard reaction from reducing sugars. HMF is found in mg quantities per kg in various foods. HMF is mainly metabolised to 5-hydroxymethyl-2-Furoic Acid (HMFA), but unknown quantities of the mutagenic 5-sulphoxymethylfurfural (SMF) may also be formed, making HMF potentially hazardous to humans. We determined the HMF content in Norwegian food items and estimated the dietary intake of HMF in 53 volunteers by means of 24h dietary recall. The estimated intakes of HMF were correlated with urinary excretion of HMFA. Coffee, prunes, dark beer, canned peaches and raisins had the highest levels of HMF. The 95th percentile of the estimated daily dietary intake of HMF and the 24h urinary excretion of HMFA were 27.6 and 28.6mg, respectively. Coffee, dried fruit, honey and alcohol were identified as independent determinants of urinary HMFA excretion. Most participants had lower estimated HMF intake than the amount of HMFA excreted in urine. In spite of this there was a significant correlation (r=0.57, P<0.001) between the estimated HMF intake and urinary HMFA. Further studies are needed to reveal alternative sources for HMF exposure.
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formation of 5 hydroxymethyl 2 furfural hmf and 5 hydroxymethyl 2 Furoic Acid during roasting of coffee
Molecular Nutrition & Food Research, 2007Co-Authors: Michael Murkovic, Mariaanna BornikAbstract:The formation of 5-hydroxymethyl-2-furfural (HMF) and 5-hydroxymethyl-2-Furoic Acid (HMFA) during roasting of coffee was studied. At 240 degrees C the maximum concentration of HMF occurs after 3 min with a quick degradation up to 10 min when most of the HMF has disappeared again. Similar to 5-hydroxymethyl-furfural, HMFA is formed in coffee but not in a model system consisting of sucrose, alanine with or without chlorogenic Acid. It was shown that HMFA is produced from different precursors than HMF namely glyceraldehyde and pyruvate. The comparison of the laboratory scale roasting with industrial roasting showed that 5-hydroxymethyl-furfural decreases with a higher degree of roasting whereas HMFA did not change. In the laboratory scale experiments, the highest concentration of 5-hydroxymethyl-furfural in coffee (909 microg/g) was obtained after 3 min and the maximum concentration of HMFA after 4 min (150 microg/g). Industrially roasted coffee contained up to 350 microg/g 5-hydroxymethyl-furfural and 140 microg/g HMFA.
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formation of 5 hydroxymethyl 2 furfural hmf and 5 hydroxymethyl 2 Furoic Acid during roasting of coffee
COST 927 Workshop, 2007Co-Authors: Michael Murkovic, Mariaanna BornikAbstract:The formation of 5-hydroxymethyl-2-furfural (HMF) and 5-hydroxymethyl-2-Furoic Acid (HMFA) during roasting of coffee was studied. At 240°C the maximum concentration of HMF occurs after 3 min with a quick degradation up to 10 min when most of the HMF has disappeared again. Similar to 5-hydroxymethyl-furfural, HMFA is formed in coffee but not in a model system consisting of sucrose, alanine with or without chlorogenic Acid. It was shown that HMFA is produced from different precursors than HMF namely glyceraldehyde and pyruvate. The comparison of the laboratory scale roasting with industrial roasting showed that 5-hydroxymethyl-furfural decreases with a higher degree of roasting whereas HMFA did not change. In the laboratory scale experiments, the highest concentration of 5-hydroxymethyl-furfural in coffee (909 μg/g) was obtained after 3 min and the maximum concentration of HMFA after 4 min (150 μg/g). Industrially roasted coffee contained up to 350 μg/g 5-hydroxymethyl-furfural and 140 μg/g HMFA.
Michael B Cohen - One of the best experts on this subject based on the ideXlab platform.
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tofa 5 tetradecyl oxy 2 Furoic Acid reduces fatty Acid synthesis inhibits expression of ar neuropilin 1 and mcl 1 and kills prostate cancer cells independent of p53 status
Cancer Biology & Therapy, 2011Co-Authors: Natalya V Guseva, Oskar W Rokhlin, Rebecca A Glover, Michael B CohenAbstract:A key player in prostate cancer development and progression is the androgen receptor (AR). Tumor-associated lipogenesis can protect cancer cells from carcinogenic- and therapeutic-associated treatments. Increased synthesis of fatty Acids and cholesterol is regulated by androgens through induction of several genes in androgen-responsive cancer cells. Acetyl-CoA-carboxylase-α (ACCA) is a key enzyme in the regulation of fatty Acids synthesis. Here we show that AR binds in vivo to intron regions of human ACCA gene. We also show that the level of ACCA protein in LNCaP depends on AR expression and that DHT treatment increases ACCA expression and fatty Acid synthesis. Inhibition of ACCA by TOFA (5-tetradecyl-oxy-2-Furoic Acid) decreases fatty Acid synthesis and induces caspase activation and cell death in most PCa cell lines. Our data suggest that TOFA can kill cells via the mitochondrial pathway since we found cytochrome c release after TOFA treatment in androgen sensitive cell lines. The results also imply tha...
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tofa 5 tetradecyl oxy 2 Furoic Acid reduces fatty Acid synthesis inhibits expression of ar neuropilin 1 and mcl 1 and kills prostate cancer cells independent of p53 status
Cancer Biology & Therapy, 2011Co-Authors: Natalya V Guseva, Oskar W Rokhlin, Rebecca A Glover, Michael B CohenAbstract:A key player in prostate cancer development and progression is the androgen receptor (AR). Tumor-associated lipogenesis can protect cancer cells from carcinogenic- and therapeutic-associated treatments. Increased synthesis of fatty Acids and cholesterol is regulated by androgens through induction of several genes in androgen-responsive cancer cells. Acetyl-CoA-carboxylase-α (ACCA) is a key enzyme in the regulation of fatty Acids synthesis. Here we show that AR binds in vivo to intron regions of human ACCA gene. We also show that the level of ACCA protein in LNCaP depends on AR expression and that DHT treatment increases ACCA expression and fatty Acid synthesis. Inhibition of ACCA by TOFA (5-tetradecyl-oxy-2-Furoic Acid) decreases fatty Acid synthesis and induces caspase activation and cell death in most PCa cell lines. Our data suggest that TOFA can kill cells via the mitochondrial pathway since we found cytochrome c release after TOFA treatment in androgen sensitive cell lines. The results also imply that the pro-apoptotic effect of TOFA may be mediated via a decrease of neuropilin-1(NRP1) and Mcl-1expression. We have previously reported that Mcl-1 is under AR regulation and plays an important role in resistance to drug-induced apoptosis in prostate cancer cells, and NRP1 is known to regulate Mcl-1 expression. Here, we show for the first time that NRP1 expression is under AR control. Taken together, our data suggest that TOFA is a potent cell death inducing agent in prostate cancer cells.
Natalya V Guseva - One of the best experts on this subject based on the ideXlab platform.
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tofa 5 tetradecyl oxy 2 Furoic Acid reduces fatty Acid synthesis inhibits expression of ar neuropilin 1 and mcl 1 and kills prostate cancer cells independent of p53 status
Cancer Biology & Therapy, 2011Co-Authors: Natalya V Guseva, Oskar W Rokhlin, Rebecca A Glover, Michael B CohenAbstract:A key player in prostate cancer development and progression is the androgen receptor (AR). Tumor-associated lipogenesis can protect cancer cells from carcinogenic- and therapeutic-associated treatments. Increased synthesis of fatty Acids and cholesterol is regulated by androgens through induction of several genes in androgen-responsive cancer cells. Acetyl-CoA-carboxylase-α (ACCA) is a key enzyme in the regulation of fatty Acids synthesis. Here we show that AR binds in vivo to intron regions of human ACCA gene. We also show that the level of ACCA protein in LNCaP depends on AR expression and that DHT treatment increases ACCA expression and fatty Acid synthesis. Inhibition of ACCA by TOFA (5-tetradecyl-oxy-2-Furoic Acid) decreases fatty Acid synthesis and induces caspase activation and cell death in most PCa cell lines. Our data suggest that TOFA can kill cells via the mitochondrial pathway since we found cytochrome c release after TOFA treatment in androgen sensitive cell lines. The results also imply tha...
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tofa 5 tetradecyl oxy 2 Furoic Acid reduces fatty Acid synthesis inhibits expression of ar neuropilin 1 and mcl 1 and kills prostate cancer cells independent of p53 status
Cancer Biology & Therapy, 2011Co-Authors: Natalya V Guseva, Oskar W Rokhlin, Rebecca A Glover, Michael B CohenAbstract:A key player in prostate cancer development and progression is the androgen receptor (AR). Tumor-associated lipogenesis can protect cancer cells from carcinogenic- and therapeutic-associated treatments. Increased synthesis of fatty Acids and cholesterol is regulated by androgens through induction of several genes in androgen-responsive cancer cells. Acetyl-CoA-carboxylase-α (ACCA) is a key enzyme in the regulation of fatty Acids synthesis. Here we show that AR binds in vivo to intron regions of human ACCA gene. We also show that the level of ACCA protein in LNCaP depends on AR expression and that DHT treatment increases ACCA expression and fatty Acid synthesis. Inhibition of ACCA by TOFA (5-tetradecyl-oxy-2-Furoic Acid) decreases fatty Acid synthesis and induces caspase activation and cell death in most PCa cell lines. Our data suggest that TOFA can kill cells via the mitochondrial pathway since we found cytochrome c release after TOFA treatment in androgen sensitive cell lines. The results also imply that the pro-apoptotic effect of TOFA may be mediated via a decrease of neuropilin-1(NRP1) and Mcl-1expression. We have previously reported that Mcl-1 is under AR regulation and plays an important role in resistance to drug-induced apoptosis in prostate cancer cells, and NRP1 is known to regulate Mcl-1 expression. Here, we show for the first time that NRP1 expression is under AR control. Taken together, our data suggest that TOFA is a potent cell death inducing agent in prostate cancer cells.
Mariaanna Bornik - One of the best experts on this subject based on the ideXlab platform.
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formation of 5 hydroxymethyl 2 furfural hmf and 5 hydroxymethyl 2 Furoic Acid during roasting of coffee
Molecular Nutrition & Food Research, 2007Co-Authors: Michael Murkovic, Mariaanna BornikAbstract:The formation of 5-hydroxymethyl-2-furfural (HMF) and 5-hydroxymethyl-2-Furoic Acid (HMFA) during roasting of coffee was studied. At 240 degrees C the maximum concentration of HMF occurs after 3 min with a quick degradation up to 10 min when most of the HMF has disappeared again. Similar to 5-hydroxymethyl-furfural, HMFA is formed in coffee but not in a model system consisting of sucrose, alanine with or without chlorogenic Acid. It was shown that HMFA is produced from different precursors than HMF namely glyceraldehyde and pyruvate. The comparison of the laboratory scale roasting with industrial roasting showed that 5-hydroxymethyl-furfural decreases with a higher degree of roasting whereas HMFA did not change. In the laboratory scale experiments, the highest concentration of 5-hydroxymethyl-furfural in coffee (909 microg/g) was obtained after 3 min and the maximum concentration of HMFA after 4 min (150 microg/g). Industrially roasted coffee contained up to 350 microg/g 5-hydroxymethyl-furfural and 140 microg/g HMFA.
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formation of 5 hydroxymethyl 2 furfural hmf and 5 hydroxymethyl 2 Furoic Acid during roasting of coffee
COST 927 Workshop, 2007Co-Authors: Michael Murkovic, Mariaanna BornikAbstract:The formation of 5-hydroxymethyl-2-furfural (HMF) and 5-hydroxymethyl-2-Furoic Acid (HMFA) during roasting of coffee was studied. At 240°C the maximum concentration of HMF occurs after 3 min with a quick degradation up to 10 min when most of the HMF has disappeared again. Similar to 5-hydroxymethyl-furfural, HMFA is formed in coffee but not in a model system consisting of sucrose, alanine with or without chlorogenic Acid. It was shown that HMFA is produced from different precursors than HMF namely glyceraldehyde and pyruvate. The comparison of the laboratory scale roasting with industrial roasting showed that 5-hydroxymethyl-furfural decreases with a higher degree of roasting whereas HMFA did not change. In the laboratory scale experiments, the highest concentration of 5-hydroxymethyl-furfural in coffee (909 μg/g) was obtained after 3 min and the maximum concentration of HMFA after 4 min (150 μg/g). Industrially roasted coffee contained up to 350 μg/g 5-hydroxymethyl-furfural and 140 μg/g HMFA.
Oskar W Rokhlin - One of the best experts on this subject based on the ideXlab platform.
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tofa 5 tetradecyl oxy 2 Furoic Acid reduces fatty Acid synthesis inhibits expression of ar neuropilin 1 and mcl 1 and kills prostate cancer cells independent of p53 status
Cancer Biology & Therapy, 2011Co-Authors: Natalya V Guseva, Oskar W Rokhlin, Rebecca A Glover, Michael B CohenAbstract:A key player in prostate cancer development and progression is the androgen receptor (AR). Tumor-associated lipogenesis can protect cancer cells from carcinogenic- and therapeutic-associated treatments. Increased synthesis of fatty Acids and cholesterol is regulated by androgens through induction of several genes in androgen-responsive cancer cells. Acetyl-CoA-carboxylase-α (ACCA) is a key enzyme in the regulation of fatty Acids synthesis. Here we show that AR binds in vivo to intron regions of human ACCA gene. We also show that the level of ACCA protein in LNCaP depends on AR expression and that DHT treatment increases ACCA expression and fatty Acid synthesis. Inhibition of ACCA by TOFA (5-tetradecyl-oxy-2-Furoic Acid) decreases fatty Acid synthesis and induces caspase activation and cell death in most PCa cell lines. Our data suggest that TOFA can kill cells via the mitochondrial pathway since we found cytochrome c release after TOFA treatment in androgen sensitive cell lines. The results also imply tha...
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tofa 5 tetradecyl oxy 2 Furoic Acid reduces fatty Acid synthesis inhibits expression of ar neuropilin 1 and mcl 1 and kills prostate cancer cells independent of p53 status
Cancer Biology & Therapy, 2011Co-Authors: Natalya V Guseva, Oskar W Rokhlin, Rebecca A Glover, Michael B CohenAbstract:A key player in prostate cancer development and progression is the androgen receptor (AR). Tumor-associated lipogenesis can protect cancer cells from carcinogenic- and therapeutic-associated treatments. Increased synthesis of fatty Acids and cholesterol is regulated by androgens through induction of several genes in androgen-responsive cancer cells. Acetyl-CoA-carboxylase-α (ACCA) is a key enzyme in the regulation of fatty Acids synthesis. Here we show that AR binds in vivo to intron regions of human ACCA gene. We also show that the level of ACCA protein in LNCaP depends on AR expression and that DHT treatment increases ACCA expression and fatty Acid synthesis. Inhibition of ACCA by TOFA (5-tetradecyl-oxy-2-Furoic Acid) decreases fatty Acid synthesis and induces caspase activation and cell death in most PCa cell lines. Our data suggest that TOFA can kill cells via the mitochondrial pathway since we found cytochrome c release after TOFA treatment in androgen sensitive cell lines. The results also imply that the pro-apoptotic effect of TOFA may be mediated via a decrease of neuropilin-1(NRP1) and Mcl-1expression. We have previously reported that Mcl-1 is under AR regulation and plays an important role in resistance to drug-induced apoptosis in prostate cancer cells, and NRP1 is known to regulate Mcl-1 expression. Here, we show for the first time that NRP1 expression is under AR control. Taken together, our data suggest that TOFA is a potent cell death inducing agent in prostate cancer cells.
