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291.
Ohne Zusammenfassung 相似文献
292.
Dr. A. v. Degen 《Plant Systematics and Evolution》1899,49(7):261-262
Ohne Zusammenfassung 相似文献
293.
Dr. A. v. Degen 《Plant Systematics and Evolution》1891,41(7):231-232
Ohne Zusammenfassung 相似文献
294.
Arpad v. Degen 《Plant Systematics and Evolution》1889,39(4):137-137
Ohne Zusammenfassung 相似文献
295.
Katherine Muñoz Meinolf BlaszkewiczGisela H. Degen 《Journal of chromatography. B, Analytical technologies in the biomedical and life sciences》2010,878(27):2623-2629
Ochratoxin A (OTA) is a frequent mycotoxin contaminant found worldwide in foods and feedstuffs. Biomonitoring has been used to assess internal OTA exposure resulting from dietary intake and from other sources. Mycotoxin levels in blood and/or urine provide good estimates of past and recent exposure since OTA binds to serum proteins and is also partly excreted via the kidney. But, measuring OTA alone does not reflect its biotransformation. In light of scarce data on its metabolites in humans, it was the aim of this study to develop a method that allows analysis of OTA and its detoxication product ochratoxin alpha (OTα) in urine and in blood plasma. The method involves enzymatic hydrolysis of conjugates, liquid–liquid extraction, and analysis of sample extracts by liquid chromatography with fluorescence detection. Application of the validated method in a pilot study with 13 volunteers revealed the presence of OTA and OTα in all samples (limit of quantification: 0.05 ng/mL in urine, and 0.1 ng/mL in plasma). In line with negative findings of others, an OTA glucuronide was not detected, neither in urine nor in plasma. By contrast, conjugates of OTα (glucuronide and/or sulfate) are major products in these samples. This was confirmed by mass spectrometry detection. As OTα represents a large fraction of ingested mycotoxin, we propose to include analyses of this metabolite in future biomonitoring studies, also in light of the observed variations for urine OTα-levels that suggest different interindividual abilities for OTA-detoxification in humans. 相似文献
296.
Ohne Zusammenfassung 相似文献
297.
Dr. A. von Degen 《Plant Systematics and Evolution》1897,47(6):195-199
Ohne Zusammenfassung 相似文献
298.
Prostaglandin H synthase (PHS) has gained interest as a drugmetabolizing enzyme and has been shown to cooxidize and metabolically activate diethylstilbestrol (DES) in vitro. Both 7,8-benzoflavone (α-naphthoflavone, ANF) and 5,6-benzoflavone (β-naphthoflavone, BNF) have now been studied for their effects on PHS from ram seminal vesicle microsomes by means of several in vitro assays. The PHS-catalyzed cooxidation of DES, as measured by high-performance liquid chromatography (HPLC) analysis, is inhibited by BNF and ANF at micromolar concentrations, with median inhibitory concentrations (IC-50) of<20 and 40 μM, respectively. The oxidation of DES is inhibited whether it is initiated by arachidonic acid or by hydrogen peroxide, indicating that the benzoflavones inhibit PHS by a mechanism different from that of indomethacin. Monitoring of cyclooxygenase activity in an oxygraph also reveals an inhibition of PHS by BNF which depends only weakly on arachidonic acid concentration; inhibition by ANF is less pronounced under these conditions. Since PHS-catalyzed conversion of the benzoflavone compounds was detected under conditions permitting cooxidation, the inhibition of PHS by benzoflavones in vitro could either be a direct effect or possibly mediated via metabolites. Our data imply that ANF and BNF, in addition to their well-known role as modifiers of mixed-function oxidases, can affect the PHS-catalyzed metabolism of xenobiotics. This is discussed in the context of adverse effects caused by DES in vivo and in cell culture and must be taken into account when interpreting the modifying effect of benzoflavones on these endpoints. 相似文献
299.
Dr. A. v. Degen 《Plant Systematics and Evolution》1891,41(6):194-195
Ohne Zusammenfassung 相似文献
300.
Dr. A. von Degen 《Plant Systematics and Evolution》1897,47(9):313-316
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