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http://hdl.handle.net/10261/11569
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Campo DC | Valor | Lengua/Idioma |
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dc.contributor.author | Thibaut, Rémi | - |
dc.contributor.author | Schnell, Sabine | - |
dc.contributor.author | Porte Visa, Cinta | - |
dc.date.accessioned | 2009-03-13T10:23:09Z | - |
dc.date.available | 2009-03-13T10:23:09Z | - |
dc.date.issued | 2006-07-07 | - |
dc.identifier.citation | Environmental Science & Technology 40(16): 5154-5160 (2006) | en_US |
dc.identifier.issn | 0013-936x | - |
dc.identifier.uri | http://hdl.handle.net/10261/11569 | - |
dc.description | 7 pages, 2 figures.-- PMID: 16955921 [PubMed].-- Printed version published Aug 15, 2006. | en_US |
dc.description.abstract | The interactions of fibrate (clofibrate, fenofibrate, bezafibrate, gemfibrozil), antiinflammatory (ibuprofen, diclofenac, naproxen, ketoprofen), and anti-depressive (fluoxetine, fluvoxamine, paroxetine) drugs with CYP catalyzed pathways (CYP1A, CYP3A-, CYP2K-, and CYP2M-like) and Phase II activities (UDP-glucuronosyltransferases and sulfotransferases), involved in both xenobiotic and endogenous metabolism in fish, were investigated in-vitro by incubating carp liver subcellular fractions in the presence of the substrate and the selected drug. Antidepressive drugs were strong inhibitors of CYP1A (92-94% inhibition), CYP3A-like (69-80% inhibition), and CYP2Klike (36-69% inhibition) catalyzed activities, while antiinflammatory drugs were potent CYP2M-like inhibitors (32-74% inhibition). Among the lipid regulators, gemfibrozil strongly inhibited CYP2M-catalyzed activity (91% inhibition) and other CYP isoforms (CYP1A and CYP3A-like). Additionally, glucuronidation of naphthol and testosterone were targeted by antiinflammatory drugs, and to a lesser extent, by fibrate drugs (48-78% inhibition). No significant alteration on sulfotransferase activities was observed, apart from a minor inhibitory effect of clofibrate, gemfibrozil, and fluoxetine on the sulfation of estradiol. Overall, gemfibrozil, diclofenac, and the three anti-depressive drugs appear to be the pharmaceuticals with the highest potential to interfere with fish metabolic systems. | en_US |
dc.description.sponsorship | This study was supported by the Spanish Ministry of Science and Education under Project ref. CGL2005-02846. S.S. acknowledges a predoctoral fellowship from the Ministerio de Educación y Ciencia. R.T. acknowledges an I3P contract from the Spanish Government. | en_US |
dc.format.extent | 162 bytes | - |
dc.format.mimetype | application/msword | - |
dc.language.iso | eng | en_US |
dc.publisher | American Chemical Society | en_US |
dc.rights | closedAccess | en_US |
dc.subject | Xenobiotic | en_US |
dc.subject | In vitro | en_US |
dc.subject | Liver | en_US |
dc.subject | Enzyme | en_US |
dc.subject | Drug | en_US |
dc.subject | Interference | en_US |
dc.title | The interference of pharmaceuticals with endogenous and xenobiotic metabolizing enzymes in carp liver: an in-vitro study | en_US |
dc.type | artículo | en_US |
dc.identifier.doi | 10.1021/es0607483 | - |
dc.description.peerreviewed | Peer reviewed | en_US |
dc.relation.publisherversion | http://dx.doi.org/10.1021/es0607483 | en_US |
dc.identifier.e-issn | 1520-5851 | - |
dc.type.coar | http://purl.org/coar/resource_type/c_6501 | es_ES |
item.openairetype | artículo | - |
item.grantfulltext | none | - |
item.cerifentitytype | Publications | - |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
item.fulltext | No Fulltext | - |
item.languageiso639-1 | en | - |
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