Unbound MEDLINE

Oxidation of atenolol, propranolol, carbamazepine and clofibric acid by a biological Fenton-like system mediated by the white-rot fungus Trametes versicolor. Water research [Water Res] Journal article

 
TitleOxidation of atenolol, propranolol, carbamazepine and clofibric acid by a biological Fenton-like system mediated by the white-rot fungus Trametes versicolor.
Author(s)Marco-Urrea E, Radjenović J, Caminal G, Petrović M, Vicent T, Barceló D 
InstitutionDepartament d'Enginyeria Química and Institut de Ciència i Tecnologia Ambiental, Universitat Autònoma de Barcelona (UAB), 08193 Bellaterra, Spain.
SourceWater Res 2009 Sep 22.
AbstractBiological advanced oxidation of the pharmaceuticals clofibric acid (CA), carbamazepine (CBZP), atenolol (ATL) and propranolol (PPL) is reported for the first time. Extracellular oxidizing species were produced through a quinone redox cycling mechanism catalyzed by an intracellular quinone reductase and any of the ligninolytic enzymes of Trametes versicolor after addition of the lignin-derived quinone 2,6-dimethoxy-1,4-benzoquinone (DBQ) and Fe(3+)-oxalate in the medium. Time-course experiments with approximately 10mg L(-1) of initial pharmaceutical concentration resulted in percent degradations above 80% after 6h of incubation. Oxidation of pharmaceuticals was only observed under DBQ redox cycling conditions. A similar degradation pattern was observed when CBZP was added at the environmentally relevant concentration of 50mug L(-1). Depletion of DBQ due to the attack of oxidizing agents was assumed to be the main limiting factor of pharmaceutical degradation. The main degradation products, that resulted to be pharmaceutical hydroxylated derivatives, were structurally elucidated. The detected 4- and 7-hydroxycarbamazepine intermediates of CBZP degradation were not reported to date. Total disappearance of intermediates was observed in all the experiments at the end of the incubation period.
LanguageENG
Pub Type(s)JOURNAL ARTICLE
PubMed ID19850317
  
Advertise on this site.