Induced cytochrome P450 1A activity in cichlid fishes from Guandu River and Jacarepaguá Lake, Rio de Janeiro, Brazil

The induction of cytochrome P4501A-mediated activity (e.g. ethoxyresorufin- O-deethylation, EROD) has been used as a biomarker for monitoring fish exposure to AhR-receptor ligands such as polycyclic aromatic hydrocarbons (PAH), polychlorinated biphenyls (PCB) and polychlorinated dibenzo-dioxins/fura...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Environmental pollution (1987) 2008-03, Vol.152 (1), p.233-238
Hauptverfasser: Parente, Thiago E.M., De-Oliveira, Ana C.A.X., Paumgartten, Francisco J.R.
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:The induction of cytochrome P4501A-mediated activity (e.g. ethoxyresorufin- O-deethylation, EROD) has been used as a biomarker for monitoring fish exposure to AhR-receptor ligands such as polycyclic aromatic hydrocarbons (PAH), polychlorinated biphenyls (PCB) and polychlorinated dibenzo-dioxins/furans (PCDD/Fs). In this study we found that hepatic EROD is induced in fish (“Nile tilapia”, Oreochromis niloticus and “acará”, Geophagus brasiliensis) from the Guandu River (7–17-fold) and Jacarepaguá Lake (7-fold), Rio de Janeiro, Brazil. Since both cichlid fish are consumed by the local population and the Guandu River is the main source of the drinking water supply for the greater Rio de Janeiro metropolitan area, pollution by cytochrome P4501A-inducing chemicals is a cause for concern and should be further investigated in sediments, water and biota. We additionally showed that EROD activity in the fish liver post-mitochondrial supernatant—simpler, cheaper and less time consuming to prepare than the microsomal fraction—is sufficiently sensitive for monitoring purposes. Increased EROD activity in the liver of cichlid fishes indicated that Guandu River, the source of drinking water supply for Rio de Janeiro is polluted by CYP1A-inducing chemicals.
ISSN:0269-7491
1873-6424
DOI:10.1016/j.envpol.2007.04.025