Anguilla anguilla L. liver ethoxyresorufin O-deethylation, glutathione S-tranferase, erythrocytic nuclear abnormalities, and endocrine responses to naphthalene and β-naphthoflavone

The effects of naphthalene (NAP) and β-naphthoflavone (BNF) on phase I biotransformation and genotoxicity in Anguilla anguilla L. were evaluated. Phase II biotransformation and cortisol levels were also assessed in NAP-treated fish. Two groups of eels were exposed to either a NAP or a BNF concentrat...

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Detalles Bibliográficos
Autores: Teles, Mariana|||0000-0001-5525-4049, Pacheco, M. Guilherme Garcês|||0000-0003-0552-9643, Santos Maroño, Mauro|||0000-0002-6478-6570
Tipo de recurso: artículo
Fecha de publicación:2003
País:España
Institución:Universitat Autònoma de Barcelona
Repositorio:Dipòsit Digital de Documents de la UAB
Idioma:inglés
OAI Identifier:oai:ddd.uab.cat:323791
Acceso en línea:https://ddd.uab.cat/record/323791
https://dx.doi.org/urn:doi:10.1016/S0147-6513(02)00134-3
Access Level:acceso abierto
Palabra clave:SDG 3 - Good Health and Well-being
Descripción
Sumario:The effects of naphthalene (NAP) and β-naphthoflavone (BNF) on phase I biotransformation and genotoxicity in Anguilla anguilla L. were evaluated. Phase II biotransformation and cortisol levels were also assessed in NAP-treated fish. Two groups of eels were exposed to either a NAP or a BNF concentration range (0.1-2.7μM) for different exposure periods (2-72h). An early significant ethoxyresorufin O-deethylation (EROD) activity inhibition was observed, especially for the highest NAP concentrations at 2-6h exposure and for BNF at 2h exposure. However, a significant EROD activity increase was detected from 16 to 72h exposure for NAP and from 4 to 72h exposure for BNF. The cytochrome P450 (P450) content was not dose related. However, with regard to BNF exposure, P450 was the first biomarker to respond. Liver alanine transaminase (ALT) activity was measured as an indicator of hepatic health condition. ALT results demonstrated that the EROD activity decrease, previously described for NAP, was not related to tissue damage. Nevertheless, the highest BNF concentrations were demonstrated to induce liver damage and to impair the EROD activity response. An increased genotoxic response, measured as erythrocytic nuclear abnormalities (ENA), was observed during the first 8h NAP exposure. However, for exposures longer than 8h, ENA frequency returned to the control levels. This response profile may reflect a considerable DNA repair capacity and/or a metabolic adaptation providing an efficient NAP biotransformation and consequent detoxification. BNF revealed no ENA alterations for all concentrations and exposure lengths. In the NAP experiment a causal relationship between immature erythrocytes (IE) and ENA frequency disappearance was not found. BNF results with regard to IE frequency revealed an ability to alter the balance between erythropoiesis and removal of erythrocytes. Liver glutathione S-transferase activity was significantly induced after 2 and 48h NAP exposure. A cortisol-impaired response seems to occur from 4 to 24h NAP exposure, demonstrating an endocrine disruption. However, an adaptation process seems to occur after 48h, since the plasma cortisol had a tendency to increase. The present findings confirm the usefulness of the adopted biomarkers. The ecological risk associated with aquatic contamination by NAP was also confirmed by the present data.