|Ethoxyresorufin-O-deethylase (EROD) and vitellogenin (VTG) in flounder (Platichthys flesus): System interaction, crosstalk and implications for monitoring|Kirby, M.F.; Smith, A.J.; Rooke, J.; Neall, P.; Scott, A.P.; Katsiadaki, I. (2007). Ethoxyresorufin-O-deethylase (EROD) and vitellogenin (VTG) in flounder (Platichthys flesus): System interaction, crosstalk and implications for monitoring. Aquat. Toxicol. 81(3): 233-244. dx.doi.org/10.1016/j.aquatox.2006.12.004
In: Aquatic Toxicology. Elsevier Science: Tokyo; New York; London; Amsterdam. ISSN 0166-445X, more
Aromatic hydrocarbons; Biomarkers; Endocrinology; Monitoring; Vitellogenesis; Marine
|Authors|| || Top |
- Kirby, M.F.
- Smith, A.J.
- Rooke, J.
- Neall, P.
- Scott, A.P.
- Katsiadaki, I.
The extent to which biological systems interact in fish from multi-contaminant areas needs to be understood for full interpretation of monitoring data. This study investigates the interaction between two biomarkers, ethoxyresorufin-O-deethylase (EROD) activity and plasma vitellogenin (VTG) in the European flounder (Platichthys flesus). Flounder were exposed to several waterborne EROD inducers and estrogenic chemicals on their own and in binary combinations. Each experimental exposure was for 10 days. The estrogenic chemicals suppressed PAH-mediated EROD induction. Ethynylestradiol (EE2) and nonylphenol (NP) had threshold concentrations of EROD inhibition similar to those at which they induced VTG production. Estradiol (E2), however, showed an ability to suppress EROD at a concentration much lower than that at which VTG was induced. This established that, although EE2 is a more potent VTG inducer than E2, it is less potent in its ability to inhibit EROD activity. The PAH, dibenz[a,h]anthracene (DbA), showed no effect on the VTG induction caused by EE2 and E2. A small effect was noted with NP at threshold concentrations for VTG induction. Archived data on flounder hepatic EROD activity collected during estuarine monitoring were reassessed in light of the project findings. It is hypothesised that published EROD monitoring data may be an underestimation of effects if it is assumed that estrogen-mediated MFO suppression is occurring in wild populations. A greater understanding of system interaction and other factors, including genetics, that influence biomarker response to contaminants would be required to interpret biomarker monitoring data.