(Oral Presentation - 2)
Chronic life-cycle effects of clofibric acid in the zebrafish
(Danio rerio)
Coimbra3, A.M, Peixoto 1,3, M.J., Coelho 1, I., Lacerda1, R., Carvalho 1,2, A.P., Gesto 1,
M., Lyssimachou 1, A., Lima 1, D., Soares 1, J., André 1, A., Capitão 1, A., Castro 1, L.
Filipe C., Santos1,2 *, M.M.
1 CIMAR/CIIMAR – Interdisciplinary Centre of Marine and Environmental Research,
University of Porto, Rua dos Bragas 177, 4050-123 Porto, Portugal.
2 FCUP – Department of Biology, Faculty of Sciences, University of Porto, Rua do
Campo Alegre, 4169-007 Porto, Portugal
3 DeBA-ECVA-UTAD - Departamento de Biologia e Ambiente - Escola de Ciências da
Vida e Ambiente – Universidade de Trás-os-Montes e Alto Douro - Quinta de Prados,
Apartado 1013, 5001-801 Vila Real, Portugal
Presenting author contact: * [email protected]
The presence of pharmaceuticals in the aquatic environment has raised considerable
concern over the last decade. Clofibric acid (CA) is an active metabolite of blood lipid
lowering agent clofibrate, and is one of the most common pharmaceuticals found in
aquatic ecosystems. Although the presence of CA in water is well described, the
knowledge on its effects in fish is still contradictory and poorly understood; furthermore,
studies on multigenerational effects are still missing. Therefore, the present study
aimed at identifying the effects and the impacted molecular pathways of CA exposure
in zebrafish (F1) and in their progeny (F2). The results indicate that CA exposure
impacts key ecological relevant endpoints such as reproduction, growth, lipid
metabolism and embryonic development. Diet exposure to CA (1 and 10 mg/g diet)
from 5 days pos-fertilization (dpf) to adulthood (144 dpf) induced a significant decrease
in fecundity at the highest dose and impacted gonad stereological endpoints of both
males and females. Similarly, CA decreased triglyceride muscle content and induced
and increase in the percentage of abnormal larvae (1 mg/g exposure). The screening
of the affected molecular pathways indicates that in accordance to the reported effects
in mammals, CA impacts pathways involved in lipid metabolism.