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- Larsson, D. G. Joakim, 1969, et al.
(författare)
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Characterization of putative ligands for a fish gonadal androgen receptor in a pulp mill effluent.
- 2006
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Ingår i: Environmental toxicology and chemistry / SETAC. - 0730-7268. ; 25:2, s. 419-27
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Tidskriftsartikel (refereegranskat)abstract
- Fish exposed to pulp and paper mill effluents often become masculinized. A plausible hypothesis is that this is caused by activation of androgen receptors. The present study aimed to investigate if ligands for the fish gonadal androgen receptor (AR2) are present in pulp mill effluent and to characterize/identify these compounds. Extracts of both primary and biologically treated effluents from a Swedish kraft pulp mill were fractionated chemically. Fractions were tested in competitive binding assays for AR2 from ovaries of the Atlantic croaker (Micropogonias undulatus). Primary effluent contained 96 ng dihydrotestosterone equivalents/ L, whereas biologically treated effluent was 16 times less potent. Further fractionations and assays of binding activities were performed on the primary effluent. Eight final fractions displaced androgen in the binding assay, and gas chromatography/mass spectrometry (GC/MS) analyses revealed that these contained 37 detectable compounds that were not present in inactive fractions. The majority were moderately polar compounds between 200 and 400 g/mol with hydroxyl/carbonyl groups. Two compounds were ruled out because of their lack of binding to AR2. The mass spectra of a third compound matched that of 4-hydroxy-3 (2-(4-hydroxy-3-methoxophenyl)ethyl)-5-metoxyacetophenon, but the remaining candidates could not be fully identified. A search for 21 known steroidal AR2 ligands showed that progesterone, a relatively strong AR2 ligand, was present in the primary effluent (1.6 microg/L) but was removed during the biological treatment step. The detection of multiple fractions with significant binding activity indicates that a variety of compounds in effluents have the potential to masculinize fish near pulp mills via an androgen receptor-mediated mechanism.
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