TY - JOUR
T1 - Sandy sediment and the bioavailability of 17β-trenbolone to adult female fathead minnows
AU - Jessick, Ashley M.
AU - Skolness, Sarah
AU - Kolok, Alan S.
N1 - Funding Information:
Funding for the project was provided by the National Science Foundation grant awards 0966858 and 0966850 . Technical assistance for the project was provided by Jodi Sangster, Lindsey Knight, Nicholas Conoan, Racine Rangel, and Bethany McAcy. Assistance for sample preparation was provided by Shannon Bartelt-Hunt in the Department of Civil Engineering at the University of Nebraska. Chemical analysis was facilitated by Daniel Snow at the Water Sciences Laboratory at the University of Nebraska at Lincoln. Sand preparation was made possible by the geotechnical lab in the Department of Civil Engineering at the University of Nebraska at Omaha.
PY - 2014/3
Y1 - 2014/3
N2 - Recent studies have detected bioavailable steroids in sediment, however, the mechanism by which these compounds become bioavailable is not completely understood. In this study, two experiments were conducted using a double aquarium system that allowed female fathead minnows to be exposed to sandy sediments without direct contact. In the first experiment, natural sediment from the Elkhorn River (Nebraska, USA) was spiked with 17β-trenbolone. Both the fish in direct contact with the sediment as well as the fish excluded from direct contact experienced significant reductions in the hepatic expression of two estrogen-responsive genes, vitellogenin and estrogen receptor α, indicating molecular defeminization. The natural sediment contained particles ranging in size from sand to clay and it was possible that the fish in experiment 1 were being exposed to trenbolone associated with the very fine particles. The sandy sediment was sieved for experiment 2, and only the particles larger than 250. μm were used. In addition, the experiment was conducted at two different Tb concentrations (1× and 10×). Furthermore nuptial tubercles, a biomarker of exposure to a masculinizing androgen, were also evaluated in the females used in experiment 2. For tubercle number and vtg expression, significant results were obtained from a two-way ANOVA due to Tb concentration, but not tank location or interaction term (location vs. concentration). For ERα expression, results were found in response to Tb concentration and tank location, but not the interaction term. Overall the results from these studies suggest that the primary route of exposure of sediment-associated trenbolone to fish is through ventilation of free compound, rather than ingestion or direct contact with the sediments.
AB - Recent studies have detected bioavailable steroids in sediment, however, the mechanism by which these compounds become bioavailable is not completely understood. In this study, two experiments were conducted using a double aquarium system that allowed female fathead minnows to be exposed to sandy sediments without direct contact. In the first experiment, natural sediment from the Elkhorn River (Nebraska, USA) was spiked with 17β-trenbolone. Both the fish in direct contact with the sediment as well as the fish excluded from direct contact experienced significant reductions in the hepatic expression of two estrogen-responsive genes, vitellogenin and estrogen receptor α, indicating molecular defeminization. The natural sediment contained particles ranging in size from sand to clay and it was possible that the fish in experiment 1 were being exposed to trenbolone associated with the very fine particles. The sandy sediment was sieved for experiment 2, and only the particles larger than 250. μm were used. In addition, the experiment was conducted at two different Tb concentrations (1× and 10×). Furthermore nuptial tubercles, a biomarker of exposure to a masculinizing androgen, were also evaluated in the females used in experiment 2. For tubercle number and vtg expression, significant results were obtained from a two-way ANOVA due to Tb concentration, but not tank location or interaction term (location vs. concentration). For ERα expression, results were found in response to Tb concentration and tank location, but not the interaction term. Overall the results from these studies suggest that the primary route of exposure of sediment-associated trenbolone to fish is through ventilation of free compound, rather than ingestion or direct contact with the sediments.
KW - Bioavailability
KW - Gene expression
KW - Route of exposure
KW - Sandy sediment
KW - Trenbolone
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U2 - 10.1016/j.aquatox.2013.12.025
DO - 10.1016/j.aquatox.2013.12.025
M3 - Article
C2 - 24441280
AN - SCOPUS:84892514137
SN - 0166-445X
VL - 148
SP - 48
EP - 54
JO - Aquatic Toxicology
JF - Aquatic Toxicology
ER -