TP9 Urban Watershed Assessment - A Pacific Northwest (USA) Example
D137-140
1:20 PM - 4:40 PM, Tuesday
() Effects of ethynylestradiol on the growth and reproductive endocrine systems of salmonid fish.
Swanson, P.1, 2, Schulz, I.3, Young, G.2, 4, Nagler, J.2, 4, Fukada, H.1, Dickey, J.5, Cooper, K.5, Hodges, N.5, 1 NOAA-Fisheries, Seattle, WA, USA2 Center of Reproductive Biology, Pullman, WA, USA3 Battelle Marine Science Laboratory, Sequim, WA, USA4 University of Idaho, Moscow, ID, USA5 University of Washington, Seattle, WA, USA
ABSTRACT- A variety of environmental contaminants disrupt reproduction in fish by binding to estrogen receptors. The most biologically potent is ethynylestradiol (EE2), a synthetic estrogen used in oral contraceptives that is present in surface waters as a result of sewage discharges. The goals of our research are two-fold: 1) to determine the endocrine mechanisms whereby EE2 potentially disrupts growth and reproduction in salmon, and 2) to determine whether exposure to EE2 during juvenile life history stages alters survival during seawater entry, growth and reproductive success as adults. In this talk I will present data from one study as an example of how we evaluated impacts of EE2 on the growth and reproductive endocrine systems of coho salmon. Our results suggest that short-term (2 or 7 days) water borne exposure to EE2 suppresses several key points of the reproductive axis. First, EE2 suppressed plasma levels of both 11-ketotestosterone (males) and estradiol-17beta (females). The actions appear to be mediated in part by reduced pituitary follicle-stimulating hormone (FSH) gene expression and plasma FSH levels, but not gonadal FSH receptor gene expression. Expression of the steroidogenic-acute regulatory protein (StAR) gene, which controls a key rate-limiting step in steroid biosynthesis, was significantly suppressed by EE2 at all concentrations tested (1-100ng/L). Exposure to EE2 also inhibited the growth axis by reducing hepatic insulin-like growth factor I (IGF-I) gene expression and plasma IGF-I levels. However, only weak effects on hepatic growth hormone receptor transcripts were observed. These results indicate that the mechanism whereby EE2 may impair growth and reproduction involves suppression of hepatic IGF I gene expression, pituitary FSH production, and steroid biosynthesis via reductions in StAR gene expression. Furthermore, reduced steroid production can occur even with short-term (2-day) exposure to low EE2 concentrations (1 or 10 ng/L) that are within ranges detected in some urban freshwater habitats in the Pacific Northwest region.
Key words: ethynylestradiol, salmon, endocrine disruption, reproduction