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Reduced embryonic survival in rainbow trout resulting from paternal exposure to the environmental estrogen 17-ethynylestradiol during late sexual maturation

Department of Biological Sciences and Center for Reproductive Biology, University of Idaho, Life Science Building Room 252, PO Box 443051, Moscow, Idaho 83844-3051, USA and ¹ Battelle PNNL-Marine Science Laboratory, 1529 West Sequim Bay Road, Sequim, Washington 98382, USA

Correspondence should be addressed to K H Brown; Email: khbrown{at}uidaho.edu

Exposure of fishes to environmental estrogens is known to affect sexual development and spawning, but little information exists regarding effects on gametes. This study evaluated embryonic survival of offspring from male rainbow trout (Oncorhynchus mykiss) exposed to 17-ethynylestradiol (EE₂) using an in vitro fertilization protocol. Males were exposed at either 1800 or 6700 degree days (°d) (i.e. 161 or 587 days post-fertilization (dpf)) to test for effects on testes linked to reproductive ontogeny. At 1800°d, fish were beginning testicular differentiation and were exposed to 109 ng EE₂/l for 21 days. At 6700° d, fish have testes containing spermatocytes and spermatids and were exposed for 56 days to either 0.8, 8.3, or 65 ng EE₂/l. Semen was collected at full sexual maturity in each group and used to fertilize eggs pooled from several non-exposed females. Significant decreases in embryonic survival were observed only with the 6700°d exposure. In 0.8 and 8.3 ng EE₂/l treatments, embryo survival was significantly reduced at 19 dpf when compared with the control. In contrast, an immediate decrease in embryonic survival at 0.5 dpf was observed in the 65 ng EE₂/l treatment. Blood samples collected at spawning from 6700° d exposed males revealed a significant decrease in 11-ketotestosterone and a significant increase in luteinizing hormone levels for the 65 ng EE₂/l treatment when compared with the other treatment groups. Results indicate that sexually maturing male rainbow trout are susceptible to EE₂ exposure with these fish exhibiting two possible mechanisms of reduced embryonic survival through sperm varying dependant on EE₂ exposure concentrations experienced.