title: Reduced embryonic survival in rainbow trout resulting from paternal exposure to the environmental estrogen 17alpha-ethynylestradiol during late sexual maturation.
abstract: 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 17alpha-ethynylestradiol (EE(2)) using an in vitro fertilization protocol. Males were exposed at either 1800 or 6700 degree days ( degrees d) (i.e. 161 or 587 days post-fertilization (dpf)) to test for effects on testes linked to reproductive ontogeny. At 1800 degrees d, fish were beginning testicular differentiation and were exposed to 109 ng EE(2)/l for 21 days. At 6700 degrees d, fish have testes containing spermatocytes and spermatids and were exposed for 56 days to either 0.8, 8.3, or 65 ng EE(2)/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 degrees d exposure. In 0.8 and 8.3 ng EE(2)/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 EE(2)/l treatment. Blood samples collected at spawning from 6700 degrees d exposed males revealed a significant decrease in 11-ketotestosterone and a significant increase in luteinizing hormone levels for the 65 ng EE(2)/l treatment when compared with the other treatment groups. Results indicate that sexually maturing male rainbow trout are susceptible to EE(2) exposure with these fish exhibiting two possible mechanisms of reduced embryonic survival through sperm varying dependant on EE(2) exposure concentrations experienced.
authors.affiliation: 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. khbrown@uidaho.edu
authors.forename: Kim H
authors.initials: KH
authors.lastname: Brown
authors.forename: Irvin R
authors.initials: IR
authors.lastname: Schultz
authors.forename: James J
authors.initials: JJ
authors.lastname: Nagler
mesh_terms: D000818:Animals; D004305:Dose-Response Relationship, Drug; D004997:Ethinyl Estradiol / Q000097:blood / Q000633:toxicity*; D005260:Female; D005307:Fertilization in Vitro; D005313:Fetal Death / Q000139:chemically induced*; D007986:Luteinizing Hormone / Q000097:blood; D008297:Male; D017686:Oncorhynchus mykiss / Q000196:embryology*; D018812:Paternal Exposure; D012741:Sexual Maturation / Q000187:drug effects; D013737:Testis / Q000187:drug effects / Q000254:growth & development; D014818:Vitellogenesis / Q000187:drug effects; D014819:Vitellogenins / Q000097:blood; D014874:Water Pollutants, Chemical / Q000633:toxicity*
chemical_list: D014819:Vitellogenins; D014874:Water Pollutants, Chemical; D004997:Ethinyl Estradiol; D007986:Luteinizing Hormone