title: Tissue-specific suppression of estrogen, androgen and glucocorticoid receptor gene expression in feral vitellogenic male Mozambique tilapia.
abstract: While vitellogenesis in male fish is commonly used as a biomarker of xenoestrogen exposure, very little is known about the impacts associated with this unusual protein synthesis in feral populations. To this end, a recent study showed elevated circulating vitellogenin (VTG) levels in male Mozambique tilapia (Oreochromis mossambicus) collected from the Aja but not Tengan Rivers in Okinawa, Japan. Here we investigated whether this unusual protein synthesis in male fish from the Aja River affect transcript abundance of estrogen (ER), androgen (AR) and glucocorticoid (GR) receptors in the liver, brain and testis. The detection of plasma VTG levels ( approximately 100 microg ml(-1)) in male tilapia confirmed xenoestrogenic exposure in the Aja, but not the Tengan River. This protein induction was not associated with any changes in the reproductive capacity as assessed by sperm mobility and testis histology in the Aja fish. Plasma levels of estradiol-17beta, 11-ketotestosterone and cortisol were not significantly different between fish from the two rivers. Quantitative real-time PCR revealed a significant reduction in transcript levels of ERalpha and ERbeta, GR and ARalpha but not ARbeta, in the livers of tilapia from the Aja compared with the Tengan River. There were no significant changes in any of the steroid receptor transcript levels in either the brain or testis between the two rivers. Overall, our results imply that xenoestrogen exposure and VTG synthesis may lead to disruption of liver responsiveness to sex steroids and glucocorticoid stimulation in feral male fish.
authors.affiliation: Marine and Environmental Research Institute, Cheju National University, Jeju 695-814, South Korea.
authors.forename: Chang-Beom
authors.initials: CB
authors.lastname: Park
authors.forename: Akihiro
authors.initials: A
authors.lastname: Takemura
authors.forename: Neelakanteswar
authors.initials: N
authors.lastname: Aluru
authors.forename: Yong-Ju
authors.initials: YJ
authors.lastname: Park
authors.forename: Byung-Ho
authors.initials: BH
authors.lastname: Kim
authors.forename: Chi-Hoon
authors.initials: CH
authors.lastname: Lee
authors.forename: Young-Don
authors.initials: YD
authors.lastname: Lee
authors.forename: Thomas W
authors.initials: TW
authors.lastname: Moon
authors.forename: Mathilakath M
authors.initials: MM
authors.lastname: Vijayan
mesh_terms: D000818:Animals; D049628:Body Size; D001921:Brain / Q000378:metabolism; D004958:Estradiol / Q000097:blood; D004967:Estrogens / Q000633:toxicity; D005786:Gene Expression Regulation; D006854:Hydrocortisone / Q000097:blood; D007564:Japan; D008099:Liver / Q000378:metabolism*; D008297:Male; D012333:RNA, Messenger / Q000378:metabolism; D011987:Receptors, Steroid / Q000235:genetics*; D045483:Rivers; D013076:Sperm Count; D013081:Sperm Motility; D013737:Testis / Q000033:anatomy & histology / Q000254:growth & development / Q000378:metabolism; D013739:Testosterone / Q000031:analogs & derivatives / Q000097:blood; D017210:Tilapia / Q000378:metabolism*; D014819:Vitellogenins / Q000097:blood; D014874:Water Pollutants, Chemical / Q000633:toxicity
chemical_list: D004967:Estrogens; D012333:RNA, Messenger; D011987:Receptors, Steroid; D014819:Vitellogenins; D014874:Water Pollutants, Chemical; D013739:Testosterone; D004958:Estradiol; C003600:11-ketotestosterone; D006854:Hydrocortisone