Tissue-specific suppression of estrogen, androgen and glucocorticoid receptor gene expression in feral vitellogenic male Mozambique tilapia.
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.
Park
Chang-Beom
CB
Marine and Environmental Research Institute, Cheju National University, Jeju 695-814, South Korea.
Takemura
Akihiro
A
Aluru
Neelakanteswar
N
Park
Yong-Ju
YJ
Kim
Byung-Ho
BH
Lee
Chi-Hoon
CH
Lee
Young-Don
YD
Moon
Thomas W
TW
Vijayan
Mathilakath M
MM
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
D004967:Estrogens; D012333:RNA, Messenger; D011987:Receptors, Steroid; D014819:Vitellogenins; D014874:Water Pollutants, Chemical; D013739:Testosterone; D004958:Estradiol; C003600:11-ketotestosterone; D006854:Hydrocortisone