Effects of 17β-estradiol, 4-nonylphenol, and β-sitosterol on the growth hormone-insulin-like growth factor system and seawater adaptation of rainbow trout (Oncorhynchus mykiss)

Previous studies show that successful adaptation of euryhaline teleost fish to seawater (SW) involves the GH-IGF system. The increasing occurrence, distribution, and concentration of environmental contaminants, including environmental estrogens (EE), in aquatic habit over recent time may compromise the hypoosmoreegulatory ability of fish. In this study, we used rainbow trout (Oncorhynchus mykiss) to assess the effects of EE on the GH-IGF system and adaptation to increased salinity. Juvenile trout (ca. 30 g) were exposed to either low (10 μg/l) or high (100 μg/l) concentrations of β-sitosterol, 4-n-nonylphenol (NP), or 17β-estradiol (E2) for 28 days in fresh water (FW); after which, fish were exposed to 20‰ SW. Plasma chloride levels in control fish rose initially, and then declined to initial levels after 48 h. By contrast, plasma chloride levels in all EE-treated groups except β-sitosterol low increased and remained elevated over initial levels after 48 h. Levels GH receptor 1 (GHR 1), GHR 2, insulin-like growth factor-1 (IGF-1), and IGF-2mRNAs in liver of control fish increased 6–12 h after SW exposure. In gill, levels of GHR 1, GHR 2, IGF-1, IGF-2, IGF receptor 1A (IGFR1A), and IGFR1B mRNAs increased in control fish 6–12 h after 20‰ SW exposure. Levels of IGFR1A and IGFR1B mRNAs in white muscle and of IGFR1A mRNA in red muscle increased in control fish 6–12 h after 20‰ SW exposure. Expression of all mRNAs in liver, gill, and red and white muscle declined from peak levels in control fish by 48 h after transfer. Exposure of fish to β-sitosterol, NP, and E2 abolished or attenuated normal salinity-induced changes in the expression of GHR, IGF, and IGFR1 mRNAs in all tissues. These results indicate that EE reduces salinity adaptation by inhibiting components of the GH-IGF system.