Meeting Abstract
35.3 Wednesday, Jan. 5 Effects of Environmental Estrogens on Organismal Growth and the Growth Hormone-Insulin-Like-Growth Factor System of Rainbow Trout HANSON, AM*; SHERIDAN, MA; North Dakota St. Univ. andrea.m.hanson@ndsu.edu
The increasing production, use, and disposal of an expanding array of chemicals that enter the environment pose a serious threat to terrestrial and aquatic animals, as well as to humans. Fish in aquatic habitats are exposed to increasing concentrations of environmental contaminants, including environmental estrogens (EE). Previous studies showed that EE affect several processes including development and reproduction. In this study, we used rainbow trout (Oncorhynchus mykiss) to assess the effects of EE on organismal growth and on the growth hormone (GH)-insulin-like growth factor (IGF) system. Juvenile trout (ca. 50 g) were exposed to varying concentrations of 17β-estradiol (E2), β-sitosterol, and 4-n-nonylphenol (NP) for 28 days (14 C; 12L:12D). EE-treated fish displayed depressed growth in terms of body mass and body length when compared to the control group. Relative growth (mass and length) was also significantly reduced for all EE-treated fish compared to controls. Hepatic levels of mRNAs encoding GH receptor 1(GHR 1), GHR 2, IGF-1, and IGF-2 decreased in a concentration-dependent fashion for all EE-treated groups. In gill, E2 reduced expression of mRNAs encoding GHR2, IGF-1, IGF-2, and IGFR1A, whereas NP reduced the expression of GHR1, GHR2, IGF1, IGF-2, and IGFR1A mRNAs. β-sitosterol had no significant effect on the expression of any GH-IGF system component in gill. The effects of EE on levels of IGFR1A and IGFR1B mRNA in red muscle and white were somewhat variable. High concentrations of E2 reduced levels of IGFR1A in white muscle and of IGFR1B in red muscle, whereas NP reduced the expression of IGFR1A and IGFR1B mRNAs in red muscle. These results indicate that EE reduce overall growth of fish by modulating the GH-IGF system in terms of GH sensitivity, IGF production, and IGF sensitivity in a tissue-specific manner. (Supported by NSF IOS 0920116)
