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). In this work, rainbow trout were used to assess the effects of EE on the growth hormone (GH)-insulin-like growth factor (IGF) system, specifically focusing on osmoregulation, organismal growth, and growth at the molecular level. Juvenile trout were exposed to varying concentrations of 17â-estradiol (E2), â-sitosterol (âS), and 4-n-nonylphenol (NP) in vivo and in vitro. Real-time quantitative-PCR was used to measure levels of mRNA expression (GH receptor 1 (GHR1), GHR2, IGF-1, IGF-2, IGF receptor 1A (IGFR1A), and IGFR1B) in multiple tissues, including liver, gill, and muscle. Western blotting was used to elucidate signaling pathways affected by EE-treatment (e.g., JAK-STAT, MAPK, PI3K). Environmental estrogen-treated fish displayed depressed growth in terms of body mass and body length. The observed effects on organismal growth appeared to be due to a decrease in food conversion, as food consumption was not significantly different between treatment groups. Hepatic, gill, and muscle levels of mRNAs encoding GHR1, GHR2, IGF-1, IGF-2, IGFR1A, and IGFR1B decreased in a concentration-, time-, and compound-dependent manner in vivo and in vitro. Furthermore, EE-treated fish displayed decreased osmoregulatory function when subjected to a salt water challenge, as evaluated by measuring plasma chloride levels and mRNA expression of GHRs, IGFs, and IGFRs. The suppression of mRNA expression of components of the GH-IGF system by EE was linked to suppressed phosphorylation of JAK-STAT, MAPK, and PI3K-Akt in a concentration- and time-dependent manner in hepatocytes and gill filaments, an effect that was ER-dependent. Classically, the ER has been thought to function as a nuclear receptor; however, the observed results support the notion that the ER (and thus EE) may have nongenomic effects as well. The results of this dissertation indicate that EE suppress growth at the organismal and molecular level via inhibition of growth-related signaling cascades and repression of gene expression elements of the GH-IGF system.