In vivo effects of 17α-ethinylestradiol, 17β-estradiol and 4-nonylphenol on hepatic insulin-like growth-factor binding protein (igfbp) mRNA levels in Atlantic salmon


Meeting Abstract

139-2  Sunday, Jan. 8 13:45 – 14:00  In vivo effects of 17α-ethinylestradiol, 17β-estradiol and 4-nonylphenol on hepatic insulin-like growth-factor binding protein (igfbp) mRNA levels in Atlantic salmon BREVES, JP*; DUFFY, TA; EINARSDOTTIR, IE; BJöRNSSON, BT; MCCORMICK, SD; Skidmore Coll.; Northeastern Univ.; Univ. of Gothenburg; Univ. of Gothenburg; USGS, Conte Anadromous Fish Res. Cen. jbreves@skidmore.edu

Feminizing endocrine disrupting compounds (EDCs) affect the growth and development of teleosts. The growth hormone (Gh)/insulin-like growth-factor (Igf) system is sensitive to estrogenic compounds and mediates some of the physiological consequences of EDC exposure. Nonetheless, there is no grasp on whether modulators of Igf activity, namely Igf binding proteins (Igfbps), are impacted by EDCs. We investigated two early life-history stages (juveniles and smolts) of Atlantic salmon (Salmo salar) and characterized how the Gh/Igf/Igfbp system responded to waterborne 17α-ethinylestradiol (EE2), 17β-estradiol (E2) and 4-nonylphenol (NP). In juveniles (~0.5 g) exposed to EE2 and NP for 21 days, hepatic vitellogenin (vtg) was induced while estrogen receptor α (erα), gh receptor (ghr), igf1 and igf2 mRNA levels were diminished. EE2 and NP reduced hepatic igfbp1b1, -2a, -2b1, -4, -5b2 and -6b1, and stimulated igfbp5a. In smolts, exposure to EE2 for 4 days diminished plasma Gh and Igf1 levels in parallel with reductions in hepatic ghr and igf1. Hepatic vtg was induced following exposure to EE2, E2 and NP, while erα only responded to EE2 and E2. EE2 and E2 diminished hepatic igfbp1b1, -4 and -6b1, and stimulated igfbp5a. We conclude that hepatic igfbps respond (directly and/or indirectly) to environmental estrogens during two key life-history stages of Atlantic salmon, and thus may modulate the growth and development of exposed individuals.

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