Estrogenic compounds decrease growth hormone receptor abundance and alter osmoregulation in Atlantic salmon

Darren T. Lerner, Mark A. Sheridan, Stephen D. McCormick

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29 Scopus citations


Exposure of Atlantic salmon smolts to estrogenic compounds is shown to compromise several aspects of smolt development. We sought to determine the underlying endocrine mechanisms of estrogen impacts on the growth hormone (GH)/insulin-like growth factor I (IGF-I) axis. Smolts in freshwater (FW) were either injected 3 times over 10days with 2μgg-1 17β-estradiol (E2) or 150μgg-1 4-nonylphenol (NP). Seawater (SW)-acclimated fish received intraperitoneal implants of 30μgg-1 E2 over two weeks. Treatment with these estrogenic compounds increased hepatosomatic index and total plasma calcium. E2 and NP reduced maximum growth hormone binding by 30-60% in hepatic and branchial membranes in FW and SW, but did not alter the dissociation constant. E2 and NP treatment decreased plasma levels of IGF-I levels in both FW and SW. In FW E2 and NP decreased plasma GH whereas in SW plasma GH increased after E2 treatment. Compared to controls, plasma chloride concentrations of E2-treated fish were decreased 5.5mM in FW and increased 10.5mM in SW. There was no effect of NP or E2 on gill sodium-potassium adenosine triphosphatase (Na+/K+-ATPase) activity in FW smolts, whereas E2 treatment in SW reduced gill Na+/K+-ATPase activity and altered the number and size of ionocytes. Our data indicate that E2 downregulates the GH/IGF-I-axis and SW tolerance which may be part of its normal function for reproduction and movement into FW. We conclude that the mechanism of endocrine disruption of smolt development by NP is in part through alteration of the GH/IGF-I axis via reduced GH receptor abundance.

Original languageEnglish
Pages (from-to)196-204
Number of pages9
JournalGeneral and Comparative Endocrinology
Issue number2
StatePublished - Nov 1 2012


  • Atlantic salmon
  • Estrogen
  • Growth hormone
  • Insulin-like growth -factor I
  • Ionocyte
  • Nonylphenol


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