PMID- 22906423
OWN - NLM
STAT- MEDLINE
DCOM- 20130405
LR  - 20191210
IS  - 1095-6840 (Electronic)
IS  - 0016-6480 (Linking)
VI  - 179
IP  - 2
DP  - 2012 Nov 1
TI  - Estrogenic compounds decrease growth hormone receptor abundance and alter 
      osmoregulation in Atlantic salmon.
PG  - 196-204
LID - S0016-6480(12)00318-8 [pii]
LID - 10.1016/j.ygcen.2012.08.001 [doi]
AB  - 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 10 days with 2 mugg(-1) 17beta-estradiol (E2) or 150mugg(-1) 4-nonylphenol 
      (NP). Seawater (SW)-acclimated fish received intraperitoneal implants of 30 
      mugg(-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.
CI  - Copyright (c) 2012 Elsevier Inc. All rights reserved.
FAU - Lerner, Darren T
AU  - Lerner DT
AD  - Organismic and Evolutionary Biology, University of Massachusetts, Amherst, MA 
      01003, USA. lerner@hawaii.edu
FAU - Sheridan, Mark A
AU  - Sheridan MA
FAU - McCormick, Stephen D
AU  - McCormick SD
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
DEP - 20120811
PL  - United States
TA  - Gen Comp Endocrinol
JT  - General and comparative endocrinology
JID - 0370735
RN  - 0 (Chlorides)
RN  - 0 (Phenols)
RN  - 0 (Water Pollutants, Chemical)
RN  - 4TI98Z838E (Estradiol)
RN  - 67763-96-6 (Insulin-Like Growth Factor I)
RN  - EC 7.2.2.13 (Sodium-Potassium-Exchanging ATPase)
RN  - I03GBV4WEL (4-nonylphenol)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Animals
MH  - Calcium/blood
MH  - Chlorides/blood
MH  - Estradiol/pharmacology
MH  - Fresh Water
MH  - Gills/metabolism
MH  - Insulin-Like Growth Factor I/metabolism
MH  - Phenols/*pharmacology
MH  - Salmo salar/*growth & development/physiology
MH  - Seawater
MH  - Sodium-Potassium-Exchanging ATPase/metabolism
MH  - Water Pollutants, Chemical/pharmacology
MH  - Water-Electrolyte Balance/*drug effects
EDAT- 2012/08/22 06:00
MHDA- 2013/04/06 06:00
CRDT- 2012/08/22 06:00
PHST- 2012/03/06 00:00 [received]
PHST- 2012/07/28 00:00 [revised]
PHST- 2012/08/03 00:00 [accepted]
PHST- 2012/08/22 06:00 [entrez]
PHST- 2012/08/22 06:00 [pubmed]
PHST- 2013/04/06 06:00 [medline]
AID - S0016-6480(12)00318-8 [pii]
AID - 10.1016/j.ygcen.2012.08.001 [doi]
PST - ppublish
SO  - Gen Comp Endocrinol. 2012 Nov 1;179(2):196-204. doi: 10.1016/j.ygcen.2012.08.001. 
      Epub 2012 Aug 11.