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Interactions between cortisol and Rhesus glycoprotein expression in ureogenic toadfish, Opsanus beta.

Tamara M Rodela1, M Danielle McDonald, Patrick J Walsh

  • 1Department of Biology, University of Ottawa, Ottawa, Ontario, Canada K1N 6N5. trodela@zoology.ubc.ca

The Journal of Experimental Biology
|December 23, 2011
PubMed
Summary

Gulf toadfish alter ammonia excretion under stress. Cortisol influences ammonia excretion by changing Rhesus (Rh) glycoprotein expression and glutamine synthetase (GS) activity.

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Area of Science:

  • * Physiology
  • * Environmental Stress Response
  • * Fish Biology

Background:

  • * Gulf toadfish normally excrete equal ammonia and urea.
  • * Stressful conditions induce ureotelism (urea excretion) in toadfish.
  • * Rhesus (Rh) glycoproteins and glutamine synthetase (GS) are key in ammonia metabolism.

Purpose of the Study:

  • * Investigate cortisol and ammonia effects on toadfish ammonia excretion.
  • * Examine the role of Rh glycoproteins and GS activity in this process.

Main Methods:

  • * In vivo infusions and injections in ureotelic toadfish.
  • * Manipulation of corticosteroid activity and plasma ammonia levels.
  • * Measurement of ammonia excretion rates, Rh mRNA expression, and GS activity.

Main Results:

  • * Lowering cortisol increased ammonia excretion and Rh expression, decreasing GS activity.
  • * Cortisol infusion decreased ammonia excretion, Rh expression, and increased hepatic GS activity.
  • * Elevated ammonia levels enhanced excretion and Rh expression, but cortisol blunted this response.

Conclusions:

  • * Cortisol modulates ammonia excretion in toadfish.
  • * Cortisol influences ammonia excretion via changes in Rh glycoprotein expression and GS activity.