Rhesus glycoprotein and urea transporter genes in rainbow trout embryos are upregulated in response to alkaline water (pH 9.7) but not elevated water ammonia

Jessica Sashaw, Michele Nawata, Sarah Thompson, Chris M. Wood, Patricia A. Wright

Research output: Contribution to journalArticle

11 Scopus citations


Recent studies have shown that genes for the putative ammonia transporter, Rhesus glycoproteins (Rh) and the facilitated urea transporter (UT) are expressed before hatching in rainbow trout (Oncorhychus mykiss Walbaum) embryos. We tested the hypothesis that Rh and UT gene expressions are regulated in response to environmental conditions that inhibit ammonia excretion during early life stages. Eyed-up embryos (22 days post-fertilization (dpf)) were exposed to control (pH 8.3), high ammonia (1.70 mmol l-1 NH4HCO3) and high pH (pH 9.7) conditions for 48 h. With exposure to high water ammonia, ammonia excretion rates were reversed, tissue ammonia concentration was elevated by 9-fold, but there were no significant changes in mRNA expression relative to control embryos. In contrast, exposure to high water pH had a smaller impact on ammonia excretion rates and tissue ammonia concentrations, whereas mRNA levels for the Rhesus glycoprotein Rhcg2 and urea transporter (UT) were elevated by 3.5- and 5.6-fold, respectively. As well, mRNAs of the genes for H+ATPase and Na+/H+ exchanger (NHE2), associated with NH3 excretion, were also upregulated by 7.2- and 13-fold, respectively, in embryos exposed to alkaline water relative to controls. These results indicate that the Rhcg2, UT and associated transport genes are regulated in rainbow trout embryos, but in contrast to adults, there is no effect of high external ammonia at this stage of development.

Original languageEnglish (US)
Pages (from-to)308-313
Number of pages6
JournalAquatic Toxicology
Issue number4
StatePublished - Mar 1 2010



  • Ammonia excretion
  • Ammonia toxicity
  • Development
  • Rh
  • Urea excretion
  • UT

ASJC Scopus subject areas

  • Aquatic Science
  • Health, Toxicology and Mutagenesis

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