Ammonia and urea excretion in the swimming crab Portunus trituberculatus exposed to elevated ambient ammonia-N.

ABSTRACT

In the present study of the swimming crab Portunus trituberculatus exposed to 0, 1, and 5 mg L(-1) NH4Cl, the effects of ammonia exposure on ammonia and urea content in hemolymph; activity of H(+)-ATPase (subunit A) and Na(+)/K(+)-ATPase (α-subunit) (NKA) in gills; mRNA expression levels of the crustacean Rh-like ammonia transporter (Rh), K(+) Channel, Na(+)/K(+)/2Cl(-) co-transporter (NKCC), Na(+)/H(+)-exchanger (NHE), urea transporter (UT) and vesicle associated membrane protein (VAMP) in gills were investigated. The ultrastructure of gills was also evaluated. All these results in this study showed a dose-dependent effect with ammonia exposure concentration. The data displayed a significant increase in hemolymph ammonia and urea concentrations under ammonia exposure. The up-regulation of Rh mRNA together with up-regulation of K(+)-channel mRNA, NKA activity, down-regulation of NKCC and NHE mRNA suggested a coordinated protective response to maintain a relatively low ammonia concentration in the body fluids during ambient ammonia exposure. The up-regulation of VAMP, H(+)-ATPase activity along with the ultrastructure of gills suggested a mechanism of exocytotic ammonia excretion that may exit in the gill of P. trituberculatus. An increased production of urea and the up-regulated expression of UT suggested that the crab can detoxify elevated ammonia levels in the body fluids into urea when pathways of ammonia excretion are decreased after long term ammonia exposure.