Abstract
A previous study showed that treatment of C6 glioma cells with 10 mM ammonium chloride monia") for 24 h decreases taurine uptake and evokes sodium-dependent taurine efflux, indicating reversal of the taurine transporter (TauT)-mediated transport as an underlying mechanism. Consistent with the involvement of TauT we now show that the ammonia-induced changes in Tau uptake and efflux are inhibited by the protein kinase C (PKC) activator phorbol 12,13-dibutyrate (PDBu). Ammonia treatment of C6 cells resulted in increased intracellular accumulation of cAMP. Incubation of the cells with dibutyryl cAMP (dbcAMP) mimicked the effects of ammonia on both taurine uptake and efflux. The effects of dbcAMP on taurine uptake and efflux were additive to the effects of ammonia. Collectively, the results suggest that the effects of ammonia on taurine uptake and efflux may be partly mediated by cAMP. Consistent with this mechanism, the adenyl cyclase inhibitor, miconazole reduced the stimulation of efflux by ammonia.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
