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MEMBRANE TRANSPORTERS, ION CHANNELS, AND PUMPS

Genistein stimulates electrogenic Cl^– secretion in mouse jejunum

Department of Physiology, School of Medical Sciences, University of Otago, Dunedin, New Zealand

Submitted 6 June 2003 ; accepted in final form 5 August 2004

We used the short-circuit current (I_sc) technique to investigate the effects of the isoflavone genistein on the electrogenic Cl^– secretion of the mouse jejunum. Genistein stimulated a sustained increase in I_sc that was dose dependent. Bumetanide inhibited 76 ± 5% of the genistein-stimulated I_sc consistent with activation of Cl^– secretion. Genistein failed to stimulate I_sc following maximal activation of the cAMP pathway by forskolin. In addition, forskolin had a reduced effect on I_sc of the mouse jejunum in the presence of genistein. Glibenclamide, a blocker of CFTR, eliminated the genistein-stimulated increase of I_sc and reduced the forskolin-activated I_sc. Clotrimazole, a Ca²⁺-activated K⁺ channel blocker, failed to reduce the genistein-stimulated I_sc. Vanadate, a blocker of tyrosine-dependent phosphatases, reduced the genistein-activated I_sc. Tyrphostin A23, a tyrosine kinase inhibitor, reduced basal I_sc, after which genistein failed to stimulate I_sc. These data suggest that genistein activated a sustained Cl^– secretory response of the mouse jejunum and that the effect of genistein was via a tyrosine-dependent phosphorylation pathway.

1-ethyl-2-benzimidazolone; vanadate; tyrphostin A23; cantharidic acid; phosphatase

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