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Título

Fructose-1,6-biphosphate and nucleoside pool modifications prevent neutrophil accumulation in the reperfused intestine

AutorSolà, Anna M. ; Panés, Julián; Xaus, Carme ; Hotter, Georgina
Palabras claveXanthine
Small intestine
F16BP
Adenosine
Adenosine deaminase
Fecha de publicación1-ene-2003
EditorFederation of American Societies for Experimental Biology
CitaciónJournal of Leukocyte Biology 73(1): 74-81 (2003)
ResumenFructose- 1,6-biphosphate (F16BP) attenuates ischemia/reperfusion (I/R) injury by inhibiting microvascular leukocyte adhesion or reducing neutrophil-derived oxygen free-radical production, but the causes of this action, the mechanisms in vivo, and the possible implication of nucleoside pool modifications are still controversial issues. We explored whether F16BP's inhibition of free-radical production and neutrophil recruitment is a result of its effect on adenosine (Ado) accumulation during intestinal I/R injury. The effects of F16BP administration were tested on the nucleotide/nucleoside metabolism at the end of the ischemic period and on microvascular neutrophil recruitment and free-radical production after reperfusion in vivo, in the presence or absence of Ado deaminase (ADA). Infusion of F16BP markedly increased endogenous Ado, decreased xanthine accumulation during the ischemic period, and inhibited neutrophil recruitment and subsequent neutrophil freeradical generation during reperfusion. Administration of ADA reversed these processes. The results provide strong evidence that F16BP prevents neutrophil accumulation and neutrophil free-radical generation during intestinal I/R by a key mechanism that modifies the nucleoside pool, leading to an endogenous accumulation of Ado and to a reduction of xanthine during ischemia.
Versión del editorhttp://dx.doi.org/10.1189/jlb.0602299
URIhttp://hdl.handle.net/10261/116485
DOI10.1189/jlb.0602299
Identificadoresdoi: 10.1189/jlb.0602299
issn: 0741-5400
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