title: Modification of glyceraldehyde-3-phosphate dehydrogenase in response to nitric oxide in intestinal preconditioning.
abstract: BACKGROUND
  Previous studies have demonstrated that intestinal preconditioning is triggered by an initial increase in nitric oxide synthesis. This confers resistance to the organ in face of a subsequently sustained period of ischemia-reperfusion. Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is a key enzyme in the glycolytic cascade that could be modulated by nitric oxide. The purpose of the present study is to evaluate a possible inhibitory effect on intestinal GAPDH by the nitric oxide generated during preconditioning. This could lead to a reduction of lactate accumulation during subsequent ischemia.
  
  
  METHODS
  GAPDH activity was measured after intestinal preconditioning, and the effect of nitric oxide synthase inhibition was evaluated.
  
  
  RESULTS
  Preconditioning induced a significant, but transient, decrease in GAPDH activity. This effect appears to be correlated with a reduced amount of lactate accumulation during ischemia. Inhibition of nitric oxide synthesis reversed these changes. In addition, increased synthesis of nitric oxide was detected after preconditioning.
  
  
  CONCLUSIONS
  In summary, this study indicates that nitric oxide generated during ischemic preconditioning could act as a glycolytic modulator during subsequent ischemia, through its effect on GAPDH activity.
authors.affiliation: Department of Medical Bioanalysis, Instituto de Investigaciones Biomédicas de Barcelona (CSIC-IDIBAPS), Spain.
authors.forename: A
authors.initials: A
authors.lastname: Sola
authors.forename: J
authors.initials: J
authors.lastname: Roselló-Catafau
authors.forename: V
authors.initials: V
authors.lastname: Alfaro
authors.forename: J
authors.initials: J
authors.lastname: Pesquero
authors.forename: L
authors.initials: L
authors.lastname: Palacios
authors.forename: E
authors.initials: E
authors.lastname: Gelpí
authors.forename: G
authors.initials: G
authors.lastname: Hotter
mesh_terms: D000818:Animals; D016166:Free Radical Scavengers / Q000494:pharmacology; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases / Q000378:metabolism*; D007422:Intestines / Q000098:blood supply* / Q000637:transplantation; D007511:Ischemia / Q000378:metabolism; D019194:Ischemic Preconditioning; D007773:Lactates / Q000378:metabolism; D008297:Male; D009569:Nitric Oxide / Q000502:physiology*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D052247:Nitric Oxide Synthase Type II; D010545:Peroxides / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000517:prevention & control
chemical_list: D016166:Free Radical Scavengers; D007773:Lactates; D010545:Peroxides; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; C496318:Nos2 protein, rat; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases