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Abstract
BACKGROUND AND AIMS Inhibition of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) by nitric oxide (NO) in intestinal preconditioning could modify the rate of formation of glycolytic intermediates. Fructose-1,6-biphosphate (F16BP) is a glycolytic intermediate that protects tissue from ischaemia/reperfusion injury. We evaluated if F16BP may be endogenously accumulated as a consequence of GAPDH inhibition by NO during intestinal preconditioning in rats.
METHODS We assessed: (1) effect of preconditioning on F16BP content; (2) effect of NO on GAPDH activity before and during sustained ischaemia; and (3) protective effect of F16BP in control, ischaemic, and preconditioned animals with or without administration ofN-nitro-l-arginine methyl ester (l-NAME), NO donor, or F16BP.
RESULTS Preconditioned rats showed a significant transient decrease in GAPDH activity and also maintained basal F16BP levels longer than ischaemic rats.l-NAME administration to preconditioned rats reversed these effects. F16BP administration to ischaemic rats decreased protein release in the perfusate. Administration of F16BP to l-NAME treated rats attenuated the harmful effect of l-NAME.
CONCLUSIONS Our study indicates that F16BP may be endogenously accumulated in preconditioned rats as a consequence of inhibition of GAPDH by NO, and this may contribute to the protection observed in intestinal preconditioning.
- fructose-1,6-biphosphate
- glyceraldehyde- 3-phosphate dehydrogenase
- intestinal preconditioning
- ischaemia/reperfusion injury
- nitric oxide
Abbreviations used in this paper
- F16BP
- fructose-1,6-biphosphate
- GAPDH
- glyceraldehyde-3-phosphate dehydrogenase
- iNOS
- inducible nitric oxide synthase
- I/R
- ischaemia/ reperfusion
- l-NAME
- N-nitro-l-arginine methyl ester
- NO
- nitric oxide
- NONOS
- spermine NONOate
- 1400W
- N-(3-(aminomethyl)benzyl) aceramidine, dihydrochloride