| dc.creator |
Solà, Anna M. |
|
| dc.creator |
Roselló-Catafau, Joan |
|
| dc.creator |
Gelpí, Emili |
|
| dc.creator |
Hotter, Georgina |
|
| dc.date |
2008-02-18T18:19:44Z |
|
| dc.date |
2008-02-18T18:19:44Z |
|
| dc.date |
2001-02 |
|
| dc.date.accessioned |
2017-01-31T01:00:11Z |
|
| dc.date.available |
2017-01-31T01:00:11Z |
|
| dc.identifier |
Gut. 2001 February; 48(2): 168–175. |
|
| dc.identifier |
http://dx.doi.org/10.1136/gut.48.2.168 |
|
| dc.identifier |
0017-5749 |
|
| dc.identifier |
http://hdl.handle.net/10261/2972 |
|
| dc.identifier |
10.1136/gut.48.2.168 |
|
| dc.identifier.uri |
http://dspace.mediu.edu.my:8181/xmlui/handle/10261/2972 |
|
| dc.description |
[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. |
|
| dc.description |
[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 of N-nitro-L-arginine methyl ester (L-NAME), NO donor, or F16BP. |
|
| dc.description |
[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. |
|
| dc.description |
[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. |
|
| dc.description |
This work was supported by grant FIS 98/002901. A Sola was supported by a grant from Institut d’Investigacions Biomèdiques
August Pi I Sunyer. |
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| dc.description |
Peer reviewed |
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application/pdf |
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| dc.language |
eng |
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| dc.publisher |
BMJ Publishing Group |
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| dc.relation |
http://dx.doi.org/10.1136/gut.48.2.168 |
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| dc.rights |
openAccess |
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| dc.subject |
Fructose-1,6-biphosphate |
|
| dc.subject |
Glyceraldehyde- 3-phosphate dehydrogenase |
|
| dc.subject |
Intestinal preconditioning |
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| dc.subject |
Ischaemia/reperfusion injury |
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| dc.subject |
Nitric Oxide |
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| dc.title |
Fructose-1,6-biphosphate in rat intestinal preconditioning: involvement of nitric oxide |
|
| dc.type |
Artículo |
|