Fructose-1,6-bisphosphate preserves intracellular glutathione and protects cortical neurons against oxidative stress
Publisher DOI
PubMed ID
12505661
Abstract
Fructose-1,6-bisphosphate (FBP), an endogenous intermediate of glycolysis, protects the brain against ischemia-reperfusion injury. The mechanisms of FBP protection after cerebral ischemia are not well understood. The current study was undertaken to determine whether FBP protects primary neurons against hypoxia and oxidative stress by preserving reduced glutathione (GSH). Cultures of pure cortical neurons were subjected to oxygen deprivation, a donor of nitric oxide and superoxide radicals (3-morpholinosydnonimine), an inhibitor of glutathione synthesis (L-buthionine-sulfoximine) or glutathione reductase (1,3-bis(2-chloroethyl)-1-nitrosourea) in the presence or absence of FBP (3.5 mM). Neuronal viability was determined using an 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide assay. FBP protected neurons against hypoxia-reoxygenation and oxidative stress under conditions of compromised GSH metabolism. The efficacy of FBP depended on duration of hypoxia and was associated with higher intracellular GSH concentration, an effect partly mediated via increased glutathione reductase activity.
Date Issued
2003
Publication Type
Article
Language(s)
en
Author(s)
Vexler, ZS | |
Wong, A | |
Francisco, C | |
Manabat, C | |
Täuber, M | |
Ferriero, DM | |
Gregory, G |
Additional Credits
Journal
Brain research
Publisher
Elsevier
ISSN
0006-8993
ISBN
12505661
Access(Rights)
metadata.only