Document Detail


Quercetin protects cutaneous tissue-associated cell types including sensory neurons from oxidative stress induced by glutathione depletion: cooperative effects of ascorbic acid.
MedLine Citation:
PMID:  9013129     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Oxidation reactions are essential biological reactions necessary for the formation of high-energy compounds used to fuel metabolic processes, but can be injurious to cells when produced in excess. Cutaneous tissue is especially susceptible to damage mediated by reactive oxygen species and low-density lipoprotein oxidation, triggered by dysmetabolic diseases, inflammation, environmental factors, or aging. Here we have examined the ability of the flavonoid quercetin to protect cutaneous tissue-associated cell types from injury induced by oxidative stress, and possible cooperative effects of ascorbic acid. Human skin fibroblasts, keratinocytes, and endothelial cells were cultured in the presence of buthionine sulfoximine (BSO), an irreversible inhibitor of glutathione (GSH) synthesis. Depletion of intracellular levels of GSH leads to an accumulation of cellular peroxides and eventual cell death. Quercetin concentration-dependently (EC50: 30-40 microM) reduced oxidative injury of BSO to all cell types, and was also effective when first added after BSO washout. BSO caused marked decreases in the intracellular level of GSH, which remained depressed in quercetin-protected cells. Ascorbic acid, while by itself not cytoprotective synergized with quercetin, lowered the quercetin EC50 and prolonged the window for cytoprotection. The related flavonoids rutin and dihydroquercetin also decreased BSO-induced injury to dermal fibroblasts, albeit less efficaciously so than quercetin. The cytoprotective effect of rutin, but not that of dihydroquercetin, was enhanced in the presence of ascorbic acid. Further, quercetin rescued sensory ganglion neurons from death provoked by GSH depletion. Direct oxidative injury to this last cell type has not been previously demonstrated. The results show that flavonoids are broadly protective for cutaneous tissue-type cell populations subjected to a chronic intracellular form of oxidative stress. Quercetin in particular, paired with ascorbic acid, may be of therapeutic benefit in protecting neurovasculature structures in skin from oxidative damage.
Authors:
S D Skaper; M Fabris; V Ferrari; M Dalle Carbonare; A Leon
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Free radical biology & medicine     Volume:  22     ISSN:  0891-5849     ISO Abbreviation:  Free Radic. Biol. Med.     Publication Date:  1997  
Date Detail:
Created Date:  1997-04-17     Completed Date:  1997-04-17     Revised Date:  2004-11-17    
Medline Journal Info:
Nlm Unique ID:  8709159     Medline TA:  Free Radic Biol Med     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  669-78     Citation Subset:  IM    
Affiliation:
Researchlife S.c.p.A., Castelfranco Veneto, Italy.
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MeSH Terms
Descriptor/Qualifier:
3T3 Cells
Animals
Ascorbic Acid / administration & dosage,  pharmacology*
Buthionine Sulfoximine / pharmacology
Cell Death / drug effects
Cells, Cultured
Chick Embryo
Drug Synergism
Free Radicals / metabolism
Glutathione / metabolism
Humans
Mice
Neurons, Afferent / drug effects*,  metabolism*
Oxidative Stress / drug effects*
Quercetin / administration & dosage,  pharmacology*
Rutin / administration & dosage,  pharmacology
Skin / drug effects*,  innervation,  metabolism*
Chemical
Reg. No./Substance:
0/Free Radicals; 117-39-5/Quercetin; 153-18-4/Rutin; 50-81-7/Ascorbic Acid; 5072-26-4/Buthionine Sulfoximine; 70-18-8/Glutathione

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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