title: Effect of quercetin, genistein and kaempferol on glutathione and glutathione-redox cycle enzymes in 3T3-L1 preadipocytes.
abstract: OBJECTIVE
  Many studies have shown that cellular redox potential is largely determined by glutathione (GSH), which accounts for more than 90% of cellular nonprotein thiols. The aim of this study was to delineate the effect of three flavonoids - namely, quercetin, kaempferol and genistein - and exogenous GSH on oxidative damage by the Fenton's pathway through the GSH and GSH-redox cycle enzymes in 3T3-L1 cells.
  
  
  METHODS
  3T3-L1 preadipocytes were exposed to each flavonoid and GSH at concentrations of 0, 5, 10, 15, 20 and 25 µM and then GSH levels and activities of glutathione peroxidase (GSH-Px), glutathione reductase (GSH-Rx) and superoxide dismutase (SOD) were measured.
  
  
  RESULTS
  Exogenous GSH did not have significant effect on intracellular GSH although slight decrease was observed at 15-25 µM doses. However, each of the three flavonoids sustained intracellular GSH levels in the cells as compared to the respective controls. Quercetin had the most profound effect, followed by kaempferol and genistein in that order. GSH-Px, GSH-Rx and SOD activities increased for all the doses tested compared to their respective controls. Again, quercetin had the maximum increase in enzyme activities followed by kaempferol and genistein for the enzymes tested.
  
  
  CONCLUSIONS
  These findings suggest that the flavonoids play an important role in diminishing oxidation-induced biochemical damages. The enhancement of these enzymes may increase the resistance of the organism against oxidative damage by the Fenton's pathway.
authors.affiliation: a Department of Chemistry , Tennessee State University , Nashville , TN , USA.
authors.forename: William Y
authors.initials: WY
authors.lastname: Boadi
authors.affiliation: a Department of Chemistry , Tennessee State University , Nashville , TN , USA.
authors.forename: Paul K
authors.initials: PK
authors.lastname: Amartey
authors.affiliation: a Department of Chemistry , Tennessee State University , Nashville , TN , USA.
authors.forename: Andrew
authors.initials: A
authors.lastname: Lo
mesh_terms: D041721:3T3-L1 Cells; D017667:Adipocytes / Q000187:drug effects* / Q000201:enzymology* / Q000378:metabolism; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D018929:Cell Culture Techniques; D004305:Dose-Response Relationship, Drug; D005419:Flavonoids / Q000494:pharmacology*; D019833:Genistein / Q000494:pharmacology; D005978:Glutathione / Q000378:metabolism* / Q000494:pharmacology; D005979:Glutathione Peroxidase / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D044949:Kaempferols / Q000494:pharmacology; D051379:Mice; D018384:Oxidative Stress / Q000187:drug effects*; D011794:Quercetin / Q000494:pharmacology; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D000975:Antioxidants; D005419:Flavonoids; D044949:Kaempferols; C006552:kaempferol; D011794:Quercetin; D019833:Genistein; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase; D005978:Glutathione
keywords: Fenton’s pathway; Flavonoids; glutathione peroxidase; glutathione reductase; oxidative damage; superoxide dismutase