These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Effect of quercetin, genistein and kaempferol on glutathione and glutathione-redox cycle enzymes in 3T3-L1 preadipocytes.
    Author: Boadi WY, Amartey PK, Lo A.
    Journal: Drug Chem Toxicol; 2016; 39(3):239-47. PubMed ID: 27063963.
    Abstract:
    CONTEXT AND 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. MATERIALS AND 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. DISCUSSION AND CONCLUSION: 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.
    [Abstract] [Full Text] [Related] [New Search]