Obesity has been reported to be a risk factor for some types of cancer, such as prostate and lung. The AKT or PI3K-AKT is a signal transduction pathway that promotes survival and growth in response to extracellular signals. The aim of this study was to investigate the effects of two flavonoids, quercetin and kaempferol, and exogenous glutathione (GSH) on the expressions of phospho- and total-AKT levels in 3T3-L1 preadipocytes. Glyceraldehyde 3-phosphate dehydrogenase (GAPDH) levels were measured in the treated samples and used as the internal standard. 3T3-L1 preadipocytes were exposed to each flavonoid and GSH at concentrations of 0, 5, 10, 15, 20, and 25 µM, and the levels of phospho- and total-Akt were measured by the MILLIPLEX MAP mates protocol, based on the Luminex xMAP technology (Millipore Corp., St. Charles, MI, USA). GAPDH levels in the preadipocytes were not significantly different at the doses tested for the flavonoids and exogenous GSH. However, significant (p <.05) decreases in phospho-AKT levels in cells treated with quercetin, kaempferol, and GSH at certain doses were observed compared to their respective controls. Total-AKT levels showed the same profile for all the tested compounds. Significant (p <.01) differences were observed for kaempferol (15-25 µM), quercetin at 10 and 20 µM, and GSH at 10 µM compared to their respective controls. Findings suggest that exposure of 3T3-L1 preadipocytes to quercetin, kaempferol, and GSH may block the activation of AKT, suggesting the role such compounds play in cell differentiation in 3T3-L1 cells.

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 non-protein 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.