Effect of quercetin, genistein and kaempferol on glutathione and glutathione-redox cycle enzymes in 3T3-L1 preadipocytes

被引:11
作者
Boadi, William Y. [1 ]
Amartey, Paul K. [1 ]
Lo, Andrew [1 ]
机构
[1] Tennessee State Univ, Dept Chem, Room 209,3500 John A Merritt Blvd, Nashville, TN 37209 USA
基金
美国食品与农业研究所;
关键词
oxidative damage; Fenton's pathway; glutathione reductase; superoxide dismutase; glutathione peroxidase; Flavonoids; MONONUCLEAR U937 CELLS; VITAMIN-E; OXYGEN-TOXICITY; LIPID PEROXIDES; STRAND BREAKS; BLOOD-CELLS; RAT-LIVER; FLAVONOIDS; SELENIUM; COPPER;
D O I
10.3109/01480545.2015.1082135
中图分类号
O6 [化学];
学科分类号
0703 ;
摘要
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 mu M 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 mu M 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.
引用
收藏
页码:239 / 247
页数:9
相关论文
共 37 条
[1]   Mechanism of protection by the flavonoids, quercetin and rutin, against tert-butylhydroperoxide- and menadione induced DNA single strand breaks in Caco-2 cells [J].
Aherne, SA ;
O'Brien, NM .
FREE RADICAL BIOLOGY AND MEDICINE, 2000, 29 (06) :507-514
[2]  
Alam ZI, 1997, J NEUROCHEM, V69, P1326
[3]   Oxidative DNA damage in the parkinsonian brain: An apparent selective increase in 8-hydroxyguanine levels in substantia nigra [J].
Alam, ZI ;
Jenner, A ;
Daniel, SE ;
Lees, AJ ;
Cairns, N ;
Marsden, CD ;
Jenner, P ;
Halliwell, B .
JOURNAL OF NEUROCHEMISTRY, 1997, 69 (03) :1196-1203
[4]   Anthocyanins in aged blueberry-fed rats are found centrally and may enhance memory [J].
Andres-Lacueva, C ;
Shukitt-Hale, B ;
Galli, RL ;
Jauregui, O ;
Lamuela-Raventos, RM ;
Joseph, JA .
NUTRITIONAL NEUROSCIENCE, 2005, 8 (02) :111-120
[5]   Lipid peroxides and glutathione status in human progenitor mononuclear (U937) cells following exposure to low doses of nickel and copper [J].
Boadi, William Y. ;
Harris, Shalandus ;
Anderson, Justin B. ;
Adunyah, Samuel E. .
DRUG AND CHEMICAL TOXICOLOGY, 2013, 36 (02) :155-162
[6]   In vitro exposure to quercetin and genistein alters lipid peroxides and prevents the loss of glutathione in human progenitor mononuclear (U937) cells [J].
Boadi, WY ;
Iyere, PA ;
Adunyah, SE .
JOURNAL OF APPLIED TOXICOLOGY, 2005, 25 (01) :82-88
[7]  
BOADI WY, 1991, VET HUM TOXICOL, V33, P105
[8]   Effect of quercetin and genistein on copper- and iron-induced lipid peroxidation in methyl linolenate [J].
Boadi, WY ;
Iyere, PA ;
Adunyah, SE .
JOURNAL OF APPLIED TOXICOLOGY, 2003, 23 (05) :363-369
[9]  
Briviba K, 1999, METHOD ENZYMOL, V301, P301
[10]   Fruit for health: the effect of flavonoids on humoral immune response and food selection in a frugivorous bird [J].
Catoni, C. ;
Schaefer, H. Martin ;
Peters, A. .
FUNCTIONAL ECOLOGY, 2008, 22 (04) :649-654