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Protective mechanism of quercetin and rutin using glutathione metabolism on HO-induced oxidative stress in HepG2 cells.
Ann N Y Acad Sci. 2009 Aug; 1171:530-7.AN

Abstract

The levels of cellular glutathione (GSH) and reactive oxygen species (ROS) simultaneously determined by fluorometric measurement, may provide important information on pro-oxidative and antioxidative balance. The dual effect of quercetin antioxidant and pro-oxidant activity was proposed from different studies. Our study demonstrated that quercetin acted as an antioxidant in HepG2 cells when cells were treated with 10 and 100 micromol/L quercetin for 30 min, but quercetin acted as a pro-oxidant when cells were incubated at 100 micromol/L quercetin for longer periods (12 and 24 h). Quercetin is capable of reducing H(2)O(2)-induced oxidative stress of HepG2 cells through different mechanisms, such as detoxification of H(2)O(2,) inhibition of ROS generation, and removal of generated ROS. We find that quercetin can block ROS generation through Fenton reaction to produce hydroxyl radicals by chelating with transition metal ions such as Cu(2+). Evidence that quercetin might exert an antioxidant effect by changing generated ROS into less reactive ROS suggests that when quercetin reacts with ROS, it becomes oxidized, which is less harmful but still reactive, and the oxidized quercetin interacts with thiol compounds as reduced GSH to return to the parent compound quercetin. In contrast, the prolonged treatment of quercetin in high concentrations (100 micromol/L) shows that quercetin may act as a pro-oxidant rather than as an antioxidant, resulting in cell death (apoptosis).

Authors+Show Affiliations

Department of Food and Nutrition, Hannam University, Daejeon, Korea.No affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19723100

Citation

Kim, Gyo-Nam, and Hae-Dong Jang. "Protective Mechanism of Quercetin and Rutin Using Glutathione Metabolism On HO-induced Oxidative Stress in HepG2 Cells." Annals of the New York Academy of Sciences, vol. 1171, 2009, pp. 530-7.
Kim GN, Jang HD. Protective mechanism of quercetin and rutin using glutathione metabolism on HO-induced oxidative stress in HepG2 cells. Ann N Y Acad Sci. 2009;1171:530-7.
Kim, G. N., & Jang, H. D. (2009). Protective mechanism of quercetin and rutin using glutathione metabolism on HO-induced oxidative stress in HepG2 cells. Annals of the New York Academy of Sciences, 1171, 530-7. https://doi.org/10.1111/j.1749-6632.2009.04690.x
Kim GN, Jang HD. Protective Mechanism of Quercetin and Rutin Using Glutathione Metabolism On HO-induced Oxidative Stress in HepG2 Cells. Ann N Y Acad Sci. 2009;1171:530-7. PubMed PMID: 19723100.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Protective mechanism of quercetin and rutin using glutathione metabolism on HO-induced oxidative stress in HepG2 cells. AU - Kim,Gyo-Nam, AU - Jang,Hae-Dong, PY - 2009/9/3/entrez PY - 2009/9/3/pubmed PY - 2009/9/24/medline SP - 530 EP - 7 JF - Annals of the New York Academy of Sciences JO - Ann N Y Acad Sci VL - 1171 N2 - The levels of cellular glutathione (GSH) and reactive oxygen species (ROS) simultaneously determined by fluorometric measurement, may provide important information on pro-oxidative and antioxidative balance. The dual effect of quercetin antioxidant and pro-oxidant activity was proposed from different studies. Our study demonstrated that quercetin acted as an antioxidant in HepG2 cells when cells were treated with 10 and 100 micromol/L quercetin for 30 min, but quercetin acted as a pro-oxidant when cells were incubated at 100 micromol/L quercetin for longer periods (12 and 24 h). Quercetin is capable of reducing H(2)O(2)-induced oxidative stress of HepG2 cells through different mechanisms, such as detoxification of H(2)O(2,) inhibition of ROS generation, and removal of generated ROS. We find that quercetin can block ROS generation through Fenton reaction to produce hydroxyl radicals by chelating with transition metal ions such as Cu(2+). Evidence that quercetin might exert an antioxidant effect by changing generated ROS into less reactive ROS suggests that when quercetin reacts with ROS, it becomes oxidized, which is less harmful but still reactive, and the oxidized quercetin interacts with thiol compounds as reduced GSH to return to the parent compound quercetin. In contrast, the prolonged treatment of quercetin in high concentrations (100 micromol/L) shows that quercetin may act as a pro-oxidant rather than as an antioxidant, resulting in cell death (apoptosis). SN - 1749-6632 UR - https://www.unboundmedicine.com/medline/citation/19723100/Protective_mechanism_of_quercetin_and_rutin_using_glutathione_metabolism_on_HO_induced_oxidative_stress_in_HepG2_cells_ L2 - https://doi.org/10.1111/j.1749-6632.2009.04690.x DB - PRIME DP - Unbound Medicine ER -