Effects of Epigallocatechin 3-O-Gallate on Cellular Antioxidative System in HepG2 Cells.

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  • MURAKAMI Chikako
    Department of Applied Biological Chemistry, Osaka Prefecture University
  • HIRAKAWA Yuki
    Department of Applied Biological Chemistry, Osaka Prefecture University
  • INUI Hiroshi
    Department of Applied Biological Chemistry, Osaka Prefecture University
  • NAKANO Yoshihisa
    Department of Applied Biological Chemistry, Osaka Prefecture University
  • YOSHIDA Hiromi
    Department of Applied Biological Chemistry, Osaka Prefecture University

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To elucidate the interactions of catechins with the cellular antioxidative system, human hepatorna HepG2 cells were incubated in a serum-free medium with catechins, and the level of thiobarbituric acid-reactive substances (TBARS) as a marker of lipid peroxidation was determined, as well as the contents of α-tocopherol (α-Toc) and glutathione (GSH) and the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). TBARS was promptly decreased by the incubation with epigallocatechin 3-O-gallate (EGCG), and 12 h later TBARS in the cells with 10μM EGCG was about 15% (p<0.05) of that in the controls (without catechins). Epigallocatechin, epicatechin 3-O-gallate, and epicatechin also had an antioxidative activity, but a higher concentration was required to induce the same effect as EGCG. In the cells incubated with EGCG, the consumption of α-Toc and the formation of the oxidized form of GSH were suppressed. Although EGCG showed no effects on the Cu/Zn-SOD activity, the Mn-SOD activity in the cells was enhanced (p<0.05) by the incubation with EGCG. Moreover, the GSH-Px activity was maintained at a higher level (p<0.05) in the cells with EGCG, compared with that in the controls. when the cells were preincubated with EGCG, the cytotoxicity of H2O2 was significantly reduced. Furthermore, the decrease of cellular α-Toc content induced by exposure to H2O2 was prevented by the pretreatment of EGCG. These results suggest that EGCG taken up into HepG2 cells is preferentially used as an antioxidant, rather than α-Toc and GSH, to suppress lipid neroxidation and to protect these cells from oxidative damages.

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