Mitochondria permeability transition-dependent tert-butyl hydroperoxide-induced apoptosis in hepatoma HepG2 cells

2004 ◽  
Vol 67 (4) ◽  
pp. 611-620 ◽  
Author(s):  
Jean-Pascal Piret ◽  
Thierry Arnould ◽  
Bruno Fuks ◽  
Pierre Chatelain ◽  
José Remacle ◽  
...  
Keyword(s):  
Hepg2 Cells ◽  
Permeability Transition ◽  
Butyl Hydroperoxide ◽  
Tert Butyl ◽  
Tert Butyl Hydroperoxide ◽  
Induced Apoptosis ◽  
Hepatoma Hepg2

scholarly journals Selenium methylselenocysteine protects human hepatoma HepG2 cells against oxidative stress induced by tert-butyl hydroperoxide

2007 ◽  
Vol 389 (7-8) ◽  
pp. 2167-2178 ◽  
Author(s):  
Susana Cuello ◽  
Sonia Ramos ◽  
Raquel Mateos ◽  
M. Angeles Martín ◽  
Yolanda Madrid ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepg2 Cells ◽  
Human Hepatoma ◽  
Butyl Hydroperoxide ◽  
Tert Butyl ◽  
Tert Butyl Hydroperoxide ◽  
Human Hepatoma Hepg2 Cells ◽  
Hepatoma Hepg2

scholarly journals Meroterpenoid-Rich Fraction of the Ethanolic Extract from Sargassum serratifolium Suppressed Oxidative Stress Induced by Tert-Butyl Hydroperoxide in HepG2 Cells

Marine Drugs ◽  
2018 ◽  
Vol 16 (10) ◽  
pp. 374 ◽  
Author(s):  
Sujin Lim ◽  
Misung Kwon ◽  
Eun-Ji Joung ◽  
Taisun Shin ◽  
Chul-Woong Oh ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepg2 Cells ◽  
Ethanolic Extract ◽  
Glutathione Depletion ◽  
Heme Oxygenase 1 ◽  
Dependent Manner ◽  
Butyl Hydroperoxide ◽  
Tert Butyl ◽  
Tert Butyl Hydroperoxide ◽  
Sargassum Serratifolium

Sargassum species have been reported to be a source of phytochemicals, with a wide range of biological activities. In this study, we evaluated the hepatoprotective effect of a meroterpenoid-rich fraction of the ethanolic extract from Sargassum serratifolium (MES) against tert-butyl hydroperoxide (t-BHP)-treated HepG2 cells. Treatment with MES recovered the cell viability from the t-BHP-induced oxidative damage in a dose-dependent manner. It suppressed the reactive oxygen species production, lipid peroxidation, and glutathione depletion in the t-BHP-treated HepG2 cells. The activity of the antioxidants induced by t-BHP, including superoxide dismutase (SOD) and catalase, was reduced by the MES treatment. Moreover, it increased the nuclear translocation of nuclear factor erythroid 2-related factor 2, leading to the enhanced activity of glutathione S transferase, and the increased production of heme oxygenase-1 and NAD(P)H:quinine oxidoreductase 1 in t-BHP-treated HepG2 cells. These results demonstrate that the antioxidant activity of MES substituted the activity of the SOD and catalase, and induced the production of detoxifying enzymes, indicating that MES might be used as a hepatoprotectant against t-BHP-induced oxidative stress.

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