Tetrandrine-induced apoptosis in rat primary hepatocytes is initiated from mitochondria: Caspases and Endonuclease G (Endo G) pathway

Toxicology ◽  
2006 ◽  
Vol 218 (1) ◽  
pp. 1-12 ◽  
Author(s):  
C YAN ◽  
Q XINMING ◽  
G LIKUN ◽  
L LINLIN ◽  
C FANGPING ◽  
...  
Keyword(s):  
Primary Hepatocytes ◽  
Endonuclease G ◽  
Rat Primary Hepatocytes ◽  
Induced Apoptosis

Oxidative stress is involved in Dasatinib-induced apoptosis in rat primary hepatocytes

2012 ◽  
Vol 261 (3) ◽  
pp. 280-291 ◽  
Author(s):  
Tao Xue ◽  
Peihua Luo ◽  
Hong Zhu ◽  
Yuqin Zhao ◽  
Honghai Wu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Primary Hepatocytes ◽  
Rat Primary Hepatocytes ◽  
Induced Apoptosis

Mechanism of Rhein-Induced Apoptosis in Rat Primary Hepatocytes: Beneficial Effect of Cyclosporine A

2015 ◽  
Vol 28 (6) ◽  
pp. 1133-1143 ◽  
Author(s):  
Gati Krushna Panigrahi ◽  
Ashish Yadav ◽  
Ashish Srivastava ◽  
Anurag Tripathi ◽  
S. Raisuddin ◽  
...  
Keyword(s):  
Beneficial Effect ◽  
Cyclosporine A ◽  
Primary Hepatocytes ◽  
Rat Primary Hepatocytes ◽  
Induced Apoptosis

Butein Up-Regulates the Expression of the π Class of GlutathioneS-Transferase in Rat Primary Hepatocytes through the ERK/AP-1 Pathway

2010 ◽  
Vol 58 (16) ◽  
pp. 8994-9000 ◽  
Author(s):  
Hebron C. Chang ◽  
Haw-Wen Chen ◽  
Hui-Shan Tung ◽  
Kai-Li Liu ◽  
Chia-Wen Tsai ◽  
...  
Keyword(s):  
Primary Hepatocytes ◽  
Rat Primary Hepatocytes

scholarly journals Overexpression of Mitochondrial Leishmania major Ascorbate Peroxidase Enhances Tolerance to Oxidative Stress-Induced Programmed Cell Death and Protein Damage

2009 ◽  
Vol 8 (11) ◽  
pp. 1721-1731 ◽  
Author(s):  
Subhankar Dolai ◽  
Rajesh K. Yadav ◽  
Swati Pal ◽  
Subrata Adak
Keyword(s):  
Oxidative Stress ◽  
Flow Cytometry ◽  
Confocal Microscopy ◽  
Ascorbate Peroxidase ◽  
Leishmania Major ◽  
Mitochondrial Respiratory Chain ◽  
Protein Carbonyl ◽  
Endonuclease G ◽  
Mitochondrial Membrane Depolarization ◽  
Induced Apoptosis

ABSTRACT Ascorbate peroxidase from Leishmania major (LmAPX) is one of the key enzymes for scavenging of reactive oxygen species generated from the mitochondrial respiratory chain. We have investigated whether mitochondrial LmAPX has any role in oxidative stress-induced apoptosis. The measurement of reduced glutathione (GSH) and protein carbonyl contents in cellular homogenates indicates that overexpression of LmAPX protects Leishmania cells against depletion of GSH and oxidative damage of proteins by H2O2 or camptothecin (CPT) treatment. Confocal microscopy and fluorescence spectroscopy data have revealed that the intracellular elevation of Ca2+ attained by the LmAPX-overexpressing cells was always below that attained in control cells. Flow cytometry assay data and confocal microscopy observation strongly suggest that LmAPX overexpression protects cells from H2O2-induced mitochondrial membrane depolarization as well as ATP decrease. Western blot data suggest that overexpression of LmAPX shields against H2O2- or CPT-induced cytochrome c and endonuclease G release from mitochondria and subsequently their accumulation in the cytoplasm. Caspase activity assay by flow cytometry shows a lower level of caspase-like protease activity in LmAPX-overexpressing cells under apoptotic stimuli. The data on phosphatidylserine exposed on the cell surface and DNA fragmentation results show that overexpression of LmAPX renders the Leishmania cells more resistant to apoptosis provoked by H2O2 or CPT treatment. Taken together, these results indicate that constitutive overexpression of LmAPX in the mitochondria of L. major prevents cells from the deleterious effects of oxidative stress, that is, mitochondrial dysfunction and cellular death.

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