scholarly journals Mitochondrial Dysfunction and Oxidative Stress Promote Apoptotic Cell Death in the Striatum via Cytochrome c/ Caspase-3 Signaling Cascade Following Chronic Rotenone Intoxication in Rats

2012 ◽  
Vol 13 (7) ◽  
pp. 8722-8739 ◽  
Author(s):  
Tsu-Kung Lin ◽  
Ching-Hsiao Cheng ◽  
Shang-Der Chen ◽  
Chia-Wei Liou ◽  
Chi-Ren Huang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Cytochrome C ◽  
Mitochondrial Dysfunction ◽  
Caspase 3 ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Signaling Cascade ◽  
And Oxidative Stress

Alginate oligosaccharide protects against endoplasmic reticulum- and mitochondrial-mediated apoptotic cell death and oxidative stress

Biomaterials ◽  
2011 ◽  
Vol 32 (23) ◽  
pp. 5438-5458 ◽  
Author(s):  
Solaleh Khoramian Tusi ◽  
Leila Khalaj ◽  
Ghorbangol Ashabi ◽  
Mahmoud Kiaei ◽  
Fariba Khodagholi
Keyword(s):  
Oxidative Stress ◽  
Endoplasmic Reticulum ◽  
Cell Death ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Alginate Oligosaccharide ◽  
And Oxidative Stress

4-hydroxynonenal induces a cellular redox status-related activation of the caspase cascade for apoptotic cell death

2000 ◽  
Vol 113 (4) ◽  
pp. 635-641 ◽  
Author(s):  
W. Liu ◽  
M. Kato ◽  
A.A. Akhand ◽  
A. Hayakawa ◽  
H. Suzuki ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Dna Fragmentation ◽  
Caspase 3 ◽  
Apoptotic Cell ◽  
K562 Cells ◽  
Apoptotic Cell Death ◽  
Jurkat Cells ◽  
Substrate Peptide ◽  
Caspase Cascade

4-Hydroxynonenal (HNE), a diffusible product of lipid peroxidation, has been suggested to be a key mediator of oxidative stress-induced cell death. In this study, we partially characterized the mechanism of HNE-mediated cytotoxicity. Incubation of human T lymphoma Jurkat cells with 20–50 μM HNE led to cell death accompanied by DNA fragmentation. Western blot analysis showed that HNE-treatment induced time- and dose-dependent activation of caspase-8, caspase-9 and caspase-3. HNE-induced caspase-3 processing was confirmed by a flow cytometric demonstration of increased catalytic activity on the substrate peptide. HNE treatment also led to remarkable cleavage of poly(ADP-ribose) polymerase (PARP), which was prevented by pretreatment of cells with DEVD-FMK as a caspase-3 inhibitor. The HNE-mediated activation of caspases, cleavage of PARP and DNA fragmentation were blocked by antioxidants cysteine, N-acety-L-cysteine and dithiothreitol, but not by two other HNE-reactive amino acids lysine and histidine, or by cystine, the oxidized form of cysteine. HNE rapidly decreased levels of intracellular reduced glutathione (GSH) and its oxidized form GSSG, and these were also attenuated by the reductants. Coincubation of Jurkat cells with a blocking anti-Fas antibody prevented Fas-induced but not HNE-induced activation of caspase-3. HNE also activated caspase-3 in K562 cells that do not express functional Fas. Our results thereby demonstrate that HNE triggers oxidative stress-linked apoptotic cell death through activation of the caspase cascade. The results also suggest a possible mechanism involving a direct scavenge of intracellular GSH by HNE.

scholarly journals Clusterin Gene Expression Mediates Resistance to Apoptotic Cell Death Induced by Heat Shock and Oxidative Stress

1999 ◽  
Vol 112 (3) ◽  
pp. 290-296 ◽  
Author(s):  
Isabelle Viard ◽  
Philippe Wehrli ◽  
Lan Jornot ◽  
Roberto Bullani ◽  
Jean-Luc Vechietti ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Cell Death ◽  
Heat Shock ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
And Oxidative Stress
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