scholarly journals Trichostatin A induces apoptotic cell death of HeLa cells in a Bcl-2 and oxidative stress-dependent manner

2012 ◽  
Vol 42 (1) ◽  
pp. 359-366 ◽  
Author(s):  
BO RA YOU ◽  
WOO HYUN PARK
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Hela Cells ◽  
Apoptotic Cell ◽  
Trichostatin A ◽  
Apoptotic Cell Death ◽  
Dependent Manner ◽  
Stress Dependent ◽  
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

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

scholarly journals Autophagy impairment as a key feature for acetaminophen-induced ototoxicity

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Tong Zhao ◽  
Tihua Zheng ◽  
Huining Yu ◽  
Bo Hua Hu ◽  
Bing Hu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Lysosomal Enzymes ◽  
Apoptotic Cell ◽  
Cell Damage ◽  
Treatment Strategies ◽  
Explant Culture ◽  
Apoptotic Cell Death ◽  
Lysosomal Dysfunction ◽  
Autophagic Degradation

AbstractMacroautophagy/autophagy is a highly conserved self-digestion pathway that plays an important role in cytoprotection under stress conditions. Autophagy is involved in hepatotoxicity induced by acetaminophen (APAP) in experimental animals and in humans. APAP also causes ototoxicity. However, the role of autophagy in APAP-induced auditory hair cell damage is unclear. In the present study, we investigated autophagy mechanisms during APAP-induced cell death in a mouse auditory cell line (HEI-OC1) and mouse cochlear explant culture. We found that the expression of LC3-II protein and autophagic structures was increased in APAP-treated HEI-OC1 cells; however, the degradation of SQSTM1/p62 protein, the yellow puncta of mRFP-GFP-LC3 fluorescence, and the activity of lysosomal enzymes decreased in APAP-treated HEI-OC1 cells. The degradation of p62 protein and the expression of lysosomal enzymes also decreased in APAP-treated mouse cochlear explants. These data indicate that APAP treatment compromises autophagic degradation and causes lysosomal dysfunction. We suggest that lysosomal dysfunction may be directly responsible for APAP-induced autophagy impairment. Treatment with antioxidant N-acetylcysteine (NAC) partially alleviated APAP-induced autophagy impairment and apoptotic cell death, suggesting the involvement of oxidative stress in APAP-induced autophagy impairment. Inhibition of autophagy by knocking down of Atg5 and Atg7 aggravated APAP-induced ER and oxidative stress and increased apoptotic cell death. This study provides a better understanding of the mechanism responsible for APAP ototoxicity, which is important for future exploration of treatment strategies for the prevention of hearing loss caused by ototoxic medications.

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