scholarly journals Methyloleanolate Induces Apoptotic And Autophagic Cell Death Via Reactive Oxygen Species Generation And c-Jun N-terminal Kinase Phosphorylation

2019 ◽  
Vol Volume 12 ◽  
pp. 8621-8635 ◽  
Author(s):  
Myoung Seok Jeong ◽  
Ji Hoon Jung ◽  
Hyemin Lee ◽  
Chang Geun Kim ◽  
Sung-Hoon Kim
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Autophagic Cell Death ◽  
Oxygen Species ◽  
Kinase Phosphorylation

scholarly journals zVAD-induced autophagic cell death requires c-Src-dependent ERK and JNK activation and reactive oxygen species generation

Autophagy ◽  
2011 ◽  
Vol 7 (2) ◽  
pp. 217-228 ◽  
Author(s):  
Szu-Ying Chen ◽  
Ling-Ya Chiu ◽  
Ming-Chei Ma ◽  
Jang-Shiun Wang ◽  
Chung-Liang Chien ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Autophagic Cell Death ◽  
Oxygen Species ◽  
Jnk Activation

scholarly journals Reactive Oxygen Species Mediate 6c-Induced Mitochondrial and Lysosomal Dysfunction, Autophagic Cell Death, and DNA Damage in Hepatocellular Carcinoma

2021 ◽  
Vol 22 (20) ◽  
pp. 10987
Author(s):  
Senzhen Wang ◽  
Xiaojuan Xu ◽  
Delu Che ◽  
Ronghui Fan ◽  
Mengke Gao ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Dna Damage ◽  
Cell Death ◽  
Cancer Cells ◽  
Reactive Oxygen ◽  
Comparative Proteomics ◽  
Autophagic Cell Death ◽  
Oxygen Species ◽  
Lysosomal Dysfunction ◽  
Mitochondrial Ros

Increasing the level of reactive oxygen species (ROS) in cancer cells has been suggested as a viable approach to cancer therapy. Our previous study has demonstrated that mitochondria-targeted flavone-naphthalimide-polyamine conjugate 6c elevates the level of ROS in cancer cells. However, the detailed role of ROS in 6c-treated cancer cells is not clearly stated. The biological effects and in-depth mechanisms of 6c in cancer cells need to be further investigated. In this study, we confirmed that mitochondria are the main source of 6c-induced ROS, as demonstrated by an increase in 2′,7′-dichlorodihydrofluorescein diacetate (DCFH-DA) and MitoSox fluorescence. Compound 6c-induced mitochondrial ROS caused mitochondrial dysfunction and lysosomal destabilization confirmed by absolute quantitation (iTRAQ)-based comparative proteomics. Compound 6c-induced metabolic pathway dysfunction and lysosomal destabilization was attenuated by N-acetyl-L-cysteine (NAC). iTRAQ-based comparative proteomics showed that ROS regulated the expression of 6c-mediated proteins, and treatment with 6c promoted the formation of autophagosomes depending on ROS. Compound 6c-induced DNA damage was characterized by comet assay, p53 phosphorylation, and γH2A.X, which was diminished by pretreatment with NAC. Compound 6c-induced cell death was partially reversed by 3-methyladenine (3-MA), bafilomycin (BAF) A1, and NAC, respectively. Taken together, the data obtained in our study highlighted the involvement of mitochondrial ROS in 6c-induced autophagic cell death, mitochondrial and lysosomal dysfunction, and DNA damage.

Polyphenol effects on CuO-nanoparticle-mediated DNA damage, reactive oxygen species generation, and fibroblast cell death

2021 ◽  
pp. 105252
Author(s):  
Carlos Angelé-Martínez ◽  
Fathima S. Ameer ◽  
Yash Raval ◽  
Guohui Huang ◽  
Tzuen-Rong J. Tzeng ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Dna Damage ◽  
Cell Death ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Fibroblast Cell ◽  
Oxygen Species ◽  
Cuo Nanoparticle
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