scholarly journals Reactive Oxygen Species Play a Central Role in Hexavalent Chromium-Induced Apoptosis in Hep3B Cells without the Functional Roles of p53 and Caspase-3

2013 ◽  
Vol 32 (2) ◽  
pp. 279-290 ◽  
Author(s):  
Ming Zeng ◽  
Fang Xiao ◽  
Xiali Zhong ◽  
Feng Jin ◽  
Lan Guan ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Hexavalent Chromium ◽  
Caspase 3 ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Functional Roles ◽  
Hep3b Cells ◽  
Induced Apoptosis

Reactive oxygen species and caspase activation mediate silica-induced apoptosis in alveolar macrophages

2001 ◽  
Vol 280 (1) ◽  
pp. L10-L17 ◽  
Author(s):  
Han-Ming Shen ◽  
Zhuo Zhang ◽  
Qi-Feng Zhang ◽  
Choon-Nam Ong
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Alveolar Macrophages ◽  
Caspase 3 ◽  
Reactive Oxygen ◽  
Parp Cleavage ◽  
Oxygen Species ◽  
Caspase Activation ◽  
Caspase 9 ◽  
Induced Apoptosis

Alveolar macrophages (AMs) are the principal target cells of silica and occupy a key position in the pathogenesis of silica-related diseases. Silica has been found to induce apoptosis in AMs, whereas its underlying mechanisms involving the initiation and execution of apoptosis are largely unknown. The main objective of the present study was to examine the form of cell death caused by silica and the mechanisms involved. Silica-induced apoptosis in AMs was evaluated by terminal deoxynucleotidyltransferase-mediated dUTP nick end-labeling assay and cell cycle/DNA content analysis. The elevated level of reactive oxygen species (ROS), caspase-9 and caspase-3 activation, and poly(ADP-ribose) polymerase (PARP) cleavage in silica-treated AMs were also determined. The results showed that there was a temporal pattern of apoptotic events in silica-treated AMs, starting with ROS formation and followed by caspase-9 and caspase-3 activation, PARP cleavage, and DNA fragmentation. Silica-induced apoptosis was significantly attenuated by a caspase-3 inhibitor, N-acetyl-Asp-Glu-Val-Asp aldehyde, and ebselen, a potent antioxidant. These findings suggest that apoptosis is an important form of cell death caused by silica exposure in which the elevated ROS level that results from silica exposure may act as an initiator, leading to caspase activation and PARP cleavage to execute the apoptotic process.

scholarly journals Bufalin Induces Reactive Oxygen Species Dependent Bax Translocation and Apoptosis in ASTC-a-1 Cells

2011 ◽  
Vol 2011 ◽  
pp. 1-12 ◽  
Author(s):  
Lei Sun ◽  
Tongsheng Chen ◽  
Xiaoping Wang ◽  
Yun Chen ◽  
Xunbin Wei
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Molecular Mechanisms ◽  
Caspase 3 ◽  
Temporal Dynamics ◽  
Reactive Oxygen ◽  
Ros Generation ◽  
Ros Production ◽  
Oxygen Species ◽  
Induced Apoptosis

Bufalin has been shown to induce cancer cell death through apoptotic pathways. However, the molecular mechanisms are not well understood. In this study, we used the confocal fluorescence microscopy (CFM) to monitor the spatio-temporal dynamics of reactive oxygen species (ROS) production, Bax translocation and caspase-3 activation during bufalin-induced apoptosis in living human lung adenocarcinoma (ASTC-a-1) cells. Bufalin induced ROS production and apoptotic cell death, demonstrated by Hoechst 33258 staining as well as flow cytometry analysis. Bax redistributed from cytosol to mitochondria from 12 to 48 h after bufalin treatment in living cells expressed with green fluorescent protein Bax. Treatment with the antioxidantN-acetyl-cysteine (NAC), a ROS scavenger, inhibited ROS generation and Bax translocation and led to a significant protection against bufalin-induced apoptosis. Our results also revealed that bufalin induced a prominent increase of caspase-3 activation blocked potently by NAC. Taken together, bufalin induced ROS-mediated Bax translocation, mitochondrial permeability transition and caspase-3 activation, implying that bufalin induced apoptosis via ROS-dependent mitochondrial death pathway in ASTC-a-1 cells.

scholarly journals Implication of mitochondria-derived reactive oxygen species, cytochrome C and caspase-3 in N-(4-Hydroxyphenyl)retinamide-induced apoptosis in cervical carcinoma cells

Oncogene ◽  
1999 ◽  
Vol 18 (46) ◽  
pp. 6380-6387 ◽  
Author(s):  
Seigo Suzuki ◽  
Masahiro Higuchi ◽  
Rita J Proske ◽  
Nobuhiko Oridate ◽  
Waun K Hong ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cytochrome C ◽  
Cervical Carcinoma ◽  
Caspase 3 ◽  
Reactive Oxygen ◽  
Carcinoma Cells ◽  
Oxygen Species ◽  
Induced Apoptosis

scholarly journals Regulation of reactive oxygen species-induced apoptosis and necrosis by caspase 3-like proteases

Oncogene ◽  
1998 ◽  
Vol 17 (21) ◽  
pp. 2753-2760 ◽  
Author(s):  
Masahiro Higuchi ◽  
Toshie Honda ◽  
Rita J Proske ◽  
Edward TH Yeh
Keyword(s):  
Reactive Oxygen Species ◽  
Caspase 3 ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Induced Apoptosis ◽  
Apoptosis And Necrosis
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