scholarly journals Cerium oxide nanoparticles protect against Aβ-induced mitochondrial fragmentation and neuronal cell death

2014 ◽  
Vol 21 (10) ◽  
pp. 1622-1632 ◽  
Author(s):  
J M Dowding ◽  
W Song ◽  
K Bossy ◽  
A Karakoti ◽  
A Kumar ◽  
...  
Keyword(s):  
Cell Death ◽  
Cerium Oxide ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Cerium Oxide Nanoparticles ◽  
Oxide Nanoparticles ◽  
Mitochondrial Fragmentation

scholarly journals Cerium Oxide Nanoparticles Induced Toxicity in Human Lung Cells: Role of ROS Mediated DNA Damage and Apoptosis

2014 ◽  
Vol 2014 ◽  
pp. 1-14 ◽  
Author(s):  
Sandeep Mittal ◽  
Alok K. Pandey
Keyword(s):  
Dna Damage ◽  
Cell Death ◽  
Cerium Oxide ◽  
Oxidative Dna Damage ◽  
Apoptotic Cell ◽  
Morphological Changes ◽  
A549 Cells ◽  
Cerium Oxide Nanoparticles ◽  
Oxide Nanoparticles ◽  
Human Lung Cells

Cerium oxide nanoparticles (CeO2NPs) have promising industrial and biomedical applications. In spite of their applications, the toxicity of these NPs in biological/physiological environment is a major concern. Present study aimed to understand the molecular mechanism underlying the toxicity of CeO2NPs on lung adenocarcinoma (A549) cells. After internalization, CeO2NPs caused significant cytotoxicity and morphological changes in A549 cells. Further, the cell death was found to be apoptotic as shown by loss in mitochondrial membrane potential and increase in annexin-V positive cells and confirmed by immunoblot analysis of BAX, BCl-2, Cyt C, AIF, caspase-3, and caspase-9. A significant increase in oxidative DNA damage was found which was confirmed by phosphorylation of p53 gene and presence of cleaved poly ADP ribose polymerase (PARP). This damage could be attributed to increased production of reactive oxygen species (ROS) with concomitant decrease in antioxidant “glutathione (GSH)” level. DNA damage and cell death were attenuated by the application of ROS and apoptosis inhibitors N-acetyl-L- cysteine (NAC) and Z-DEVD-fmk, respectively. Our study concludes that ROS mediated DNA damage and cell cycle arrest play a major role in CeO2NPs induced apoptotic cell death in A549 cells. Apart from beneficial applications, these NPs also impart potential harmful effects which should be properly evaluated prior to their use.

Mitochondrial fragmentation and neuronal cell death in response to the Bcl-2/Bcl-xL/Bcl-w antagonist ABT-737

2010 ◽  
Vol 58 (8) ◽  
pp. 1258-1267 ◽  
Author(s):  
Kenneth W. Young ◽  
Lucia G.P. Piñón ◽  
Dalbir Dhiraj ◽  
Davina Twiddy ◽  
Marion MacFarlane ◽  
...  
Keyword(s):  
Cell Death ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Mitochondrial Fragmentation

Cerium Oxide Nanoparticles Prevent Nitrosative Stress in Neuronal Cell Culture Model

2010 ◽  
Vol 49 ◽  
pp. S181 ◽  
Author(s):  
Janet M Dowding ◽  
Sarah Lubitz ◽  
Ajay Karakoti ◽  
Andrew Kim ◽  
Sudipta Seal ◽  
...  
Keyword(s):  
Cell Culture ◽  
Cerium Oxide ◽  
Nitrosative Stress ◽  
Neuronal Cell ◽  
Cerium Oxide Nanoparticles ◽  
Oxide Nanoparticles ◽  
Cell Culture Model ◽  
Neuronal Cell Culture ◽  
Culture Model

scholarly journals Zinc Oxide Nanoparticles Induce Ferroptotic Neuronal Cell Death in vitro and in vivo

2020 ◽  
Vol Volume 15 ◽  
pp. 5299-5315
Author(s):  
Xia Qin ◽  
Qianghu Tang ◽  
Xuejun Jiang ◽  
Jun Zhang ◽  
Bin Wang ◽  
...  
Keyword(s):  
Cell Death ◽  
Zinc Oxide ◽  
Zinc Oxide Nanoparticles ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Oxide Nanoparticles

scholarly journals c-Abl-mediated Drp1 phosphorylation promotes oxidative stress-induced mitochondrial fragmentation and neuronal cell death

2017 ◽  
Vol 8 (10) ◽  
pp. e3117-e3117 ◽  
Author(s):  
Lujun Zhou ◽  
Qiang Zhang ◽  
Peng Zhang ◽  
Lei Sun ◽  
Can Peng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Mitochondrial Fragmentation

scholarly journals Zika Virus-Induced Neuronal Apoptosis via Increased Mitochondrial Fragmentation

2020 ◽  
Vol 11 ◽  
Author(s):  
Shu Yang ◽  
Kirill Gorshkov ◽  
Emily M. Lee ◽  
Miao Xu ◽  
Yu-Shan Cheng ◽  
...  
Keyword(s):  
Cell Death ◽  
Zika Virus ◽  
Neuronal Apoptosis ◽  
Mitochondrial Dynamics ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Mitochondrial Fragmentation ◽  
Zikv Infection ◽  
Mitofusin 2 ◽  
Infected Cells

The 2015 to 2016 outbreak of Zika virus (ZIKV) infections in the Americas coincided with a dramatic increase in neurodevelopmental abnormalities, including fetal microcephaly, in newborns born to infected women. In this study, we observed mitochondrial fragmentation and disrupted mitochondrial membrane potential after 24 h of ZIKV infection in human neural stem cells and the SNB-19 glioblastoma cell line. The severity of these changes correlated with the amount of ZIKV proteins expressed in infected cells. ZIKV infection also decreased the levels of mitofusin 2, which modulates mitochondria fusion. Mitochondrial division inhibitor 1 (Mdivi-1), a small molecule inhibiting mitochondria fission, ameliorated mitochondria disruptions and reduced cell death in ZIKV-infected cells. Collectively, this study suggests that abnormal mitochondrial fragmentation contributes to ZIKV-induced neuronal cell death; rebalancing mitochondrial dynamics of fission-fusion could be a therapeutic strategy for drug development to treat ZIKV-mediated neuronal apoptosis.

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