Polyhydroxylated fullerene derivative C60(OH)24prevents mitochondrial dysfunction and oxidative damage in an MPP+-induced cellular model of Parkinson's disease

2008 ◽  
Vol 86 (16) ◽  
pp. 3622-3634 ◽  
Author(s):  
Xiaoqing Cai ◽  
Haiqun Jia ◽  
Zhongbo Liu ◽  
Bei Hou ◽  
Cheng Luo ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Oxidative Damage ◽  
Mitochondrial Dysfunction ◽  
Fullerene Derivative ◽  
Cellular Model

scholarly journals Parkinson’s Disease: The Mitochondria-Iron Link

2016 ◽  
Vol 2016 ◽  
pp. 1-21 ◽  
Author(s):  
Yorka Muñoz ◽  
Carlos M. Carrasco ◽  
Joaquín D. Campos ◽  
Pabla Aguirre ◽  
Marco T. Núñez
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Oxidative Damage ◽  
Mitochondrial Dysfunction ◽  
Iron Homeostasis ◽  
Regulatory Protein ◽  
Iron Chelation ◽  
Causal Link ◽  
Iron Accumulation ◽  
Published Evidence

Mitochondrial dysfunction, iron accumulation, and oxidative damage are conditions often found in damaged brain areas of Parkinson’s disease. We propose that a causal link exists between these three events. Mitochondrial dysfunction results not only in increased reactive oxygen species production but also in decreased iron-sulfur cluster synthesis and unorthodox activation of Iron Regulatory Protein 1 (IRP1), a key regulator of cell iron homeostasis. In turn, IRP1 activation results in iron accumulation and hydroxyl radical-mediated damage. These three occurrences—mitochondrial dysfunction, iron accumulation, and oxidative damage—generate a positive feedback loop of increased iron accumulation and oxidative stress. Here, we review the evidence that points to a link between mitochondrial dysfunction and iron accumulation as early events in the development of sporadic and genetic cases of Parkinson’s disease. Finally, an attempt is done to contextualize the possible relationship between mitochondria dysfunction and iron dyshomeostasis. Based on published evidence, we propose that iron chelation—by decreasing iron-associated oxidative damage and by inducing cell survival and cell-rescue pathways—is a viable therapy for retarding this cycle.

Curcumin Rescues a PINK1 Knock Down SH-SY5Y Cellular Model of Parkinson’s Disease from Mitochondrial Dysfunction and Cell Death

2016 ◽  
Vol 54 (4) ◽  
pp. 2752-2762 ◽  
Author(s):  
Celia van der Merwe ◽  
Hayley Christy van Dyk ◽  
Lize Engelbrecht ◽  
Francois Hendrikus van der Westhuizen ◽  
Craig Kinnear ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cell Death ◽  
Mitochondrial Dysfunction ◽  
Cellular Model ◽  
Knock Down
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