scholarly journals The Execution Step in Parkinson’s Disease – On the Vicious Cycle of Mitochondrial Complex I Inhibition, Iron Dishomeostasis and Oxidative Stress

10.5772/17618 ◽  
2012 ◽  
Author(s):  
Marco T. ◽  
Pamela Urrutia ◽  
Natalia Mena ◽  
Pabla Aguirre
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Complex I ◽  
Mitochondrial Complex I ◽  
Vicious Cycle ◽  
Mitochondrial Complex ◽  
And Oxidative Stress

scholarly journals Chloramphenicol Mitigates Oxidative Stress by Inhibiting Translation of Mitochondrial Complex I in Dopaminergic Neurons of Toxin-Induced Parkinson’s Disease Model

2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Jeongsu Han ◽  
Soo Jeong Kim ◽  
Min Jeong Ryu ◽  
Yunseon Jang ◽  
Min Joung Lee ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Dopaminergic Neurons ◽  
Complex I ◽  
Cell Loss ◽  
Preventive Strategy ◽  
Mitochondrial Complex I ◽  
Ros Production ◽  
Mitochondrial Complex

Paraquat (PQ), an herbicide considered an environmental contributor to the development of Parkinson’s disease (PD), induces dopaminergic neuronal loss through reactive oxygen species (ROS) production and oxidative stress by mitochondrial complex I. Most patients with PQ-induced PD are affected by chronic exposure and require a preventive strategy for modulation of disease progression. To identify drugs that are effective in preventing PD, we screened more than 1000 drugs that are currently used in clinics and in studies employing PQ-treated cells. Of these, chloramphenicol (CP) showed the most powerful inhibitory effect. Pretreatment with CP increased the viability of PQ-treated SN4741 dopaminergic neuronal cells and rat primary cultured dopaminergic neurons compared with control cells treated with PQ only. CP pretreatment also reduced PQ-induced ROS production, implying that mitochondrial complex I is a target of CP. This effect of CP reflected downregulation of the mitochondrial complex I subunit ND1 and diminished PQ recycling, a major mechanism of ROS production, and resulted in the prevention of cell loss. Notably, these effects of CP were not observed in rotenone-pretreated SN4741 cells and Rho-negative cells, in which mitochondrial function is defective. Consistent with these results, CP pretreatment of MPTP-treated PD model mice also ameliorated dopaminergic neuronal cell loss. Our findings indicate that the inhibition of mitochondrial complex I with CP protects dopaminergic neurons and may provide a strategy for preventing neurotoxin-induced PD.

scholarly journals Mitochondrial Complex I Reversible S-Nitrosation Improves Bioenergetics and Is Protective in Parkinson's Disease

2018 ◽  
Vol 28 (1) ◽  
pp. 44-61 ◽  
Author(s):  
Chiara Milanese ◽  
Victor Tapias ◽  
Sylvia Gabriels ◽  
Silvia Cerri ◽  
Giovanna Levandis ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Complex I ◽  
Mitochondrial Complex I ◽  
Mitochondrial Complex

scholarly journals Bacopa monnieri Phytochemicals Mediated Synthesis of Platinum Nanoparticles and Its Neurorescue Effect on 1-Methyl 4-Phenyl 1,2,3,6 Tetrahydropyridine-Induced Experimental Parkinsonism in Zebrafish

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Jayshree Nellore ◽  
Cynthia Pauline ◽  
Kanchana Amarnath
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Platinum Nanoparticles ◽  
Complex I ◽  
Leaf Extract ◽  
Bacopa Monnieri ◽  
Mitochondrial Complex I ◽  
Mitochondrial Complex ◽  
Zebrafish Model ◽  
Experimental Parkinsonism

Current discovery demonstrates the rapid formation of platinum nanoparticles using leaf extract of a neurobeneficial plant, Bacopa monnieri (BmE). The nanoparticles (BmE-PtNPs) were stabilized and then coated with varied phytochemicals present within the leaf extract. These nanoparticles demonstrated the same activity of Complex I, as that of oxidizing NADH to NAD+ using a spectrophotometric method. This suggests that BmE-PtNPs are a potential medicinal substance for oxidative stress mediated disease with suppressed mitochondrial complex I, namely, Parkinson's disease (PD). Hence, the neuroprotective potentials of the phytochemical coated nanoparticle were explored in 1-methyl 4-phenyl 1,2,3,6 tetrahydropyridine- (MPTP-)induced experimental Parkinsonism in zebrafish model. BmE-PtNPs pretreatment significantly reversed toxic effects of MPTP by increasing the levels of dopamine, its metabolites, GSH and activities of GPx, catalase, SOD and complex I, and reducing levels of MDA along with enhanced locomotor activity. Taken together, these findings suggest that BmE-PtNPs have protective effect in MPTP-induced neurotoxicity in this model of Parkinson's disease via their dual functions as mitochondrial complex I and antioxidant activity.

scholarly journals Parkinson’s disease and mitochondrial complex I: a perspective on the Ndi1 therapy

2009 ◽  
Vol 41 (6) ◽  
pp. 493-497 ◽  
Author(s):  
Mathieu Marella ◽  
Byoung Boo Seo ◽  
Takao Yagi ◽  
Akemi Matsuno-Yagi
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Complex I ◽  
Mitochondrial Complex I ◽  
Mitochondrial Complex

Mitochondrial Complex I Deficiency in Parkinson's Disease

1990 ◽  
Vol 54 (3) ◽  
pp. 823-827 ◽  
Author(s):  
A. H. V. Schapira ◽  
J. M. Cooper ◽  
D. Dexter ◽  
J. B. Clark ◽  
P. Jenner ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Complex I ◽  
Mitochondrial Complex I ◽  
Mitochondrial Complex ◽  
Complex I Deficiency
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