Quercetin up-regulates mitochondrial complex-I activity to protect against programmed cell death in rotenone model of Parkinson’s disease in rats

Neuroscience ◽  
2013 ◽  
Vol 236 ◽  
pp. 136-148 ◽  
Author(s):  
S.S. Karuppagounder ◽  
S.K. Madathil ◽  
M. Pandey ◽  
R. Haobam ◽  
U. Rajamma ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Complex I ◽  
Mitochondrial Complex I ◽  
Mitochondrial Complex ◽  
Complex I Activity

scholarly journals Mitochondrial Complex I Activity is Conditioned by Supercomplex I–III2–IV Assembly in Brain Cells: Relevance for Parkinson’s Disease

2017 ◽  
Vol 42 (6) ◽  
pp. 1676-1682 ◽  
Author(s):  
Irene Lopez-Fabuel ◽  
Monica Resch-Beusher ◽  
Monica Carabias-Carrasco ◽  
Angeles Almeida ◽  
Juan P. Bolaños
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Complex I ◽  
Brain Cells ◽  
Mitochondrial Complex I ◽  
Mitochondrial Complex ◽  
Complex I Activity

scholarly journals Loss of mitochondrial complex I activity potentiates dopamine neuron death induced by microtubule dysfunction in a Parkinson’s disease model

2011 ◽  
Vol 192 (5) ◽  
pp. 873-882 ◽  
Author(s):  
Won-Seok Choi ◽  
Richard D. Palmiter ◽  
Zhengui Xia
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Complex I ◽  
Dopamine Neuron ◽  
Dopamine Neurons ◽  
Substantia Nigra Pars Compacta ◽  
Mitochondrial Complex I ◽  
Mitochondrial Complex ◽  
Neuron Death ◽  
Complex I Activity

Mitochondrial complex I dysfunction is regarded as underlying dopamine neuron death in Parkinson’s disease models. However, inactivation of the Ndufs4 gene, which compromises complex I activity, does not affect the survival of dopamine neurons in culture or in the substantia nigra pars compacta of 5-wk-old mice. Treatment with piericidin A, a complex I inhibitor, does not induce selective dopamine neuron death in either Ndufs4+/+ or Ndufs4−/− mesencephalic cultures. In contrast, rotenone, another complex I inhibitor, causes selective toxicity to dopamine neurons, and Ndufs4 inactivation potentiates this toxicity. We identify microtubule depolymerization and the accumulation of cytosolic dopamine and reactive oxygen species as alternative mechanisms underlying rotenone-induced dopamine neuron death. Enhanced rotenone toxicity to dopamine neurons from Ndufs4 knockout mice may involve enhanced dopamine synthesis caused by the accumulation of nicotinamide adenine dinucleotide reduced. Our results suggest that the combination of disrupting microtubule dynamics and inhibiting complex I, either by mutations or exposure to toxicants, may be a risk factor for Parkinson’s disease.

scholarly journals A novel neuroprotective therapy for Parkinson’s disease using a viral noncoding RNA that protects mitochondrial Complex I activity

2011 ◽  
Vol 209 (1) ◽  
pp. 1-10 ◽  
Author(s):  
Wei-Li Kuan ◽  
Emma Poole ◽  
Michael Fletcher ◽  
Sharon Karniely ◽  
Pam Tyers ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Complex I ◽  
Neurodegenerative Disorder ◽  
Dopamine Neurons ◽  
Mitochondrial Complex I ◽  
Mitochondrial Complex ◽  
Neuroprotective Therapy ◽  
Nigrostriatal Dopamine Neurons ◽  
Complex I Activity

Parkinson’s disease (PD) is a neurodegenerative disorder that results in the loss of nigrostriatal dopamine neurons. The etiology of this cell loss is unknown, but it involves abnormalities in mitochondrial function. In this study, we have demonstrated that the administration of a novel noncoding p137 RNA, derived from the human cytomegaloviral β2.7 transcript, can prevent and rescue dopaminergic cell death in vitro and in animal models of PD by protecting mitochondrial Complex I activity. Furthermore, as this p137 RNA is fused to a rabies virus glycoprotein peptide that facilitates delivery of RNA across the blood–brain barrier, such protection can be achieved through a peripheral intravenous administration of this agent after the initiation of a dopaminergic lesion. This approach has major implications for the potential treatment of PD, especially given that this novel agent could have the same protective effect on all diseased neurons affected as part of this disease process, not just the dopaminergic nigrostriatal pathway.

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.

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