Inhibition of mitochondrial NADH-ubiquinone oxidoreductase activity by 1-methyl-4-phenylpyridinium ion

Mizuno, Yoshikuni; Saitoh, Tomohiko; Sone, Nobuhito

doi:10.1016/0006-291x(87)90664-4

Cited by 97 publications

(28 citation statements)

References 18 publications

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“…Two groups reported inhibition of complex I by MPP C (Nicklas et al 1985;Ramsay et al 1986). We independently made the same observation ( Mizuno et al 1987a). Furthermore, we found inhibition of the a-ketoglutarate dehydrogenase complex of the mitochondrial tricarboxylic acid cycle by MPP C (Mizuno et al 1987b).…”

Section: Neurotoxin-based Models Of Pdsupporting

confidence: 60%

Progress in the pathogenesis and genetics of Parkinson's disease

Mizuno

Hattori

Kubo

et al. 2008

Phil. Trans. R. Soc. B

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Recent progresses in the pathogenesis of sporadic Parkinson's disease (PD) and genetics of familial PD are reviewed. There are common molecular events between sporadic and familial PD, particularly between sporadic PD and PARK1-linked PD due to a-synuclein (SNCA) mutations. In sporadic form, interaction of genetic predisposition and environmental factors is probably a primary event inducing mitochondrial dysfunction and oxidative damage resulting in oligomer and aggregate formations of a-synuclein. In PARK1-linked PD, mutant a-synuclein proteins initiate the disease process as they have increased tendency for self-aggregation. As highly phosphorylated aggregated proteins are deposited in nigral neurons in PD, dysfunctions of proteolytic systems, i.e. the ubiquitin-proteasome system and autophagy-lysosomal pathway, seem to be contributing to the final neurodegenerative process. Studies on the molecular mechanisms of nigral neuronal death in familial forms of PD will contribute further on the understanding of the pathogenesis of sporadic PD.

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Section: Neurotoxin-based Models Of Pdsupporting

confidence: 60%

Progress in the pathogenesis and genetics of Parkinson's disease

Mizuno

Hattori

Kubo

et al. 2008

Phil. Trans. R. Soc. B

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“…Within the SNpc neurons, MPP þ enters mitochondria and inhibits complex I of the mitochondrial respiratory chain, ultimately leading to cell apoptosis. 3,7 Tyrosine hydroxylase (TH), which is the rate-limiting enzyme in dopamine biosynthesis, is widely used as a marker of dopaminergic cells. 8 The apoptosis induced by oxidative stress is associated with the bcl-2 family members, 9 the release of cytochrome c from mitochondria, and the activation of caspases.…”

Section: Introductionmentioning

confidence: 99%

Preventive role of PD‐1 on MPTP‐induced dopamine depletion in mice

Jung

Son

Jin

et al. 2010

Cell Biochemistry & Function

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Many current studies of Parkinson's disease (PD) suggest that inflammation is involved in the neurodegenerative process. PD-1, a traditional Korean medicine, used to treat various brain diseases in Korea. This study was designed to investigate the effect of PD-1 extract in the Parkinson's model of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) lesioned mice. The MPTP administration caused the dopamine neuron loss in the striatum and substantia nigra pars compacta (SNpc), which was demonstrated by a depletion of tyrosine hydroxylase (TH). In addition, a reduction of bcl-2 expression with elevation of bax expression, caspase-3 activation, and release of cytochrome c into cytosol in dopaminergic neurons of SNpc were noted. Oral administration of PD-1 extract (50 and 100 mg kg(-1)) attenuated the MPTP-induced depletion of TH proteins in the striatum and SNpc and prevented the apoptotic effects. These results indicate that PD-1 extract is able to protect dopaminergic neurons from MPTP-induced neuronal death, with important implications for the treatment of PD.

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“…1 More recently, a PD-like phenotype has been induced in rodents using rotenone, another potent inhibitor of complex I. 2 Partially defective complex I activity has also been documented in tissues 3 and cybrids derived from PD patients.…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial DNA haplogroup K is associated with a lower risk of Parkinson's disease in Italians

et al. 2005

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It has been proposed that European mitochondrial DNA (mtDNA) haplogroups J and K, and their shared 10398G single-nucleotide polymorphism (SNP) in the ND3 gene, are protective from Parkinson's disease (PD). We evaluated the distribution of the different mtDNA haplogroups in a large cohort of 620 Italian patients with adult-onset (450, o65 years of age) idiopathic PD vs two groups of ethnic-matched controls. Neither the frequencies of haplogroup J nor that of 10398G were significantly different. However, the frequency of haplogroup K was significantly lower in PD. Stratification by sex and age indicated that the difference in the distribution of haplogroup K was more prominent in 450year old males. In spite of the common 10398G SNP, haplogroups J and K belong to widely diverging mitochondrial clades, a consideration that may explain the different results obtained for the two haplogroups in our cohorts. Our study suggests that haplogroup K might confer a lower risk for PD in Italians, corroborating the idea that the mitochondrial oxidative phosphorylation pathway is involved in the susceptibility to idiopathic PD.

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Inhibition of mitochondrial NADH-ubiquinone oxidoreductase activity by 1-methyl-4-phenylpyridinium ion

Cited by 97 publications

References 18 publications

Progress in the pathogenesis and genetics of Parkinson's disease

Progress in the pathogenesis and genetics of Parkinson's disease

Preventive role of PD‐1 on MPTP‐induced dopamine depletion in mice

Mitochondrial DNA haplogroup K is associated with a lower risk of Parkinson's disease in Italians

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