Mitochondrial NAD+-linked State 3 respiration and complex-I activity are compromised in the cerebral cortex of 3-nitropropionic acid-induced rat model of Huntington's disease. (Q45306770)

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English	Mitochondrial NAD+-linked State 3 respiration and complex-I activity are compromised in the cerebral cortex of 3-nitropropionic acid-induced rat model of Huntington's disease.	scientific article

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9 January 2020

Mitochondrial NAD+-linked State 3 respiration and complex-I activity are compromised in the cerebral cortex of 3-nitropropionic acid-induced rat model of Huntington's disease (English)

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9 January 2020

Huntington's disease

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Merina Varghese

2

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9 January 2020

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Mritunjay Pandey

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9 January 2020

Kizhakke M Sindhu

3

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9 January 2020

Sen Sreetama

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9 January 2020

A K Navneet

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Kochupurackal P Mohanakumar

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Rajamma Usha

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22 October 2007

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15

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Journal of Neurochemistry

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420-434

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2

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9 January 2020

Complex I defect in muscle from patients with Huntington's disease.

1 reference

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Chronic systemic pesticide exposure reproduces features of Parkinson's disease

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Chronic intoxication with 3-nitropropionic acid in rats induces the loss of striatal dopamine terminals without affecting nigral cell viability.

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Oxidative damage and metabolic dysfunction in Huntington's disease: selective vulnerability of the basal ganglia.

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Inhibition of the mitochondrial respiratory chain complex activities in rat cerebral cortex by methylmalonic acid.

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Direct evidence for S-nitrosation of mitochondrial complex I.

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Beta-amyloid fragment 25-35 causes mitochondrial dysfunction in primary cortical neurons

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Melatonin protects against 6-OHDA-induced neurotoxicity in rats: a role for mitochondrial complex I activity

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Energy thresholds in brain mitochondria. Potential involvement in neurodegeneration.

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Molecular Pathways of Neurodegeneration in Parkinson's Disease

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Death of cortical and striatal neurons induced by mitochondrial defect involves differential molecular mechanisms

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Increased mitochondrial respiration maintains the mitochondrial membrane potential and promotes survival of cerebellar neurons in an endogenous model of glutamate receptor activation.

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Brain enzyme and clinical alterations induced in rats and mice by nitroaliphatic toxicants.

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Mitochondrial defect in Huntington's disease caudate nucleus

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Evidence for impairment of energy metabolism in vivo in Huntington's disease using localized 1H NMR spectroscopy

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Measuring the quantity and activity of mitochondrial electron transport chain complexes in tissues of central nervous system using blue native polyacrylamide gel electrophoresis.

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Mitochondrial electron transport chain complex dysfunction in a transgenic mouse model for amyotrophic lateral sclerosis

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Excitotoxicity is required for induction of oxidative stress and apoptosis in mouse striatum by the mitochondrial toxin, 3-nitropropionic acid

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Elevated serotonin and reduced dopamine in subregionally divided Huntington's disease striatum

1 reference

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21 January 2018

Energy metabolism defects in Huntington's disease and effects of coenzyme Q10.

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21 January 2018

3-nitropropionic acid induced in vivo protein oxidation in striatal and cortical synaptosomes: insights into Huntington's disease

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Cleavage of Structural Proteins during the Assembly of the Head of Bacteriophage T4

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Preparation of synaptic and nonsynaptic mitochondria from mammalian brain

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Differential expression of oxidative phosphorylation genes in patients with Alzheimer's disease: implications for early mitochondrial dysfunction and oxidative damage.

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Coenzyme Q10 administration increases brain mitochondrial concentrations and exerts neuroprotective effects

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Inhibition of mitochondrial respiration by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in mouse brain in vivo

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Oxidative damage to mitochondrial complex I due to peroxynitrite: identification of reactive tyrosines by mass spectrometry

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Influence of cytosolic and mitochondrial Ca2+, ATP, mitochondrial membrane potential, and calpain activity on the mechanism of neuron death induced by 3-nitropropionic acid

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Acute 3-nitropropionic acid intoxication induces striatal astrocytic cell death and dysfunction of the blood-brain barrier: involvement of dopamine toxicity.

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Evidence for a defect in NADH: ubiquinone oxidoreductase (complex I) in Huntington's disease

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Increased formation of reactive oxygen species, but no changes in glutathione peroxidase activity, in striata of mice transgenic for the Huntington's disease mutation

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4-Hydroxy-2(E)-nonenal inhibits CNS mitochondrial respiration at multiple sites.

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Oxidative damage to mitochondrial DNA in Huntington's disease parietal cortex

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Acute intranigral infusion of rotenone in rats causes progressive biochemical lesions in the striatum similar to Parkinson's disease

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L-deprenyl protects against rotenone-induced, oxidative stress-mediated dopaminergic neurodegeneration in rats

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Melatonin protects against rotenone-induced oxidative stress in a hemiparkinsonian rat model.

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Quantification of oxidative phosphorylation enzymes after blue native electrophoresis and two-dimensional resolution: normal complex I protein amounts in Parkinson's disease conflict with reduced catalytic activities.

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Huntington's disease: Changes in striatal proteins reflect astrocytic gliosis

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Comparison of intrastriatal injections of quinolinic acid and 3-nitropropionic acid for use in animal models of Huntington's disease

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Carbidopa/levodopa and selegiline do not affect platelet mitochondrial function in early parkinsonism

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Neurochemical alterations in Huntington's chorea: a study of post-mortem brain tissue

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Biochemical abnormalities and excitotoxicity in Huntington's disease brain.

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Mitochondrial dysfunction and free radical damage in the Huntington R6/2 transgenic mouse.

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Assessment of mitochondrial oxidative phosphorylation in patient muscle biopsies, lymphoblasts, and transmitochondrial cell lines

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The mitochondrial toxin 3-nitropropionic acid induces differential expression patterns of apoptosis-related markers in rat striatum

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Heat shock protein 27 prevents cellular polyglutamine toxicity and suppresses the increase of reactive oxygen species caused by huntingtin

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