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Abstract Parkinson’s disease is characterized by dopamine cell loss of the substantia nigra. Parkinson’s disease and the neurotoxin 1-methyl-4-phenyl-1,2,5,6 tetrahydropyridine may destroy dopamine neurons through oxidative stress. Coenzyme Q is a cofactor of mitochondrial uncoupling proteins that enhances state-4 respiration and eliminate superoxides. Here we report that short-term oral administration of coenzyme Q induces nigral mitochondrial uncoupling and prevents dopamine cell loss after 1-methyl-4-phenyl-1,2,5,6 tetrahydropyridine administration in monkeys.
Male, Ubiquinone, Uncoupling Agents, Dopamine, Cell Respiration, Gene Expression, Membrane Transport Proteins, Proteins, Cell Count, Ion Channels, Mitochondria, Mitochondrial Proteins, Substantia Nigra, Disease Models, Animal, Parkinsonian Disorders, Chlorocebus aethiops, Animals, Uncoupling Protein 2, RNA, Messenger
Male, Ubiquinone, Uncoupling Agents, Dopamine, Cell Respiration, Gene Expression, Membrane Transport Proteins, Proteins, Cell Count, Ion Channels, Mitochondria, Mitochondrial Proteins, Substantia Nigra, Disease Models, Animal, Parkinsonian Disorders, Chlorocebus aethiops, Animals, Uncoupling Protein 2, RNA, Messenger
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