Oxidative damage in nucleic acids and Parkinson's disease.

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Oxidative damage in nucleic acids and Parkinson's disease.

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Article
Kyushu Univ. Production Kyushu Univ. Production
Responsibility:
Nakabeppu, Yusaku(Division of Neurofunctional Genomics, Department of Immunobiology and Neuroscience, Medical Institute of Bioregulation, Kyushu University)
中別府, 雄作(九州大学生体防御医学研究所個体機能制御部門脳機能制御学分野)
Tsuchimoto, Daisuke(Division of Neurofunctional Genomics, Department of Immunobiology and Neuroscience, Medical Institute of Bioregulation, Kyushu University)

土本, 大介(九州大学生体防御医学研究所個体機能制御部門脳機能制御学分野)
Yamaguchi, Hiroo(Division of Neurofunctional Genomics, Department of Immunobiology and Neuroscience, Medical Institute of Bioregulation, Kyushu University)
山口, 浩雄(九州大学生体防御医学研究所個体機能制御部門脳機能制御学分野)
Sakumi, Kunihiko(Division of Neurofunctional Genomics, Department of Immunobiology and Neuroscience, Medical Institute of Bioregulation, Kyushu University)
作見, 邦彦(九州大学生体防御医学研究所個体機能制御部門脳機能制御学分野)

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Language:
English
Publication info:
Journal of Neuroscience Research. 85, (5), pp. 919-934, 2007-04. Wiley InterScience
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Abstract:
Oxidative DNA lesions, such as 8-oxoguanine (8-oxoG), accumulate in nuclear and mitochondrial genomes during aging, and such accumulation can increase dramatically in patients with Parkinson's disease (PD). To counteract oxidative damage to nucleic acids, human and rodents are equipped with three distinct enzymes. One of these, MTH1, hydrolyzes oxidized purine nucleoside triphosphates, such as 8-oxo-2-deoxyguanosine triphosphate and 2-hydroxy-2-deoxyadenosine triphosphate, to their monophosphate forms. The other two enzymes are 8-oxoG DNA glycosylase encoded by the OGG1 gene and adenine/2-hydroxyadenine DNA glycosylase encoded by the MUTYH gene. We have shown a significant increase in 8-oxoG in mitochondrial DNA as well as an elevated expression of MTH1, OGG1, and MUTYH in nigrostriatal dopaminergic neurons of PD patients, suggesting that the buildup of these lesions may cause dopamine neuron loss. We established MTH1-null mice and found that MTH1-null fibroblasts were highly susceptible to cell death caused by H_2O_2 characterized by pyknosis and electron-dense deposits in the mitochondria, and that this was accompanied by an ongoing accumulation of 8-oxoG in nuclear and mitochondrial DNA. We also showed that MTH1-null mice exhibited an increased accumulation of 8-oxoG in striatal mitochondrial DNA, followed by more extreme neuronal dysfunction after 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine administration than that of wild-type mice. In conclusion, oxidative damage in nucleic acids is likely to be a major risk factor for Parkinson's disease, indicating that a solid understanding of the defense mechanisms involved will enable us to develop new strategies for protecting the brain against oxidative stress. Read more
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