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• W2090825344 abstract "Increased oxidative stress and mitochondrial abnormalities contribute to neuronal dysfunction in Huntington's disease (HD). We investigated whether these pathological changes in HD brains may also be present in peripheral tissues. Leukocyte 8-hydroxydeoxyguanosine (8-OHdG) and plasma malondialdehyde (MDA) were elevated, and activities of erythrocyte Cu/Zn-superoxide dismutase (Cu/Zn-SOD) and glutathione peroxidase (GPx) reduced in 16 HD patients when compared to 36 age- and gender-matched controls. Deleted and total mitochondrial DNA (mtDNA) copy numbers were increased, whereas the mRNA expression levels of mtDNA-encoded mitochondrial enzymes are not elevated in HD leukocytes compared to the normal controls. Plasma MDA levels also significantly correlated with HD disease severity. These results indicate means to suppress oxidative damage or to restore mitochondrial functions may be beneficial to HD patients. Plasma MDA may be used as a potential biomarker to test treatment efficacy in the future, if confirmed in a larger, longitudinal study." @default.
• W2090825344 created "2016-06-24" @default.
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• W2090825344 date "2007-07-01" @default.
• W2090825344 modified "2023-10-16" @default.
• W2090825344 title "Increased oxidative damage and mitochondrial abnormalities in the peripheral blood of Huntington’s disease patients" @default.
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• W2090825344 doi "https://doi.org/10.1016/j.bbrc.2007.05.093" @default.
• W2090825344 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/17543886" @default.
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