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Isobe, C., Abe, T. and Terayama, Y. (2010) Levels of Reduced and Oxidized CoenzymeQ-10 and 8-hydroxy-2-deoxyguanosine in the Cerebrospinal Fluid of Patients with Living Parkinson’s Disease Demonstrate That Mitochondrial Oxidative Damage and/or Oxidative DNA Damage Contributes to the Neurodegenerative Process. Neuroscience Letters, 469, 159-163.
http://dx.doi.org/10.1016/j.neulet.2009.11.065

has been cited by the following article:

• TITLE: Influence of Therapy on Some Important Final Products of Oxidation of Lipids, Proteins and Nucleic Acids in Patients with Parkinson’s Diseases

  AUTHORS: Galina D. Nikolova, Boncho G. Grigorov, Antoaneta M. Zheleva, Veselina G. Gadjeva

  KEYWORDS: Free Radicals, Malondialdehyde, 8-Hydroxy-2’-Deoxyguanosine, Protein Carbonyl Content

  JOURNAL NAME: Advances in Biological Chemistry, Vol.4 No.4, June 26, 2014

  ABSTRACT: The major clinical disturbances in Parkinson’s disease (PD) are consequence of dopamine depletion in the neostriatum, due to degeneration of dopaminergic neurons. The aim of the present study was to determine whether oxidative stress (OS) occurs during the clinical course of Parkinson’s disease and to evaluate the influence of therapy on the levels of some important final products of oxidation of lipids, proteins and nucleic acids in PD patients with drug therapy. For this purpose, we investigated the levels of malondialdehid (MDA), protein carbonyl content (PCC) and 8-hydroxy-2’-deoxyguanosine quantity (8-OHdG) in PD patients with and without drug therapy. The observed changes in MDA levels, PCC and 8-OHdG quantity in blood of untreated PD patients, suggested impaired antioxidant status and presence of oxidative stress in Parkinson disease. After treatment with Madopar, the elevation in by-products significantly progresses. Our results demonstrate that administration of Madopar causes in greater degree oxidative stress than that induced by Parkinson disease, by itself.