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Oxidative damage and cytogenetic analysis in leukocytes of Parkinson’s disease patients

From the Department of Human and Environmental Sciences (Dr. Scarpato and L. Migliore, F. Trippi, and R. Barale), Department of Neuroscience–Section of Neurology (Drs. Lucetti, Gambaccini, Bernardini, and Bonuccelli, and L. Petrozzi), Department of Human Morphology and Applied Biology (Dr. Frenzilli), University of Pisa, Italy; and Department of Pharmacology and Pharmaceutical Technology (Dr. Rodilla), Universidad Cardenal Herrera CEU, Moncada (Valencia), Spain.

Address correspondence and reprint requests to Dr. Ubaldo Bonuccelli, Department of Neuroscience–Section of Neurology, Movement Disorders Unit, University of Pisa, Via Roma 67, 56126 Pisa, Italy; e-mail: u.bonuccelli{at}med.unipi.it

Background: Postmortem studies suggest excessive free radical toxicity in the substantia nigra of patients with PD. Increased lipid peroxidation and oxidative DNA damage have been reported in the CNS. Markers of oxidative stress have been identified in the blood of patients with PD.

Objective: To assess the presence of spontaneous chromosome and primary or oxidative DNA damage in peripheral blood leukocytes of patients with untreated PD.

Methods: Patients with de novo PD (20) and control subjects (16), matched for age, sex, and smoking habits, underwent cytogenetic analysis using the human lymphocyte micronucleus assay coupled with the fluorescence in situ hybridization technique and the Comet assay.

Results: Compared with controls, patients with PD showed an increase in the incidence of spontaneous micronuclei (p < 0.001); single strand breaks (p < 0.001); and oxidized purine bases (p < 0.05). Fluorescence in situ hybridization analysis showed micronuclei harboring acentric fragments.

Conclusions: There is chromosomal, primary DNA damage and oxidative DNA damage demonstrable in lymphocytes of patients with untreated PD.

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