Chromosome and oxidative damage biomarkers in lymphocytes of Parkinson's disease patients

As cancer development usually results from exposure to several environmenta l risk factors in interaction with the genetic susceptibility of the host, it could be of interest to investigate if neurodegeneration, as occurs in P arkinson's disease (PD) patients can be attributed at least partially, to e nvironmental risk factors. There is growing evidence that oxidative stress could play a significant ro le as a risk factor in the aetiology and pathogenesis of neurodegenerative diseases, emphasising the need for new individual and human-based approache s. The aim of our research is to explore the relation between chromosome insta bility and oxidative stress biomarkers in Parkinson's disease using a varie ty of strategies. We determined peripheral markers for oxidative damage in PD by testing for spontaneous and induced chromosomal damage, DNA strand br eaks, oxidised pyrimidines and altered purines both in peripheral blood and cultured lymphocytes. We also measured glutathione S-transferase activity in the plasma of patients and controls. Compared to healthy controls, PD patients show higher frequencies of micron uclei (17.2 +/- 4.8 vs. 9.0 +/- 3.4, p < 0.001) and a significant increase in the levels of single strand breaks (SSB). Significant differences were a lso obtained in the distribution of oxidised purine bases between the two g roups. Preliminary data obtained by fluorescence in situ hybridization anal ysis showed that the percentage of centromere negative micronuclei is highe r than that of centromere positive micronuclei. Glutathione S-transferase a ctivity in plasma from PD patients and controls was also measured and the e nzymatic activity in PD patients was lower than in healthy controls.