**2.1.3 Results**

In the patients with PD (Table 1), the levels of 8-oxo2dG in peripheral blood lymphocytes were significantly increased (p<0.05), as compared to the controls.


Table 1. Levels of DNA oxidative damage (8-oxo2dG/dG x 10-5) in the PD patients and in control group. Results are expressed as a means ± SD. The nonparametric of Mann-Whitney test for unlinked variables was used. Differences significant at \*p<0.05, as compared to the controls.

In the PD patients (Table 2) disease progress from stage I to IV (according to the scale of Hoehn and Yahr) resulted in higher level of 8-oxo2dG in DNA (p<0.05) also observed between stages I and III, and a tendency to further decrease in stage IV.


Table 2. Levels of oxidative DNA damage (8-oxo2dG/dG x 10-5), as related to the stage of the PD according to the scale of Hoehn and Yahr. Results are expressed as means ± SD. The nonparametric of Mann-Whitney test for unlinked variables was used. Differences significant at \*p<0.05, between stages I and IV of PD.

Pharmacotherapy with L-dopa (Table 3) affected the level of 8-oxo2dG (p<0.01), as compared to the healthy controls.


Table 3. Levels of oxidative DNA damage (8-oxo2dG/dG x 10-5), as related to pharmacotherapy with L-dopa (+) in the patients with PD. Results are expressed as means ± SD. The nonparametric of Mann-Whitney test for unlinked variables was used. Differences significant at \*\*p<0.01, as compared to the controls.

Our results indicated that, L-dopa can modify the level of oxidative DNA damage (8 oxo2dG) in the peripheral blood cells of PD patients. On the other hand, it is interesting that in PD a significant increase in DNA damage has been observed in the IVth stage of the disease development (according to Hoehn and Yahr), even so 8-oxo2dG levels are increased between the stages I and III of the disease evolution. It seems that in PD the reason for increasing levels of oxidative process altered nucleic acids is thought to involve overproduction of free radicals as well as decreased levels of enzymatic and non-enzymatic antioxidants and less effective repair mechanisms. In AD patients have been found to contain lowered activity of specific 8-oxoguanine glycosylase 1, OGG1, and more oxidative DNA damage which might induce of apoptosis (Dorszewska et al., 2005, 2009a, 2010).

It seems that analysis of the level of oxidative stress (8-oxo2dG) may be represented targets for diagnosis of PD and therapy in future.

#### **2.2 Influence of L-dopa treatment on the level of apoptotic factors in peripheral blood lymphocytes of Parkinson's disease patients**

At the neuropathological studies, PD is mainly characterized by neuronal intracellular inclusions named Lewy's bodies with α-synuclein. These inclusions are now known to be comprised of filamentous polymers of α-synuclein, which may generate oxidative stress in the brain of PD patients. It could results from several mechanisms, such as depletion of antioxidants, defects in mitochondrial electron transport, neurotoxin exposure, and excessive oxidation of dopamine in the patients given L-dopa. Conway et al. (2001) showed that dopamine or L-dopa inhibits the fibrillization of α-synuclein filaments by stabilization of their structure.

However Alves Da Costa et al. (2002) showed that α-synuclein drastically lowered caspase-3 activity and p53 protein expression, and transcriptional activity, proteins controlled the apoptotic cascade. Blandini et al. (2004), Dorszewska et al. (2009b) and Iwashita (2004) showed that, apoptotic proteins such as: Bcl-2 family proteins and PARP are involved in the pathogenesis of PD as well.

The aim of the study was to estimate the levels of p53, and PARP proteins, and 85 kDa fragment, and two Bcl-2 family proteins: Bcl-2 and Bax in peripheral lymphocytes of patients with PD and in control group. The attention was also paid to L-dopa pharmacotherapy in PD.
