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

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 8hydroxy-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.

Oxidative Stress in Neurodegenerative Diseases

“…This finding suggests that patients in the off-medication state handled acute stress better than those in the on-medication state, indicating that medication may impede the ability to tolerate acute OS [ 165 ]. Similar conclusions were obtained in a very recent study by Nikolova et al [ 166 ], who observed a greater rise in PC and 8-OHdG levels in the blood of PD patients who were treated with l -DOPA in comparison to untreated PD patients, demonstrating that administration of l -DOPA may cause greater OS than PD itself [ 166 ].…”