A multi-biomarker analysis of the antioxidant efficacy of Parkinson's disease therapy

Abstract Substantial evidences suggest that reactive oxygen species participate in the normal aging process and in cancer and neurodegenerative age-related diseases. Parkinson's disease (PD), one of the most common oxidative stress-associated pathology in aging people, is treated with a standard pharmacological protocol consisting in a combined therapy l -dopa plus an inhibitor of dopa-decarboxylase, such as carbidopa. The therapy is well validated for the ability to restoring dopaminergic neurotransmission in PD patients, while l -dopa and carbidopa ability in modulating oxidative stress is currently under discussion. Our aim was to evaluate the impact of l -dopa and carbidopa on several biomarkers of exogenously-induced oxidative stress to validate the overall antioxidant effectiveness of the therapy. For this purpose we used peripheral blood lymphocytes from healthy donors treated in vitro with l -dopa and carbidopa and then challenged by different concentrations of H 2 O 2 . Glutathione (GSH, GSSG, GSH/GSSG), malondialdehyde (TBARs), protein carbonyls as well as DNA damage (8-oxo-7,8-dihydro-2′-deoxyguanosine (8-oxodG) and micronuclei (MN)), modulation was evaluated. Our results show that l -dopa, but not carbidopa, decreases the markers of lipid and protein oxidation and increases the total content of glutathione. Both l -dopa and carbidopa (alone or in combination) are able to counteract the formation of 8-oxodG and to reduce H 2 O 2 -induced micronuclei.