Abstract
Oxidative stress results from an imbalance between the generation of reactive oxygen and nitrogen species and the antioxidant capacity of the cell.1,2 Failure of the cell to effectively eliminate reactive species can lead to the oxidative modification of lipids, nucleic acids, proteins, and other cellular constituents, modifications which have been consistently detected in human postmortem brain tissue from Parkinson’s disease (PD) patients.3-13 In addition to the increasing burden of oxidatively damaged proteins, lipids, and nucleic acids in the substantia nigra (SN) from PD patients, there is also a 40%-50% reduction in glutathione (GSH) levels.9,14-17 A pathogenic role for oxidative stress in disease progression has been suggested for other neurodegenerative diseases as well, including Alzheimer’s disease (AD),18 dementia with Lewy bodies (DLB),19 amyotrophic lateral sclerosis (ALS),20 and Huntington’s disease (HD).21. © 2013 by Taylor & Francis Group, LLC.