Oxidative damage to macromolecules in human Parkinson disease and the rotenone model.

Published

Journal Article (Review)

Parkinson disease (PD), the most common neurodegenerative movement disorder, is associated with selective degeneration of nigrostriatal dopamine neurons. Although the underlying mechanisms contributing to neurodegeneration in PD seem to be multifactorial, mitochondrial impairment and oxidative stress are widely considered to be central to many forms of the disease. Whether oxidative stress is a cause or a consequence of dopaminergic death, there is substantial evidence for oxidative stress both in human PD patients and in animal models of PD, especially using rotenone, a complex I inhibitor. There are many indices of oxidative stress, but this review covers the recent evidence for oxidative damage to nucleic acids, lipids, and proteins in both the brain and the peripheral tissues in human PD and in the rotenone model. Limitations of the existing literature and future perspectives are discussed. Understanding how each particular macromolecule is damaged by oxidative stress and the interplay of secondary damage to other biomolecules may help us design better targets for the treatment of PD.

Full Text

Duke Authors

Cited Authors

  • Sanders, LH; Timothy Greenamyre, J

Published Date

  • September 2013

Published In

Volume / Issue

  • 62 /

Start / End Page

  • 111 - 120

PubMed ID

  • 23328732

Pubmed Central ID

  • 23328732

Electronic International Standard Serial Number (EISSN)

  • 1873-4596

Digital Object Identifier (DOI)

  • 10.1016/j.freeradbiomed.2013.01.003

Language

  • eng

Conference Location

  • United States