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Oxidative Damage to Nucleic Acids pp 123–140Cite as

The Role of Oxidative Damage to Nucleic Acids in the Pathogenesis of Neurological Disease

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Part of the book series: Molecular Biology Intelligence Unit ((MBIU))

Abstract

Oxidative stress involving reactive oxygen species (ROS) and reactive nitrogen species (RNS) is integral to the process of aging and age-related diseases such as Alzheimer disease (AD), Parkinson’s disease, and amyotrophic lateral sclerosis (ALS). Oxidative stress-induced modification of nucleic acids impacts on the function of the cell, which can have an important role in the cause of AD. ROS induces hydroxylation of nucleic acid bases (e.g., formation of 8-hydroxy-2′ deoxyguanosine (8-OHdG) from deoxyguanosine), and RNS induces their hydroxylative deamination (e.g. cytosine to uracil conversion). 8-OHdG is commonly used as a marker of DNA damage in AD and other age-related diseases, and is approximately 10-fold higher than other oxidized bases. It is present in significant amounts in the mitochondrail and nuclear DNA of AD brains, as compared to control cases. Mitochondrial DNA is relatively more prone to damage as it is exposed to increased concentrations of ROS. In addition to transversion mutations of nucleic acid bases, oxidative stress-induced DNA damage results in delterious DNA-DNA and DNA-protein crosslinking. DNA-DNA crosslinks may also be initiated by RNS-induced deamination of nucleic acid bases. ROS can also modify amyloid-β, through the oxidation of its constituent methionines to the corresponding radical cations, which initiate free radical chain reactions leading to its aggregation. Nucleic acids are also damaged through the mediation of advanced lipid peroxidation products, such as trans-4-hydroxynonenal (HNE) and 4-oxo-2-nonenal (ONE), which result in the formation of the corresponding “propano-” and “etheno-” adducts. The substantial DNA damage in AD reflects impaired mitochondrial function in the cases of AD, which results in increased ROS/RNS and decreased ATP formation, the latter impacting on the DNA repair.

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Authors and Affiliations

  1. Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, Ohio, 44106, USA

    George Perry & Mark A. Smith

  2. Department of Chemistry, University of Missouri-Rolla, Rolla, Missouri, 65409, USA

    V. Prakash Reddy & Ayse Beyaz

  3. Department of Chemistry, Case Western Reserve University, Cleveland, Ohio, USA

    Lawrence M. Sayre

Authors
  1. V. Prakash Reddy
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  2. Ayse Beyaz
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  3. George Perry
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  4. Marcus S. Cooke
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  5. Lawrence M. Sayre
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  6. Mark A. Smith
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Editor information

Editors and Affiliations

  1. Radiation and Oxidative Stress Group Department of Cancer Studies and Molecular Medicine RKCSB, Leicester Royal Infirmary, University of Leicester, Leicester, UK

    Mark D. Evans B.Sc., Ph.D.

  2. Department of Cancer Studies and Molecular Medicine and Department of Genetics, University of Leicester, Leicester, UK

    Marcus S. Cooke B.Sc., M.Sc., Ph.D.

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© 2007 Landes Bioscience and Springer Science+Business Media

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Reddy, V.P., Beyaz, A., Perry, G., Cooke, M.S., Sayre, L.M., Smith, M.A. (2007). The Role of Oxidative Damage to Nucleic Acids in the Pathogenesis of Neurological Disease. In: Evans, M.D., Cooke, M.S. (eds) Oxidative Damage to Nucleic Acids. Molecular Biology Intelligence Unit. Springer, New York, NY. https://doi.org/10.1007/978-0-387-72974-9_10

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