Oxidative Stress and Its Mitigation in Neurodegenerative Disorders

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: 30 July 2025 | Viewed by 740

Special Issue Editor


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Guest Editor
Department of Chemistry, and Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY 40506, USA
Interests: aging; age-related disorders; oxidative stress; neurodegenerative disorders; Alzheimer's disease; brain

Special Issue Information

Dear Colleagues,

Oxidative stress, commonly defined as excessive production of free radicals, decreases the scavenging of free radicals by antioxidant enzymes and/or small-molecule antioxidants, and it is now widely accepted as a critical aspect of neuronal loss, with consequent abnormal pathology and symptomology, in neurodegenerative disorders. Among the latter disorders are Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, amyotrophic lateral sclerosis and Down syndrome.

In biological cells, the predominant indices of protein oxidation include excessive levels of protein-resident carbonyls or 3-nitrotyrosine, while the major indices of lipid peroxidation include protein-bound 4-hydroxynonenal (HNE), isoprostanes (mostly derived from peroxidation of arachidonic acid) and neuroprostanes (derived from the peroxidation of neuronal-resident docosahexaenoic acid). The major indices of the oxidation of DNA or RNA are 8-hydroxy-2-deoxyguanosine and 8-hydroxyguanosine, respectively.

The mechanisms of elevated oxidative stress are numerous and diverse, and they include mitochondrial dysfunction; metabolic dysfunction, including glucose dysfunction and insulin resistance and other metabolic processes; the activation of the mTORC1 pathway; the peroxidation of membrane bilayer-resident lipids; and roles involving the oligomeric forms of peptides, proteins and oligosaccharides.

Potential mitigation of oxidative stress can be achieved by certain endogenous antioxidant enzymes or small-molecule antioxidants, as well as by the application of exogenous small-molecule antioxidants, i.e., naturally occurring or synthetic molecules.

Papers discussing various aspects of oxidative stress and its mitigation in neurodegenerative disorders will be considered for inclusion in this Special Issue of Antioxidants.

Prof. D. Allan Butterfield
Guest Editor

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Keywords

  • oxidative stress
  • neurodegenerative disorders
  • brain
  • Alzheimer’s disease
  • Parkinson’s disease
  • Huntington’s disease

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Published Papers (1 paper)

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Review

24 pages, 3218 KiB  
Review
Biological Models of Oxidative Purine DNA Damage in Neurodegenerative Disorders
by Chryssostomos Chatgilialoglu
Antioxidants 2025, 14(5), 578; https://doi.org/10.3390/antiox14050578 - 11 May 2025
Viewed by 330
Abstract
Most DNA damage caused by oxidative metabolism consists of single lesions that can accumulate in tissues. This review focuses on two classes of lesions: the two 8-oxopurine (8-oxo-Pu) lesions that are repaired by the base excision repair (BER) enzyme and the four 5′,8-cyclopurine [...] Read more.
Most DNA damage caused by oxidative metabolism consists of single lesions that can accumulate in tissues. This review focuses on two classes of lesions: the two 8-oxopurine (8-oxo-Pu) lesions that are repaired by the base excision repair (BER) enzyme and the four 5′,8-cyclopurine (cPu) lesions that are repaired exclusively by the nucleotide excision repair (NER) enzyme. The aim is to correlate the simultaneous quantification of these two classes of lesions in the context of neurological disorders. The first half is a summary of reactive oxygen species (ROS) with particular attention to the pathways of hydroxyl radical (HO) formation, followed by a summary of protocols for the quantification of six lesions and the biomimetic chemistry of the HO radical with double-stranded oligonucleotides (ds-ODN) and calf thymus DNA (ct-DNA). The second half addresses two neurodegenerative diseases: xeroderma pigmentosum (XP) and Cockayne syndrome (CS). The quantitative data on the six lesions obtained from genomic and/or mitochondrial DNA extracts across several XP and CS cell lines are discussed. Oxidative stress contributes to oxidative DNA damage by resulting in the accumulation of cPu and 8-oxo-Pu in DNA. The formation of cPu is the postulated culprit inducing neurological symptoms associated with XP and CS. Full article
(This article belongs to the Special Issue Oxidative Stress and Its Mitigation in Neurodegenerative Disorders)
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