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Related Concept Videos

Nucleotide Excision Repair01:38

Nucleotide Excision Repair

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DNA Distortion and Damage
Cells are regularly exposed to mutagens—factors in the environment that can damage DNA and generate mutations. UV radiation is one of the most common mutagens and is estimated to introduce a significant number of changes in DNA. These include bends or kinks in the structure, which can block DNA replication or transcription. If these errors are not fixed, the damage can cause mutations, which in turn can result in cancer or disease depending on which sequences are...
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Overview of DNA Repair02:25

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In order to be passed through generations, genomic DNA must be undamaged and error-free. However, every day, DNA in a cell undergoes several thousand to a million damaging events by natural causes and external factors. Ionizing radiation such as UV rays, free radicals produced during cellular respiration, and hydrolytic damage from metabolic reactions can alter the structure of DNA. Damages caused include single-base alteration, base dimerization, chain breaks, and cross-linkage.
Chemically...
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Spontaneous and Induced Mutations01:30

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Spontaneous mutations arise infrequently during DNA replication due to errors in the process. A key factor behind these errors is tautomeric shifts in nitrogenous bases, where bases transition from keto to enol forms or amino to imino forms. This shift can alter base-pairing rules, leading to mutations. Additionally, reactive oxygen species (ROS) arising from aerobic metabolism can damage DNA, resulting in depurination (loss of a purine base) or depyrimidination (loss of a pyrimidine base).
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Disorders of the Nervous Tissue01:28

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Nervous tissue is a vital component of the human body's communication system, enabling us to perceive and respond to stimuli. However, like all other tissues, it is vulnerable to disorders and diseases that can significantly impact our neurological functioning.
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Aging01:26

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Aging is a complex biological phenomenon influenced by various processes that affect cellular and systemic functions. Several prominent theories attempt to explain its mechanisms, highlighting cellular limitations, oxidative damage, and hormonal changes as central factors in aging.
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Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...
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Related Experiment Video

Updated: Aug 26, 2025

Quantification of three DNA Lesions by Mass Spectrometry and Assessment of Their Levels in Tissues of Mice Exposed to Ambient Fine Particulate Matter
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Oxidative DNA Damage: A Role in Altering Neuronal Function.

Adib Behrouzi1, Mark R Kelley1,2,3,4, Jill C Fehrenbacher1,2,5

  • 1Department of Pharmacology and Toxicology, Indiana University School of Medicine, Indianapolis, IN 46202, USA.

Journal of Cellular Signaling
|October 7, 2022
PubMed
Summary
This summary is machine-generated.

Oxidative DNA damage contributes to neurological diseases. Inhibiting DNA repair enzymes worsens neurotoxicity, while enhancing repair may mitigate neurodegeneration.

Keywords:
8-oxoguanine DNA glycosylase-1AgingAlzheimer’s diseaseAmyotrophic lateral sclerosisApurinic/apyrimidinic endonuclease/redox effector factor 1Base excision repairChemotherapy-induced peripheral neuropathyInflammatory bowel diseaseOxidative DNA damageOxidative stress

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Oxidative stress is implicated in many neurological disorders.
  • The specific role of oxidative DNA damage in neuronal dysfunction is less understood.
  • Previous research showed inhibiting DNA repair enzymes exacerbates cisplatin neurotoxicity.

Purpose of the Study:

  • To explore the role of oxidative DNA damage in various neuropathologies.
  • To highlight the potential of enhancing DNA repair as a therapeutic strategy for neurodegeneration.

Main Methods:

  • Review of existing literature on oxidative DNA damage and neuropathologies.
  • Analysis of clinical data correlating DNA damage with disease progression.
  • Examination of findings from animal models investigating DNA repair mechanisms.

Main Results:

  • Clinical evidence shows increased oxidative DNA damage in neuropathology biopsies.
  • Animal models demonstrate that impaired DNA repair worsens disease, while enhanced repair improves outcomes.
  • Inhibition of OGG1 glycosylase and APE1 endonuclease activities exacerbates cisplatin neurotoxicity.

Conclusions:

  • Oxidative DNA damage is a significant factor in the progression of central and peripheral nervous system diseases.
  • Targeting oxidative DNA repair pathways presents a promising therapeutic avenue for neurodegenerative conditions.