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Related Concept Videos

DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
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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.
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Comet Assay as an Indirect Measure of Systemic Oxidative Stress
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Published on: May 22, 2015

High DNA oxidative damage in systemic sclerosis.

Jerome Avouac1, Didier Borderie, Ovanesse Garabed Ekindjian

  • 1Service de Rhumatologie A, Hôpital Cochin, Université Paris Descartes, AP-HP, Paris, France.

The Journal of Rheumatology
|September 17, 2010
PubMed
Summary
This summary is machine-generated.

This study found higher levels of DNA damage biomarker 8-hydroxy-2'-deoxyguanosine (8-oxodG) in patients with systemic sclerosis (SSc), indicating significant oxidative stress. Elevated 8-oxodG levels were linked to fibrotic complications in SSc patients.

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Area of Science:

  • Biochemistry
  • Immunology
  • Pathophysiology

Background:

  • Reactive oxygen species (ROS) play a key role in systemic sclerosis (SSc) pathogenesis.
  • While protein and lipid damage are documented, oxidative DNA damage in SSc is less understood.
  • 8-hydroxy-2 -deoxyguanosine (8-oxodG) is a validated biomarker for endogenous oxidative DNA damage.

Purpose of the Study:

  • To evaluate urinary 8-oxodG levels in SSc patients.
  • To compare 8-oxodG levels with F2-isoprostane, a marker of lipid peroxidation.
  • To assess the association of 8-oxodG with SSc clinical manifestations and fibrotic phenotypes.

Main Methods:

  • Urinary 8-oxodG and 8-isoprostaglandin-F(2α) (8-iso-PGF(2α)) were measured using competitive ELISA.
  • The study included 80 SSc patients and 39 age- and sex-matched controls.
  • Multivariate analysis was employed to identify associations with clinical parameters.

Main Results:

  • SSc patients exhibited significantly higher urinary 8-oxodG and 8-iso-PGF(2α) levels compared to controls.
  • Elevated 8-oxodG levels correlated with pulmonary fibrosis, reduced forced vital capacity, and decreased DLCO/alveolar volume.
  • In diffuse cutaneous SSc, a modified Rodnan skin score > 14 was independently associated with higher 8-oxodG.

Conclusions:

  • The study confirms substantial oxidative stress in SSc.
  • Increased 8-oxodG levels in SSc patients are associated with a fibrotic phenotype.
  • Further research is needed to determine the predictive value of 8-oxodG in SSc and its role in fibrotic processes.