Related Experiment Video

Updated: Aug 18, 2026

Laser Micro-Irradiation to Study DNA Recruitment During S Phase
07:11

Laser Micro-Irradiation to Study DNA Recruitment During S Phase

Published on: April 16, 2021

p21(Cip1/WAF1/Sdi1) does not affect expression of base excision DNA repair enzymes during chronic oxidative stress

Michael A O'reilly1, Peter F Vitiello, Sean C Gehen

  • 1Department of Pediatrics, School of Medicine and Dentistry, University of Rochester, Rochester, NY 14642, USA. michael_oreilly@urmc.rochester.edu

Antioxidants & Redox Signaling
|May 14, 2005
PubMed

Insights

Chronic oxidative stress from hyperoxia increases p21, a cell cycle inhibitor. This study found p21 does not alter base excision repair (BER) enzyme expression, suggesting other protective mechanisms against DNA damage.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Biochemistry

Background:

  • Chronic oxidative stress from hyperoxia induces DNA damage and cell cycle arrest via p21.
  • p21-induced G(1) arrest correlates with reduced DNA damage and improved cell survival.
  • This suggests p21 may influence base excision repair (BER) pathways for oxidized DNA repair.

Purpose of the Study:

  • To investigate the relationship between p21 expression and BER enzyme levels under hyperoxia.
  • To determine if p21 deficiency impacts the expression of key BER enzymes.
  • To elucidate the protective mechanisms of p21 against hyperoxia-induced cellular damage.

Main Methods:

  • Utilized p21 wild-type and p21-deficient mice.
  • Employed human lung adenocarcinoma H1299 cells with inducible p21 expression.
  • Measured mRNA and protein levels of BER enzymes (Ogg1, Tdg, Udg, Mpg, Nth1, Mgmt, APE) after hyperoxia exposure.

Main Results:

  • Hyperoxia exposure increased p21 levels in cells.
  • mRNA levels of BER enzymes remained constant during 3 days of hyperoxia.
  • Protein levels of Ogg1, Nth1, and APE were unchanged.
  • p21 deficiency did not significantly alter the expression of these BER repair enzymes.

Conclusions:

  • Hyperoxia induces p21 expression without significantly altering BER enzyme expression.
  • p21 may protect cells from oxidative stress by modulating BER enzyme activity rather than expression.
  • Alternative mechanisms, such as apoptosis, may also contribute to p21-mediated cell protection.

More Related Videos

Laser Microirradiation to Study In Vivo Cellular Responses to Simple and Complex DNA Damage10:44

Laser Microirradiation to Study In Vivo Cellular Responses to Simple and Complex DNA Damage

Published on: January 31, 2018

Visualizing and Quantifying Endonuclease-Based Site-Specific DNA Damage10:59

Visualizing and Quantifying Endonuclease-Based Site-Specific DNA Damage

Published on: August 21, 2021

Related Concept Videos

Long-patch Base Excision Repair01:02

Long-patch Base Excision Repair

Since the discovery of the two BER pathways, there has been a debate about how a cell chooses one pathway over the other and the factors determining this selection. Numerous in vitro experiments have pointed out multiple determinants for the sub-pathway selection. These are:
Nucleotide Excision Repair01:38

Nucleotide Excision Repair

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...
Nucleotide Excision Repair01:08

Nucleotide Excision Repair

Overview
Base Excision Repair01:54

Base Excision Repair

One of the common DNA damages is the chemical alteration of single bases by alkylation, oxidation, or deamination. The altered bases cause mispairing and strand breakage during replication. This type of damage causes minimal change to the DNA double helix structure and can be repaired by the base excision repair (BER) pathways. BER corrects damaged DNA sequences by removing the damaged base and restoring the original base sequence using the complementary strand as a template.
The first step of...
Base Excision Repair01:54

Base Excision Repair

One of the common DNA damages is the chemical alteration of single bases by alkylation, oxidation, or deamination. The altered bases cause mispairing and strand breakage during replication. This type of damage causes minimal change to the DNA double helix structure and can be repaired by the base excision repair (BER) pathways. BER corrects damaged DNA sequences by removing the damaged base and restoring the original base sequence using the complementary strand as a template.
The first step of...
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...