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Nucleotide Excision Repair

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 Repair

Nucleotide Excision Repair

Nucleotide Excision Repair

Nucleotide Excision Repair

Overview of DNA Repair

Overview of DNA Repair

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...

Overview of DNA Repair

Overview of DNA Repair

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...

Mutations

Mutations

Mutations are changes in the sequence of DNA. These changes can occur spontaneously or they can be induced by exposure to environmental factors. Mutations can be characterized in a number of different ways: whether and how they alter the amino acid sequence of the protein, whether they occur over a small or large area of DNA, and whether they occur in somatic cells or germline cells.
Chromosomal Alterations Are Large-Scale Mutations
While point mutations are changes in a single nucleotide in...

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Related Experiment Video

Updated: Jul 4, 2026

Immunofluorescence Imaging of DNA Damage and Repair Foci in Human Colon Cancer Cells

Immunofluorescence Imaging of DNA Damage and Repair Foci in Human Colon Cancer Cells

Published on: June 9, 2020

A radiation damage repair model for normal tissues.

Mike Partridge¹

¹The Institute of Cancer Research, Downs Road, Sutton, SM2 5PT, UK.

Physics in Medicine and Biology

|June 19, 2008

Summary

This study introduces a simplified cellular Monte Carlo model for radiation damage and repair in normal tissues. The model accurately predicts tissue responses to radiation, including re-epithelialization and radiosensitivity, aligning with experimental data.

Area of Science:

Radiation Biology
Computational Biology
Tissue Engineering

Background:

Understanding radiation damage and repair mechanisms in normal tissues is crucial for radiotherapy.
Existing models often lack the necessary detail to capture complex cellular responses.

Purpose of the Study:

To develop and validate a simplified cellular Monte Carlo model for simulating radiation damage and repair in normal epithelial tissues.
To assess the model's ability to reproduce experimentally observed radiobiological phenomena.

Main Methods:

A cellular Monte Carlo model incorporating cell cycling, motility, and radiation damage response (cell cycle arrest, cell death).
Simulation of stable equilibrium systems with varying cell cycle times (24-96 h).
Irradiation of simulated systems to observe and quantify tissue responses.

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Immunofluorescence Imaging of DNA Damage and Repair Foci in Human Colon Cancer Cells

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Measuring DNA Damage and Repair in Mouse Splenocytes After Chronic In Vivo Exposure to Very Low Doses of Beta- and Gamma-Radiation

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Main Results:

The model achieved stable equilibrium for cell cycle times between 24-96 hours.
Simulated irradiation produced responses consistent with experimental and clinical observations.
Accurate predictions of re-epithelialization, radiosensitivity, time to maximum toxicity, low-dose hyper-radiosensitivity, and lesion repopulation rates were achieved.

Conclusions:

The simplified cellular Monte Carlo model effectively captures key aspects of radiation damage and repair in normal epithelial tissues.
The model's predictions align quantitatively with a range of experimental and clinical radiobiological data.
This model serves as a valuable tool for understanding and predicting tissue responses to radiation therapy.