DNA damage and repair during photodynamic therapy

L. Vorster, H. Abrahamse

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review


Cells are constantly stressed by, not only environmental factors, but also its own metabolism. This can lead to chemical alterations and/or errors in synthesis. Such changes or errors are known as DNA damage. There are two main types of DNA damage: endogenous and exogenous. Endogenous DNA damage is caused by metabolic by-products such as reactive oxygen species (ROS) and by replication errors. Exogenous DNA damage is induced by external factors such as UV radiation and viruses [1]. Altered bases, single strand breaks, double strand breaks and fragmentation are known as primary damage. Deletions, chromosomal rearrangements and protein-DNA crosslinking are secondary damage. These errors can lead to mutations, genomic instability, development of cancer and cell death [2]. Radiation induced DNA damage has been widely studied in resent times due to the properties of DNA such as ionization potential and electron affinity [4]. UV radiation experiments have been conducted even before the DNA double helix was postulated. Radiation effects not only DNA but also RNA, proteins and even cell structures such as cell membranes [5].Low Intensity Laser Irradiation (LILI) or biostimulation is used in conjunction with photosensitizers (PS) in photodynamic therapy (PDT) to treat cancer. A single wavelength is used that emits no heat, sound or vibration and reacts with the PS to induce various changes in cellular functions. These changes are a consequence of changes in epigenetic regulation of genes. When the laser light reacts with the PS, in the presence of oxygen, it generates ROS. The ROS is highly reactive and damages DNA on such a scale that the repair pathways can not repair the DNA and thus lead to cell death. PDT is used in cancer treatment for two main reasons. Firstly the PS has a high affinity for cancer cells. Secondly, due to the fact that the ROS is highly reactive and has a short half-life, only molecules in close proximity of it are directly affected [5]. Recent studies have identified two mechanisms in PDT. One is the necrosis of a cell and the second involves apoptosis. Necrosis implies fragmentation of the cell membranes, causing the cell to rupture. Apoptosis is a form of controlled cell death where the chromatin fragments and the cell converts to an apoptotic body (dead cell) [4]. This chapter will review the mechanisms of DNA damage, DNA repair and the effect on these mechanisms during PDT.

Original languageEnglish
Title of host publicationDNA Repair
Subtitle of host publicationNew Research
PublisherNova Science Publishers, Inc.
Number of pages16
ISBN (Print)9781621007562
Publication statusPublished - Jan 2012

ASJC Scopus subject areas

  • General Medicine
  • General Biochemistry,Genetics and Molecular Biology


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