Doctor of Natural Sciences (Dr. rer. Nat.)
Doctor Honoris Causa (Nicolaus Copernicus University, Collegium Medicum, Bydgoszcz, Poland)
Doctor Honoris Causa (Dokuz Eylul University, Izmir, Turkey)
DNA Damage and Repair
Oxidative stress is produced in cells by oxygen-derived species resulting from cellular metabolism and from interaction with cells of exogenous sources such as carcinogenic compounds, redox-cycling drugs and ionizing radiations. DNA damage caused by oxygen-derived species including free radicals is the most frequent type encountered by aerobic cells. When this type of damage occurs to DNA, it is called oxidative DNA damage and it can produce a multiplicity of modifications in DNA including base and sugar lesions, strand breaks, DNA-protein cross-links and base-free sites. Accurate measurement of these modifications is essential for understanding of mechanisms of oxidative DNA damage and its biological effects. Numerous DNA lesions have been identified in cells and tissues at steady-state levels and upon exposure to free radical-generating systems. Data accumulated over many years clearly show that oxidative DNA damage plays an important role in a number of disease processes. Thus, oxidative DNA damage is implicated in carcinogenesis and neurodegenerative diseases such as Alzheimer's disease. There is also strong evidence for the role of this type of DNA damage in the aging process. The accumulation of oxidative DNA damage in non-dividing cells is thought to contribute to age-associated diseases. DNA damage is countered in cells by DNA repair, which is a basic and universal process to protect the genetic integrity of organisms. The genomes of organisms encode DNA repair enzymes that continuously monitor chromosomes to correct DNA damage. Multiple processes such as base- and nucleotide-excision pathways exist to repair the wide range of DNA damages. If left unrepaired, oxidative DNA damage can lead to detrimental biological consequences in organisms, including cell death, mutations and transformation of cells to malignant cells. Therefore, DNA repair is regarded as one of the essential events in all life forms. There is an increasing awareness of the importance of oxidative DNA damage and its repair to human health. Thus, it becomes exceedingly important to understand, at the fundamental level, the mechanisms of oxidative DNA damage, and its processing by DNA repair enzymes as well as how unrepaired DNA lesions may lead to cytotoxicity, mutagenesis and eventually to diseases and aging. More detailed knowledge of mechanisms of DNA damage and repair might allow us to modulate DNA repair. This could lead to drug developments and clinical applications including the improvement of cancer therapy by inhibiting DNA repair in drug- or radiation-resistant tumors and/or the increase in the resistance of normal cells to DNA damage by overexpressing DNA repair genes.
Journal Editorships
Conferences Organized
h-Index
80 (according to Web of Science)
93 (according to Google Scholar)
Number of citations
23514 (according to Web of Science)
34833 (according to Google Scholar)
Detailed list of Dr. Dizdaroglu's Publications
Detailed list of Dr. Dizdaroglu's Invited Presentations