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Updated: Jan 10, 2026

Visualizing and Quantifying Endonuclease-Based Site-Specific DNA Damage
Published on: August 21, 2021
Cellular and Molecular Mechanisms of Oxidative DNA Damage and Repair
Adnan Ayna1, Cuneyt Caglayan2, Seyithan Taysi3
1Department of Chemistry, Faculty of Science and Literature, Bingol University, 12000 Bingol, Turkey.
Abstract:
DNA is continuously exposed to endogenous and exogenous factors that induce oxidative modifications leading to mutations and genomic instability. Oxidative DNA damage plays a dual role, contributing to physiological signaling at low levels while promoting mutagenesis, carcinogenesis and degenerative diseases when unpaired. Among various lesions, an oxidized base, such as 8-oxo-2'-deoxyguanosine (8-oxodG), is one of the major biomarkers of oxidative stress and genomic damage. Cells have evolved sophisticated repair processes, including base excision repair (BER), nucleotide excision repair (NER), and mismatch repair (MMR), to maintain genomic integrity. Dysregulation or polymorphism of these repair genes has been linked with cancer, neurologic, and cardiovascular disorders. This review discusses an overview of what is presently known concerning oxidative DNA damage and repair mechanisms, particularly emphasizing their molecular players, signaling routes, and human disease implications. It further refers to the latest advances in CRISPR-based technologies and multi-omics approaches that are redefining our understanding of DNA damage response (DDR) networks and creating new frontiers for therapeutic interventions.
Insights
Oxidative DNA damage, marked by 8-oxo-2'-deoxyguanosine (8-oxodG), can cause mutations and disease. DNA repair pathways like base excision repair (BER) are crucial for genomic stability and preventing cancer.
Area of Science:
- Molecular Biology
- Genetics
- Biochemistry
Background:
- DNA is susceptible to oxidative damage from internal and external sources, leading to mutations and genomic instability.
- Oxidative DNA damage has a dual role: low levels are involved in signaling, while excessive damage promotes mutagenesis, cancer, and degenerative diseases.
- 8-oxo-2'-deoxyguanosine (8-oxodG) is a key biomarker for oxidative stress and DNA damage.
Purpose of the Study:
- To review current knowledge on oxidative DNA damage and repair mechanisms.
- To emphasize the molecular players, signaling pathways, and implications for human diseases.
- To highlight recent advances in CRISPR and multi-omics for understanding DNA damage response (DDR) and therapeutic development.
Main Methods:
- Literature review of oxidative DNA damage and repair mechanisms.
- Focus on molecular players, signaling routes, and disease connections.
- Inclusion of recent advances in CRISPR-based technologies and multi-omics approaches.
Main Results:
- Oxidative DNA damage, particularly 8-oxodG, is a significant factor in genomic instability and disease.
- Cellular repair pathways, including base excision repair (BER), nucleotide excision repair (NER), and mismatch repair (MMR), are essential for maintaining genomic integrity.
- Dysregulation of DNA repair genes is linked to various disorders, including cancer, neurological, and cardiovascular diseases.
Conclusions:
- Understanding oxidative DNA damage and repair is critical for comprehending disease pathogenesis.
- Advances in technologies like CRISPR and multi-omics are crucial for exploring DNA damage response (DDR) networks.
- New therapeutic strategies targeting DDR pathways offer promising avenues for disease intervention.
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