DNAStrangbrüche

DNAStrangbrüche, also known as DNA strand breaks, are disruptions in the phosphodiester backbone of a DNA molecule. These breaks can occur in either one or both strands of the DNA double helix. Single-strand breaks (SSBs) affect only one of the two complementary DNA strands, while double-strand breaks (DSBs) involve breaks in both strands at or near the same location.

The formation of DNA strand breaks can be caused by various endogenous and exogenous agents. Endogenous sources include reactive oxygen species generated during normal metabolic processes, errors during DNA replication or repair, and enzymatic activities. Exogenous sources encompass ionizing radiation (like X-rays and gamma rays), ultraviolet radiation, certain chemicals, and mechanical stress.

DNA strand breaks are considered highly cytotoxic lesions, particularly DSBs, as they can lead to significant genomic instability, mutations, chromosomal rearrangements, and ultimately cell death if not accurately repaired. Cells have evolved sophisticated DNA repair pathways to counteract these damaging events. The primary repair mechanisms for SSBs include base excision repair (BER) and nucleotide excision repair (NER). For DSBs, the main pathways are non-homologous end joining (NHEJ) and homologous recombination (HR). NHEJ is a more error-prone but rapid process, while HR is generally more accurate and relies on a homologous template for repair, typically occurring during the S and G2 phases of the cell cycle.

The study of DNA strand breaks and their repair mechanisms is crucial in understanding cell biology, aging, and diseases such as cancer, where unrepaired DNA damage can drive tumorigenesis. Therapeutic strategies, particularly in cancer treatment, often aim to induce or exploit DNA strand breaks to trigger cell death in cancer cells.