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These reactive chemical species can reach DNA by diffusion and the bimolecular reaction damages the DNA (oxidative stress). Unlike direct DNA damage which causes sunburn, indirect DNA damage does not result in any warning signal or pain in the human body. The bimolecular reactions that cause the indirect DNA damage are illustrated in the figure:
Nucleotide excision repair (NER) is a particularly important excision mechanism that removes DNA damage induced by ultraviolet light (UV). UV DNA damage results in bulky DNA adducts — these adducts are mostly thymine dimers and 6,4-photoproducts. Recognition of the damage leads to removal of a short single-stranded DNA segment that contains ...
The major acute effects of UV irradiation on normal human skin comprise sunburn inflammation erythema, tanning, and local or systemic immunosuppression. [42] The most deadly form, malignant melanoma, is mostly caused by indirect DNA damage from UVA radiation.
This process of absorption works to reduce the risk of DNA damage and the formation of pyrimidine dimers. UVA light makes up 95% of the UV light that reaches earth, whereas UVB light makes up only about 5%. UVB light is the form of UV light that is responsible for tanning and burning. Sunscreens work to protect from both UVA and UVB rays.
UV light, specifically non-ionizing shorter-wavelength radiation such as UVC and UVB, causes direct DNA damage by initiating a synthesis reaction between two thymine molecules. The resulting dimer is very stable. Although they can be removed through excision repairs, when UV damage is extensive, the entire DNA molecule breaks down and the cell ...
The sun is, by far, the greatest source of ultraviolet (UV) radiation, which is the culprit that causes most skin cancers—the most common form of cancer in the U.S. According to the Skin Cancer ...
After DNA damage, cell cycle checkpoints are activated. Checkpoint activation pauses the cell cycle and gives the cell time to repair the damage before continuing to divide. DNA damage checkpoints occur at the G1/S and G2/M boundaries. An intra-S checkpoint also exists. Checkpoint activation is controlled by two master kinases, ATM and ATR.
An arsenal of DNA repair mechanisms exists to repair various forms of damaged DNA and minimize genomic instability. Most DNA repair mechanisms require an intact DNA strand as template to fix the damaged strand. DNA damage prevents the normal enzymatic synthesis of DNA by the replication fork.