Pyrimidine dimer

Pyrimidine dimers represent molecular lesions originating from thymine or cytosine bases within DNA, resulting from photochemical reactions.

[1][2] These lesions, commonly linked to direct DNA damage,[3] are induced by ultraviolet light (UV), particularly UVC, result in the formation of covalent bonds between adjacent nitrogenous bases along the nucleotide chain near their carbon–carbon double bonds,[4] the photo-coupled dimers are fluorescent.

Conversely, certain bacteria utilize photolyase, powered by sunlight, to repair pyrimidine dimer-induced DNA damage.

Overwhelming DNA damage can precipitate mutations within an organism's genome, potentially culminating in cancer cell formation.

Notably, pyrimidine dimers contribute to sunburn and melanin production, and are a primary factor in melanoma development in humans.

[12] A third type of molecular lesion is a Dewar pyrimidinone, resulting from the reversible isomerization of a 6–4 photoproduct under further light exposure.

Despite thymine-thymine CPDs being the most common lesions induced by UV, translesion polymerases show a tendency to incorporate adenines, resulting in the accurate replication of thymine dimers more often than not.

[14] Pyrimidine dimers introduce local conformational changes in the DNA structure, which allow recognition of the lesion by repair enzymes.

[7] Some common features and symptoms of XP include skin discoloration, and the formation of multiple tumors proceeding UV exposure.

Typically, the lesion associated with the pyrimidine dimer blocks cellular machinery from synthesizing past the damaged site.

[21] Sunscreen primarily works by absorbing the UV light from the sun through the use of organic compounds, such as oxybenzone or avobenzone.