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Xeroderma pigmentosum (XP) is a genetic disorder in which there is a decreased ability to repair DNA damage such as that caused by ultraviolet (UV) light. [1] Symptoms may include a severe sunburn after only a few minutes in the sun, freckling in sun-exposed areas, dry skin and changes in skin pigmentation. [1]
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.
One cause of cataracts is exposure to ultraviolet light. Provided the level of UV emission from lamps is within safe limits, and the lamp a sufficient distance away from the individual, there should be no increased risk of developing cataracts. Photophobia is a symptom of excessive sensitivity to light which affects 5 to 20% of the population ...
Patients with systemic lupus erythematosus experience skin symptoms after sunlight exposure; some types of porphyria are aggravated by sunlight. A rare hereditary condition xeroderma pigmentosum (a defect in DNA repair) is thought to increase the risk of UV-light-exposure-related cancer by increasing photosensitivity.
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 ...
Indirect DNA damage occurs when a UV-photon is absorbed in the human skin by a chromophore that does not have the ability to convert the energy into harmless heat very quickly. [2] Molecules that do not have this ability have a long-lived excited state.
Phytophotodermatitis, also known as berloque dermatitis, [1] [2] [3] margarita photodermatitis, [4] [5] lime disease [6] or lime phytodermatitis [6] is a cutaneous phototoxic inflammatory reaction resulting from contact with a light-sensitizing botanical agent (such as lime juice) followed by exposure to ultraviolet A (UV-A) light (from the sun, for instance).
Photolyases (EC 4.1.99.3) are DNA repair enzymes that repair damage caused by exposure to ultraviolet light. These enzymes require visible light (from the violet/blue end of the spectrum) both for their own activation [1] and for the actual DNA repair. [2] The DNA repair mechanism involving photolyases is called photoreactivation.