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dc.contributor.authorSheehan, John M
dc.contributor.authorCragg, Nicola
dc.contributor.authorChadwick, Caroline A
dc.contributor.authorPotten, Christopher S
dc.contributor.authorYoung, Antony R
dc.date.accessioned2009-10-16T11:01:51Z
dc.date.available2009-10-16T11:01:51Z
dc.date.issued2002-05
dc.identifier.citationRepeated ultraviolet exposure affords the same protection against DNA photodamage and erythema in human skin types II and IV but is associated with faster DNA repair in skin type IV. 2002, 118 (5):825-9 J. Invest. Dermatol.en
dc.identifier.issn0022-202X
dc.identifier.pmid11982760
dc.identifier.doi10.1046/j.1523-1747.2002.01681.x
dc.identifier.urihttp://hdl.handle.net/10541/84317
dc.description.abstractWe have investigated the photoprotective properties of induced pigmentation using erythema and epidermal DNA photodamage as endpoints. Previously unexposed buttock skin of 12 young, healthy adults (six skin type II and six skin type IV) was exposed daily (Monday to Friday) for 2 wk (days 1-12) with 0.65 minimal erythema dose of solar simulated radiation. Mean skin type IV minimal erythema dose was 1.8-fold greater than for skin type II. Compared to skin type II, solar simulated radiation treatments produced less erythema and more tanning in skin type IV. To assess DNA photodamage, biopsies were taken and prepared for paraffin sections that were stained with a monoclonal antibody for thymine dimers. Thymine dimers were quantified by image analysis. The single exposure data (0.65 and 2 minimal erythema dose) showed that DNA damage was related to physical dose (J per cm2) independent of skin type. Our data also showed that DNA photodamage accumulates in both skin types with repeated, suberythemal doses of solar simulated radiation. On day 12, there were more thymine dimers in skin type IV than skin type II, again indicating that physical rather than biologic dose determines the level of DNA damage. Comparisons on days 12 and 19, however, showed a much greater loss of thymine dimers in skin type IV, suggesting better thymine dimer repair. Protection factors for erythema and thymine dimers were calculated and shown to be about 2 in both skin types. This provides further indirect evidence that DNA is a chromophore for erythema, but also suggests that a tan may not be the major factor in natural photoprotection.
dc.language.isoenen
dc.subject.meshDNA Damage
dc.subject.meshDNA Repair
dc.subject.meshEpidermis
dc.subject.meshErythema
dc.subject.meshHumans
dc.subject.meshMelanins
dc.subject.meshPyrimidine Dimers
dc.subject.meshSkin Pigmentation
dc.subject.meshUltraviolet Rays
dc.titleRepeated ultraviolet exposure affords the same protection against DNA photodamage and erythema in human skin types II and IV but is associated with faster DNA repair in skin type IV.en
dc.typeArticleen
dc.contributor.departmentPaterson Institute for Cancer Research, Christie Hopsital, Masnchester M20 4BX, UKen
dc.identifier.journalThe Journal of Investigative Dermatologyen
html.description.abstractWe have investigated the photoprotective properties of induced pigmentation using erythema and epidermal DNA photodamage as endpoints. Previously unexposed buttock skin of 12 young, healthy adults (six skin type II and six skin type IV) was exposed daily (Monday to Friday) for 2 wk (days 1-12) with 0.65 minimal erythema dose of solar simulated radiation. Mean skin type IV minimal erythema dose was 1.8-fold greater than for skin type II. Compared to skin type II, solar simulated radiation treatments produced less erythema and more tanning in skin type IV. To assess DNA photodamage, biopsies were taken and prepared for paraffin sections that were stained with a monoclonal antibody for thymine dimers. Thymine dimers were quantified by image analysis. The single exposure data (0.65 and 2 minimal erythema dose) showed that DNA damage was related to physical dose (J per cm2) independent of skin type. Our data also showed that DNA photodamage accumulates in both skin types with repeated, suberythemal doses of solar simulated radiation. On day 12, there were more thymine dimers in skin type IV than skin type II, again indicating that physical rather than biologic dose determines the level of DNA damage. Comparisons on days 12 and 19, however, showed a much greater loss of thymine dimers in skin type IV, suggesting better thymine dimer repair. Protection factors for erythema and thymine dimers were calculated and shown to be about 2 in both skin types. This provides further indirect evidence that DNA is a chromophore for erythema, but also suggests that a tan may not be the major factor in natural photoprotection.


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