Repeated 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

被引:95
作者
Sheehan, JM [1 ]
Cragg, N
Chadwick, CA
Potten, CS
Young, AR
机构
[1] Univ London Kings Coll, St Thomas Hosp, Guys Kings & St Thomas Sch Med, St Johns Inst Dermatol,Dept Environm Dermatol, London SE1 7EH, England
[2] Paterson Inst Canc Res, Manchester M20 9BX, Lancs, England
关键词
melanogenesis; protection factor; thymine dimers;
D O I
10.1046/j.1523-1747.2002.01681.x
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 ;
摘要
We 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 cm(2) ) 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.
引用
收藏
页码:825 / 829
页数:5
相关论文
共 37 条
[1]  
AUBIN F, 1989, PHOTODERMATOLOGY, V6, P118
[2]   Photoadaptation to ultraviolet (UV) radiation in vivo:: photoproducts in epidermal cells following UVB therapy for psoriasis [J].
Bataille, V ;
Bykov, VJ ;
Sasieni, P ;
Harulow, S ;
Cuzick, J ;
Hemminki, K .
BRITISH JOURNAL OF DERMATOLOGY, 2000, 143 (03) :477-483
[3]   Defective global genome repair in XPC mice is associated with skin cancer susceptibility but not with sensitivity to UVB induced erythema and edema [J].
Berg, RJW ;
Ruven, HJT ;
Sands, AT ;
de Gruijl, FR ;
Mullenders, LHF .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 1998, 110 (04) :405-409
[4]  
DEFINE OF, 1997, ARCH DERMATOL RES, V289, P501
[5]   Enhancement of DNA repair in human skin cells by thymidine dinucleotides: Evidence for a p53-mediated mammalian SOS response [J].
Eller, MS ;
Maeda, T ;
Magnoni, C ;
Atwal, D ;
Gilchrest, BA .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1997, 94 (23) :12627-12632
[6]   THE VALIDITY AND PRACTICALITY OF SUN-REACTIVE SKIN TYPE-I THROUGH TYPE-VI [J].
FITZPATRICK, TB .
ARCHIVES OF DERMATOLOGY, 1988, 124 (06) :869-871
[7]   DNA photodamage stimulates melanogenesis and other photoprotective responses [J].
Gilchrest, BA ;
Eller, MS .
JOURNAL OF INVESTIGATIVE DERMATOLOGY SYMPOSIUM PROCEEDINGS, 1999, 4 (01) :35-40
[8]  
Gniadecka M, 1996, ACTA DERM-VENEREOL, V76, P429
[9]  
Green A, 1992, Epithelial Cell Biol, V1, P47
[10]   Clearance of UVB-induced erythema in patients with non-melanoma skin cancer [J].
Holmes, SC ;
Aitchison, TC ;
MacKie, RM .
PHOTODERMATOLOGY PHOTOIMMUNOLOGY & PHOTOMEDICINE, 1997, 13 (5-6) :189-192