Also see:
Unsaturated Fats and Age Pigment
Phospholipases, PUFA, and Inflammation
PUFA Accumulation & Aging
Topical Vitamin E and ultraviolet radiation on human skin
Niacinamide and the Skin
Caffeine and Skin Protection
Benefits of Aspirin
J Invest Dermatol. 1993 Jan;100(1):35S-41S.
Mechanisms of UV-induced inflammation.
Hruza LL, Pentland AP.
The inflammation produced by exposure to ultraviolet (UV) light has been well documented clinically and histologically. However, the mechanisms by which mediators induce this clinical response remain poorly defined. It is clear that photochemistry occurring after UV absorption must be responsible for initiating these events. Some of these underlying mechanisms have been defined. After exposure to UV light, the formation of prostaglandins and the release of histamine are increased. In addition to an increase in the quantity of these mediators, an increase in sensitivity of irradiated tissue to agonist stimulation also occurs. This increased sensitivity may cause tissue to respond to agonist levels previously present. Phospholipase activity also increases, making more substrate available for prostaglandin formation. Oxygen radical-induced peroxidation of membrane lipids caused by irradiation may contribute to increased phospholipase activity. Oxygen-free radicals also participate in sunburn cell formation and in UV-induced decreases in Langerhans cell numbers. Several enzymatic and non-enzymatic mechanisms are present in skin for reducing these highly reactive oxygen species.
J Am Acad Dermatol. 1981 Oct;5(4):411-22.
The human sunburn reaction: histologic and biochemical studies.
Gilchrest BA, Soter NA, Stoff JS, Mihm MC Jr.
The ultraviolet-induced erythema reaction was investigated histologically and biochemically in four subjects, utilizing suction blister aspirates, analyzed for histamine and prostaglandin E2 (PGE2), and Epon-embedded 1-mu skin biopsy sections from control skin and from irradiated skin at intervals for 72 hours after exposure to a Hanovia lamp. Major histologic alterations in the epidermis included dyskeratotic and vacuolated keratinocytes (sunburn cells), and disappearance of Langerhans cells. In the dermis the major changes were vascular, involving both the superficial and deep venular plexuses. Endothelial cell enlargement was first apparent within 30 minutes of irradiation, peaked at 24 hours, and persisted throughout the 72-hour study period. Mast cell degranulation and associated perivenular edema were first apparent at 1 hour and striking at the onset of erythema, 3 to 4 hours postirradiation; edema was absent and mast cells were again normal in number and granule content at 24 hours. Histamine levels rose approximately fourfold above control values immediately after the onset of erythema and returned to baseline within 24 hours. PGE2 levels were statistically elevated even before the onset of erythema and reached approximately 150% of the control value at 24 hours. These data provide the first evidence that histamine may mediate the early phase of the human sunburn reaction and increase our understanding of its complex histologic and biochemical sequelae.
J Invest Dermatol. 1983 Jun;80(6):496-9.
Increased concentrations of arachidonic acid, prostaglandins E2, D2, and 6-oxo-F1 alpha, and histamine in human skin following UVA irradiation.
Hawk JL, Black AK, Jaenicke KF, Barr RM, Soter NA, Mallett AI, Gilchrest BA, Hensby CN, Parrish JA, Greaves MW.
The buttock skin of clinically normal human subjects was subjected to approximately 2.5 minimal erythema doses of ultraviolet A irradiation. Deep red erythema developed during irradiation, faded slightly within the next few hours, increased to maximum intensity between 9-15 h, and decreased gradually thereafter although still persisting strongly at 48 h. Suction blister exudates were obtained at 0, 5, 9, 15, 24, and 48 h after irradiation as well as suction blister exudates from a contralateral control site and assayed for arachidonic acid, prostaglandins D2 and E2, and the prostacyclin breakdown product 6-oxo-prostaglandin F1 alpha by gas chromatography-mass spectrometry, and for histamine by radioenzyme assay. Increased concentrations of arachidonic acid and prostaglandins D2, E2, and 6-oxo-prostaglandin F1 alpha were found maximally between 5-9 h after irradiation, preceding the phase of maximal erythema. Elevations of histamine concentration occurred 9-15 h after irradiation, preceding and coinciding with the phase of maximal erythema. At 24 h, still at the height of the erythemal response, all values had returned to near control levels. Hence increased concentrations of arachidonic acid and its products from the cyclooxygenase pathway, and of histamine, accompany the early stages up to 24 h. A causal role in production of the erythema seems likely for these substances although other mediators are almost certainly involved.
Adv Exp Med Biol. 1994;366:87-97.
Active oxygen mechanisms of UV inflammation.
Pentland AP.
Active oxygen radicals are important in the pathogenesis of UV irradiation injury. The initiating mechanisms involve the generation of hydroxyl radicals, superoxide, and organic hydroperoxides due to photochemical reactions. These active oxygen species lead to DNA strand breakage, mutation and the generation of inflammatory mediators such as cytokines and arachidonic acid metabolites which amplify the irradiation-induced inflammation. Several compounds have recently been utilized to successfully decrease these effects. Improved understanding of the mechanisms by which active oxygen species induce injury in skin now promises improved treatment.
Semin Dermatol. 1990 Mar;9(1):11-5.
Acute effects of ultraviolet radiation on the skin.
Soter NA.
The responses of normal skin to ultraviolet (UV) irradiation are an example of inflammation. The chromophores initiating the reaction are unknown. Characteristic clinical findings are erythema, heat, swelling, and pain. Histopathologic changes include epidermal keratinocyte damage with Langerhans cell depletion and dermal edema, endothelial swelling, mast cell degranulation, and cellular infiltration with neutrophils and monocytes. Biochemical changes include release of histamine, cyclo-oxygenase, and lipoxygenase-derived products of arachidonic acid, kinins, and cytokines, probably from a range of epidermal and dermal cell types. These substances very likely assist in mediation of the reaction. The response is more pronounced in young subjects. UVB (280 to 315 nm) and UVA (315 to 400 nm) radiation both produce inflammation, but with marked qualitative and quantitative differences. UVB having more effect on the epidermis, UVA more on the dermis.
J Cosmet Sci. 2006 Mar-Apr;57(2):203-4.
Salicylic acid protects the skin from UV damage.
Mammone T, Gan D, Goyarts E, Maes D.
Aspirin(acetyl salicylate) has long been used as an analgesic. Salicylic acid has been reported to have anti-inflammatory properties. These activities include inhibiting activity of cox-1, cox-2, and NF-kb. In addition, salicylic acid has also been shown in some systems to induce Hsp70. We have demonstrated that salicylic acid inhibits UVB-induced sunburn cell formation, as well as increase the removal of UVB induced TT dimer formation in living skin equivalents. Given these protective properties of salicylic acid, we propose the use of salicylic acid as a topical therapeutic to protect the skin from sun damage.
J Dermatol Sci. 2009 Jul;55(1):10-7. Epub 2009 May 2.
The effects of topically applied glycolic acid and salicylic acid on ultraviolet radiation-induced erythema, DNA damage and sunburn cell formation in human skin.
Kornhauser A, Wei RR, Yamaguchi Y, Coelho SG, Kaidbey K, Barton C, Takahashi K, Beer JZ, Miller SA, Hearing VJ.
BACKGROUND:
alpha-Hydroxy acids (alphaHAs) are reported to reduce signs of aging in the skin and are widely used cosmetic ingredients. Several studies suggest that alphaHA can increase the sensitivity of skin to ultraviolet radiation. More recently, beta-hydroxy acids (betaHAs), or combinations of alphaHA and betaHA have also been incorporated into antiaging skin care products. Concerns have also arisen about increased sensitivity to ultraviolet radiation following use of skin care products containing beta-HA.
OBJECTIVE:
To determine whether topical treatment with glycolic acid, a representative alphaHA, or with salicylic acid, a betaHA, modifies the short-term effects of solar simulated radiation (SSR) in human skin.
METHODS:
Fourteen subjects participated in this study. Three of the four test sites on the mid-back of each subject were treated daily Monday-Friday, for a total of 3.5 weeks, with glycolic acid (10%), salicylic acid (2%), or vehicle (control). The fourth site received no treatment. After the last treatment, each site was exposed to SSR, and shave biopsies from all four sites were obtained. The endpoints evaluated in this study were erythema (assessed visually and instrumentally), DNA damage and sunburn cell formation.
RESULTS:
Treatment with glycolic acid resulted in increased sensitivity of human skin to SSR, measured as an increase in erythema, DNA damage and sunburn cell formation. Salicylic acid did not produce significant changes in any of these biomarkers.
CONCLUSIONS:
Short-term topical application of glycolic acid in a cosmetic formulation increased the sensitivity of human skin to SSR, while a comparable treatment with salicylic acid did not.
Dermatologica. 1976;152(2):87-99.
Dermatopharmacology of salicylic acid. III. Topical contra-inflammatory effect of salicylic acid and other drugs in animal experiments.
Weirich EG, Longauer JK, Kirkwood AH.
The acute contra-inflammatory effects of salicylic acid, three standard dermatocorticoids and four contact antiphlogistics have been investigated by means of a UV dermatitis inhibition test in the guinea pig. The substances tested had a distinct inhibitory effect on the development of erythema and can be ranked in the following ascending order of activity (percent of maximum possible score): bufexamac = 36%, salicylic acid = 37%, hydrocortisone = 44%, acetylsalicylic acid = 48%, flumethasone pivalate = 51%, fluocinolone acetonide = 51%, phenylbutazone = 56%, and indomethacin = 58%.
Z Hautkr. 1981 Nov 15;56(22):1437-46.
[The influence of acetylosalicyclic acid on the cutaneous effect of UV-A (author’s transl)].
[Article in German]
Jablonski KP, Pullmann H, Steigleder GK.
This study deals with the influence of acetylosalicyclic acid (Colfarit Bayer) on the cutaneous effect of UV-A. Each of 24 volunteers received UV-A doses from 5 J/cm2 to 50 J/cm2. The immediate and the delayed UV-A erythema were reduced by prophylactic application of acetylosalicylic acid, 3 g daily three days before exposure and three days afterwards. 72 h after exposure to UV-A the reduction of delayed erythema formation was most obvious. Acetylosalicyclic acid had no influence, however, on the pigmentation caused by UV-A radiation.
