Increased prostaglandins E2 and F2alpha in human skin at 6 and 24 h after ultraviolet B irradiation (290− 320 nm).

Black, A. Kobza; Greaves, M.W.; Hensby, C.N.; Plummer, N. A.

doi:10.1111/j.1365-2125.1978.tb01650.x

Cited by 140 publications

(63 citation statements)

References 18 publications

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“…and arachidonic acid in human skin and for their elevation 24 h after irradiation with three MED u.v.B and six MED u.v.C. We have previously shown that the maximum increase of prostaglandin-like compounds occurs at approximately 24 h after three MED u.v.B when the erythema is maximal (Black et al, 1978). Six MED of u.v.C.…”

Section: Discussionmentioning

confidence: 99%

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The effects of indomethacin on arachidonic acid and prostaglandins e2 and f2alpha levels in human skin 24 h after u.v.B and u.v.C irradiation.

Black¹,

Greaves²,

Hensby³

et al. 1978

Brit J Clinical Pharma

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100

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1 Clinically normal human abdominal skin was irradiated with either three times its minimal erythema dose (MED) of ultraviolet B (u.v.B) or six MEDs of ultraviolet C (u.v.C) radiation. In both instances erythema was maximal at 24 h. 2 Exudate was recovered by a suction bulla technique from normal and irradiated skin at 24 h after irradiation. 3 Arachidonic acid, prostaglandins E2 and FSalpha, as measured by GC–MS, were significantly elevated at 24 h. Radioimmunoassay also showed increased PGF2alpha‐like concentrations. 4 Oral indomethacin only partially reduced the erythema resulting from both types of radiation but totally suppressed the elevation of PGE 2 and F2alpha concentrations. 5 Topical indomethacin also suppressed u.v.B‐induced increases in prostaglandins E2 and F2alpha. Unexpectedly, the vehicle alone produced a similar suppressive effect on prostaglandins although erythema appeared unaltered. 6 Most of the arachidonic acid metabolized by indomethacin‐sensitive pathways is not converted to prostaglandins E2 and F2alpha in human skin.

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Section: Discussionmentioning

confidence: 99%

“…We have previously presented evidence for increased amounts of arachidonic acid, prostaglandin E2 and F2 -like materials in human skin exudate 24 h after irradiation with u.v.B (290-320 nm) (Black, Greaves, Hensby & Plummer, 1978);and u.v.C. (100-290 nm) (Camp, Greaves, Hensby, Plummer & Warin, 1978).…”

Section: Introduceton Methodsmentioning

confidence: 99%

The effects of indomethacin on arachidonic acid and prostaglandins e2 and f2alpha levels in human skin 24 h after u.v.B and u.v.C irradiation.

Black¹,

Greaves²,

Hensby³

et al. 1978

Brit J Clinical Pharma

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100

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“…For example, significant elevations of arachidonic acid and its cyclooxygenase and lipoxygenase products are observed in dermal perfusates and in suction blisters raised on irradiated skin (3)(4)(5), and inhibition of cyclooxygenase-derived prostaglandins by indomethacin treatment blocks 50% of the erythema that develops during the first 24 h after UVB injury (3,(8)(9)(10)(11)(12). Studies of UV-irradiated keratinocytes.…”

Section: Introductionmentioning

confidence: 99%

Enhanced prostaglandin synthesis after ultraviolet injury is mediated by endogenous histamine stimulation. A mechanism for irradiation erythema.

Pentland¹,

Mahoney²,

Jacobs³

et al. 1990

J. Clin. Invest.

116

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Acute ultraviolet light B (UVB) injury is associated with dermal mast cell histamine release. The possibility that histamine-stimulated prostaglandin (PG) synthesis could be a mechanism for irradiation erythema was therefore examined using human skin explants. Explants responded to UV irradiation (120 mJ/cm2) with a fivefold increase in synthesis of prostaglandins E2, F2. and 6-keto PGFIt. Incubating explants with the H1 antihistamines brompheniramine (50 MM) or pyrilamine (30 1AM) inhibited PG release from irradiated explants 63±4.9% (mean±SEM) 6 h after UV exposure. Antihistamines did not affect PG synthesis in control explants. Irradiation increased the histamine concentration in explant conditioned medium only 50% over basal values, suggesting that irradiation enhanced histamine responsiveness. Explants were therefore incubated with exogenous histamine. In irradiated explants, PG synthesis was stimulated threefold by 3 MM histamine. Unirradiated explants' PG synthesis was unaffected by histamine.Enhanced histamine sensitivity was also examined in epidermal cell cultures. In irradiated cultures, histamine sensitivity was again markedly potentiated: as little as 1 MM histamine stimulated significant PGE2 release and the response to 10-30 MAM histamine was increased six to eight times compared with that of unirradiated cultures. These studies demonstrate that endogenous histamine stimulates PG synthesis in human skin after UV injury by potentiation of histamine-induced prostaglandin release. Potentiated agonist responses induced by UV exposure may contribute to the effects of UVB irradiation injury and in particular to irradiation erythema. (J. Clin. Invest. 1990. 86:566-574.) Key words: ultraviolet light-skin -injury.

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“…Regarding the kinetics of the increase in their concentration, there is a fast release of prostaglandins (PG) E 2 , F 2 , D 2 and 12-R-HETE, even before the erythema has become clinically perceptible, and they persist for 48 h reaching a maximum level 18-24 h after exposure to UVB (14,73,77,82). In vitro studies have confirmed the dose-dependent increase in the levels of the released eicosanoids (65).…”

Section: Biochemical Mediators In the Pathogenesis Of Erythemamentioning

confidence: 61%

“…Both the nature of the eicosanoids and the levels they reach depend on the wavelength of the radiation (73,74). For example, cyclooxygenase inhibitors administered during the first 24 h after UVB exposure reduced by about 50% the severity of photoinduced erythema (77)(78)(79)(80). However, indomethacin administered either topically or intradermally has no effect on erythema when the latter is induced only by UVA radiation (81).…”

Section: Biochemical Mediators In the Pathogenesis Of Erythemamentioning

confidence: 99%

Photochemistry and photobiology of actinic erythema: defensive and reparative cutaneous mechanisms

Tedesco¹,

Martínez²,

González³

1997

Braz J Med Biol Res

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Sunlight is part of our everyday life and most people accept it as beneficial to our health. With the advance of our knowledge in cutaneous photochemistry, photobiology and photomedicine over the past four decades, the terrestrial solar radiation has become a concern of dermatologists and is considered to be a major damaging environmental factor for our skin. Most photobiological effects (e.g., sunburn, suntanning, local and systemic immunosuppression, photoaging or dermatoheliosis, skin cancer and precancer, etc.) are attributed to ultraviolet radiation (UVR) and more particularly to UVB radiation (290-320 nm). UVA radiation (320-400 nm) also plays an important role in the induction of erythema by the photosensitized generation of reactive oxygen species (singlet oxygen OH)) that damage DNA and cellular membranes, and promote carcinogenesis and the changes associated with photoaging. Therefore, research efforts have been directed at a better photochemical and photobiological understanding of the so-called sunburn reaction, actinic or solar erythema. To survive the insults of actinic damage, the skin appears to have different intrinsic defensive mechanisms, among which antioxidants (enzymatic and non-enzymatic systems) play a pivotal role. In this paper, we will review the basic aspects of the action of UVR on the skin: a) photochemical reactions resulting from photon absorption by endogenous chromophores; b) the lipid peroxidation phenomenon, and c) intrinsic defensive cutaneous mechanisms (antioxidant systems). The last section will cover the inflammatory response including mediator release after cutaneous UVR exposure and adhesion molecule expression.Correspondence

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Increased prostaglandins E2 and F2alpha in human skin at 6 and 24 h after ultraviolet B irradiation (290− 320 nm).

Cited by 140 publications

References 18 publications

The effects of indomethacin on arachidonic acid and prostaglandins e2 and f2alpha levels in human skin 24 h after u.v.B and u.v.C irradiation.

The effects of indomethacin on arachidonic acid and prostaglandins e2 and f2alpha levels in human skin 24 h after u.v.B and u.v.C irradiation.

Enhanced prostaglandin synthesis after ultraviolet injury is mediated by endogenous histamine stimulation. A mechanism for irradiation erythema.

Photochemistry and photobiology of actinic erythema: defensive and reparative cutaneous mechanisms

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