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.

Self Cite

1. Human abdominal skin was irradiated with six times the minimal erythema dose of ultraviolet C (100–290 nm) radiation. Erythema appeared at 3 h, was of moderate degree by 6 h and was maximal at 12‐ 24 h. It was reduced at 48 h and by 72 h had disappeared. 2. A suction bulla technique was used for the recovery of exudate from normal and inflamed skin at 6, 18, 24 and 48 h after irradiation. 3. Prostaglandin‐ like activity, estimated by bioassay, showed maximum increase at 18 h, when erythema was also maximum. PGF 2alpha, measured by both radioimmunoassay and by combined gas‐liquid chromatography‐gas spectrometry, followed a similar time course then fell to normal, or near normal, levels at 48 h. 4. Prostaglandin E2 and arachidonic acid concentrations, measured by gas chromatography‐mass spectrometry, were maximally raised at 18–24 h. At 48 h, when some erythema was still present, though reduced, prostaglandin E2 concentrations were still raised above control values. 5. The results provide direct evidence in support of the view that the erythma following irradiation of human skin by u.v.C involves activation of arachidonic acid metabolism. However, the relationship between the erythema and increased prostaglandin activity is not fully understood.

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Irradiation of human skin by short wavelength ultraviolet radiation (100–290 nm) (u.v.C): increased concentrations of arachidonic acid and prostaglandines E2 and F2alpha.

Camp¹,

Greaves²,

Hensby³

et al. 1978

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“…That the concentrations of eicosanoids in untreated and base treated skin did not change significantly during the 72 h study suggests that systemic effects resulting from absorption of the drug into the systemic circulation were unlikely to have occurred. Although base treatment alone has been shown to affect AA metabolism in human skin (Hammarstrom et al, 1977;Black et al, 1978) we did not detect significant differences in the concentrations of metabolites between base and untreated lesions at the various time points except at 72 h when LTB4 appeared significantly higher in the base treated site than in the corresponding untreated control site (P = 0.04).…”

Section: Discussionmentioning

confidence: 59%

Topical steroid treatment reduces arachidonic acid and leukotriene B4 in lesional skin of psoriasis.

Wong¹,

Barr²,

Fm³

et al. 1986

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Topical clobetasol propionate or vehicle ointment was applied daily for 3 days to psoriatic plaques on eight patients. Skin chamber exudates from untreated, steroid and vehicle treated lesions were assayed for arachidonic acid (AA), leukotriene B4 (LTB4), prostaglandin E2 (PGE2) and 12‐hydroxy‐5,8,10,14‐eicosatetraenoic acid (12‐HETE) before, and at 24 h and 72 h after treatment. Significant reductions in AA and LTB4 were observed at 72 h in steroid treated lesions. The reduction in 12‐ HETE levels observed after steroid treatment was not statistically significant. PGE2 levels in lesional psoriatic skin were unaltered. The reduction of AA, and LTB4 was associated with clinical improvement of psoriasis.

“…Treatment of subjects with oral indomethacin prior to irradiation with u.v.B completely suppressed the increase in cyclo-oxygenase activity but was only partially effective in reducing erythema (Black et al, 1978). In contrast, a drug which had no effect on PGE2 levels was also ineffective in reducing erythma (Barr et al, 1982).…”

Section: Controlmentioning

confidence: 93%

“…Leukotriene B4 (LTB4), et al, 1980). The rise in prostaglandin levels a 5,12-dihydroxyeicosatetraenoic acid product after ultraviolet B irradiation (u.v.B) can be of the 5-lipoxygenase pathway, is one of the reduced by prior administration of indome-most potent chemokinetic agents for polythacin, an inhibitor of the cyclo-oxygenase morphonuclear cells in vitro (Ford-Hutchinson enzyme system (Black et al, 1978). However, et al, 1980) and is chemokinetic in vivo (Camp al., 1983a).…”

Section: Introductionmentioning

confidence: 99%

Lipoxygenase products of arachidonic acid in human inflamed skin.

Black¹,

Barr²,

Wong³

et al. 1985

Self Cite

Monohydroxy acids (HETEs) and leukotriene B4 (LTB4) metabolites of arachidonic acid were measured in skin of healthy volunteers after ultraviolet B irradiation, and in the uninvolved skin of psoriatics after topical dithranol application. Exudate was collected from suction bullae on control and inflamed abdominal skin, and analysed for 12‐HETE and PGE2 by GC‐MS and LTB4 by bioassay. 12‐HETE and PGE2 were raised at 24 h but not at 72 h after u.v.B irradiation: control and 24 h values were 13.7 and 41.5 ng ml‐1 (P less than 0.05, n = 6) for 12‐HETE respectively, and 4.5 and 30.2 ng ml‐1 (P less than 0.01, n = 6) for PGE2. Dithranol application raised PGE2 levels from 23.1 ng ml‐1 in control exudate to 62 ng ml‐1 (P less than 0.01, n = 6) at 24 h before declining to base levels at 72 h. However, 12‐HETE was raised at 72 h (200 ng ml‐1, P less than 0.01, n = 5) but not at 24 h (104 ng ml‐1) compared to control levels (50 ng ml‐1, n = 5). The levels of the LTB4 were low (less than 100 pg ml‐1), and no significant increases were observed. Arachidonic acid in inflamed skin can be metabolised by the cyclo‐oxygenase and lipoxygenase pathway. It is probable that the lipoxygenase product 12‐HETE is involved in these inflammatory reactions.