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1 Clinically normal human abdominal skin was irradiated with three minimal‐erythema doses of ultraviolet B irradiation, (u.v.B). 2 Erythema was assessed visually, and exudate recovered by a suction bulla technique from normal skin, and at 10 min, 2, 6, 18, 24 and 48 h after irradiation. 3 Erythema was barely visible at 2 h, but increased to maximum at 24 h, which was maintained at 48 h. 4 Increased arachidonic acid and prostaglandin E2, F2 alpha and D2 concentrations in the exudate, measured by gas chromatography‐mass spectrometry, accompanied the developing erythema, with the maximal rise of arachidonic acid, prostaglandin E2 and D2 occurring at the height of the erythema at 24 h. 5 At 48 h, still at the height of the erythemal response, arachidonic acid and PGE2 levels had returned to near normal. 6 Concentrations of arachidonic acid and of its products from the cyclo‐ oxygenase pathway, parallel the development of i.u.B. erythema in the first 24 h.

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.

SUMMARY This is the first report of human gastrointestinal arachidonate and prostanoids measured quantitatively by gas chromatography-mass spectrometry (GC-MS) The methods for gas chromatography-mass spectrometry (GC-MS) were as reported previously.' In brief, the dried extract obtained as described above was dissolved in dichloromethane. An aliquot was taken for GC-MS and further purified by LH20 column chromatography; non-polar impurities were eluted with dichloromethane, and the eicosanoids were eluted with methanol which was then evaporated. Deuterated standards were added, and each dried methanol extract was dissolved in doubledistilled water acidified to pH 3 with hydrochloric acid. Each solution was percolated through an Amberlite column which was then washed with distilled water, and the eicosanoids were eluted with 315 on 11 May 2018 by guest. Protected by copyright.

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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