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Ultraviolet-B-induced erythema is mediated by nitric oxide and prostaglandin E2 in combination

Ultraviolet-B-induced erythema is mediated by nitric oxide and prostaglandin E2 in combination
Ultraviolet-B-induced erythema is mediated by nitric oxide and prostaglandin E2 in combination
Ultraviolet-B-induced erythema (one, two, or four times the minimal erythema dose) was reduced but not abolished by application of 1% indomethacin gel immediately after irradiation of human skin. Continuous synthesis of prostaglandins is reflected by similar levels of indomethacin-mediated inhibition of erythema at any time within 48 h after irradiation. Repeated applications of indomethacin did not increase the inhibition. Twenty-four hours after irradiation with four minimal erythema doses, mean prostaglandin E2 levels in suction blisters were 27.2 ng per ml (SEM 11) compared with 8.6 ng per ml in unirradiated skin (n = 25; p < 0.01). Prosta glandin E2 levels in dermal tissues, sampled by microdialysis (depth 0.6 +/- 0.1 mm), were 310 pg per ml (SEM 123) and 237 pg per ml (SEM 88) in irradiated and unirradiated skin, respectively (n = 7, n.s.). Nitric oxide also made a significant contribution to ultraviolet-B-induced erythema. Ultraviolet erythema was inhibited by L-NAME in a dose-related fashion with 2 mM L-NAME causing total abolition of the response. L-NAME was effective at all time points up to 48 h suggesting that NO was produced continuously. NO was undetectable in suction blister fluid but in dermal microdialysate NO was present at 44.3 ng per ml (SEM 6.2) following ultraviolet B compared with 26.0 ng per ml (SEM 8.0) in unirradiated skin (p < 0.05), approximately 1000 times the molar concentration of prostaglandin E2. These findings confirm prostaglandin E2 and NO to be mediators of ultraviolet-induced erythema. They also show that there is prolonged synthesis of both mediators within the erythemal response and that synthesis of NO is induced by lower doses of ultraviolet B compared with that of prostaglandin E2.
Abbreviations: COX, cyclo-oxygenase; NOS, nitric oxide synthase
indomethacin, L-NAME, microdialysis, nitric oxide, prosta glandin E2
0022-202X
880-885
Rhodes, L.E.
3a291b8d-eb3e-4989-a8da-b7f2a99010ca
Belgi, G.
17ddcd76-ce91-414d-b573-08dd4950b0d4
Parslew, R.
e0e7492a-817b-4097-a7d5-618f9025648a
McLoughlin, L.
1c7d973a-81e6-4da8-ad17-d965fb6fa195
Clough, G.F.
9f19639e-a929-4976-ac35-259f9011c494
Friedmann, P.S.
d50bac23-f3ec-4493-8fa0-fa126cbeba88
Rhodes, L.E.
3a291b8d-eb3e-4989-a8da-b7f2a99010ca
Belgi, G.
17ddcd76-ce91-414d-b573-08dd4950b0d4
Parslew, R.
e0e7492a-817b-4097-a7d5-618f9025648a
McLoughlin, L.
1c7d973a-81e6-4da8-ad17-d965fb6fa195
Clough, G.F.
9f19639e-a929-4976-ac35-259f9011c494
Friedmann, P.S.
d50bac23-f3ec-4493-8fa0-fa126cbeba88

Rhodes, L.E., Belgi, G., Parslew, R., McLoughlin, L., Clough, G.F. and Friedmann, P.S. (2001) Ultraviolet-B-induced erythema is mediated by nitric oxide and prostaglandin E2 in combination. Journal of Investigative Dermatology, 117 (4), 880-885. (doi:10.1046/j.0022-202x.2001.01514.x).

Record type: Article

Abstract

Ultraviolet-B-induced erythema (one, two, or four times the minimal erythema dose) was reduced but not abolished by application of 1% indomethacin gel immediately after irradiation of human skin. Continuous synthesis of prostaglandins is reflected by similar levels of indomethacin-mediated inhibition of erythema at any time within 48 h after irradiation. Repeated applications of indomethacin did not increase the inhibition. Twenty-four hours after irradiation with four minimal erythema doses, mean prostaglandin E2 levels in suction blisters were 27.2 ng per ml (SEM 11) compared with 8.6 ng per ml in unirradiated skin (n = 25; p < 0.01). Prosta glandin E2 levels in dermal tissues, sampled by microdialysis (depth 0.6 +/- 0.1 mm), were 310 pg per ml (SEM 123) and 237 pg per ml (SEM 88) in irradiated and unirradiated skin, respectively (n = 7, n.s.). Nitric oxide also made a significant contribution to ultraviolet-B-induced erythema. Ultraviolet erythema was inhibited by L-NAME in a dose-related fashion with 2 mM L-NAME causing total abolition of the response. L-NAME was effective at all time points up to 48 h suggesting that NO was produced continuously. NO was undetectable in suction blister fluid but in dermal microdialysate NO was present at 44.3 ng per ml (SEM 6.2) following ultraviolet B compared with 26.0 ng per ml (SEM 8.0) in unirradiated skin (p < 0.05), approximately 1000 times the molar concentration of prostaglandin E2. These findings confirm prostaglandin E2 and NO to be mediators of ultraviolet-induced erythema. They also show that there is prolonged synthesis of both mediators within the erythemal response and that synthesis of NO is induced by lower doses of ultraviolet B compared with that of prostaglandin E2.
Abbreviations: COX, cyclo-oxygenase; NOS, nitric oxide synthase

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More information

Published date: 2001
Keywords: indomethacin, L-NAME, microdialysis, nitric oxide, prosta glandin E2

Identifiers

Local EPrints ID: 27366
URI: http://eprints.soton.ac.uk/id/eprint/27366
ISSN: 0022-202X
PURE UUID: 9d99a5cd-adbc-4161-96ec-cb601402157e
ORCID for G.F. Clough: ORCID iD orcid.org/0000-0002-6226-8964

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Date deposited: 28 Apr 2006
Last modified: 16 Mar 2024 02:54

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Contributors

Author: L.E. Rhodes
Author: G. Belgi
Author: R. Parslew
Author: L. McLoughlin
Author: G.F. Clough ORCID iD
Author: P.S. Friedmann

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