Toggle Main Menu Toggle Search

Open Access padlockePrints

The eicosanoid response to high dose UVR exposure of individuals prone and resistant to sunburn

Lookup NU author(s): Professor Anthony Thody


Full text for this publication is not currently held within this repository. Alternative links are provided below where available.


High personal UVR doses can be gained during leisure activities, causing intense self-resolving inflammation (sunburn) of unprotected skin. UVR activates release of membrane fatty acids and upregulates their metabolism by cyclooxygenases (COX) and lipoxygenases (LOX) to different eicosanoids. While COX-derived prostaglandin (PG)E-2 is a potent mediator of sunburn vasodilatation, LOX-derived 15-hydroxyeicosatetraenoic acid (HETE) and its lipoxin metabolites may contribute to sunburn limitation. We explored the relationships between expression of these lipid mediators and the clinical and histological outcomes, comparing responses of individuals prone and more resistant to sunburn. An acute UVR exposure of 12 SED (standard erythema dose) was applied to buttock skin of 32 white Caucasians (n = 16 phototype I/II, n = 16 phototype III/IV), and over the subsequent 72 h assessments were made of skin erythema, immunohistochemical expression of leukocyte markers, COX-2, 12-LOX, 15-LOX and nitric oxide synthase (NOS), and eicosanoid levels by LC/ESI-MS/MS. Evidence of a significant inflammatory response was seen earlier in phototype I/II with regard to expression of erythema (4h, p < 0.001), neutrophil infiltration (24 h, p = 0.01), epidermal COX-2 (24 h, p < 0.05) and 12-LOX (24 h, p < 0.01), and dermal eNOS (24 h, p < 0.05) proteins, although CD3+ lymphocyte infiltration showed an earlier increase in phototype III/IV (24 h, p < 0.05). Although erythema was equivalent at 72 h in both groups, phototype I/II showed higher PGE(2) accompanied by elevated 15-HETE, and a strong positive correlation was seen between these mediators (n = 18, r = 0.805, p = 0.0001). Hence anti-inflammatory eicosanoid 15-HETE may temper the pro-inflammatory milieu in sunburn, having greater influence in those prone to sunburn than those more resistant, given the same high UVR exposure conditions.

Publication metadata

Author(s): Nicolaou A, Masoodi M, Gledhill K, Haylett AK, Thody AJ, Tobin DJ, Rhodes LE

Publication type: Article

Publication status: Published

Journal: Photochemical & Photobiological Sciences

Year: 2012

Volume: 11

Issue: 2

Pages: 371-380

Print publication date: 16/12/2011

ISSN (print): 1474-905X

ISSN (electronic): 1474-9092

Publisher: Royal Society of Chemistry


DOI: 10.1039/c1pp05272a


Altmetrics provided by Altmetric


Funder referenceFunder name
Manchester Academic Health Sciences Centre (MAHSC)
NIHR Manchester Biomedical Research Centre
WT077714Wellcome Trust