Green tea catechins (GTC) reduce UV radiation (UVR)-induced inflammation in experimental models, but human studies are scarce and their cutaneous bioavailability and mechanism of photoprotection are unknown. We aimed to examine oral GTC cutaneous uptake, ability to protect human skin against erythema induced by a UVR dose range and impact on potent cyclo-oxygenase-and lipoxygenase-produced mediators of UVR inflammation, PGE 2 and 12-hydroxyeicosatetraenoic acid (12-HETE), respectively. In an open oral intervention study, sixteen healthy human subjects (phototype I/II) were given low-dose GTC (540 mg) with vitamin C (50 mg) daily for 12 weeks. Preand post-supplementation, the buttock skin was exposed to UVR and the resultant erythema quantified. Skin blister fluid and biopsies were taken from the unexposed and the UVR-exposed skin 24 h after a pro-inflammatory UVR challenge (three minimal erythema doses). Urine, skin tissue and fluid were analysed for catechin content and skin fluid for PGE 2 and 12-HETE by liquid chromatography coupled to tandem MS. A total of fourteen completing subjects were supplement compliant (twelve female, median 42·5 years, range 29-59 years). Benzoic acid levels were increased in skin fluid post-supplementation (P¼0·03), and methylated gallic acid and several intact catechins and hydroxyphenyl-valerolactones were detected in the skin tissue and fluid. AUC analysis for UVR erythema revealed reduced response post-GTC (P¼0·037). Pre-supplementation, PGE 2 and 12-HETE were UVR induced (P¼ 0·003, 0·0001). After GTC, UVR-induced 12-HETE reduced from mean 64 (SD 42) to 41 (SD 32) pg/ml (P¼0·01), while PGE 2 was unaltered. Thus, GTC intake results in the incorporation of catechin metabolites into human skin associated with abrogated UVR-induced 12-HETE; this may contribute to protection against sunburn inflammation and potentially longer-term UVR-mediated damage.Key words: Green tea catechins: Bioavailability: Skin: 12-Hydroxyeicosatetraenoic acid UV radiation (UVR) in sunlight is a key environmental stressor that makes an impact on skin health. Acute effects include sunburn (an inflammatory response), immune suppression and photosensitivity, while repeated exposures lead to photoageing and photocarcinogenesis (1) . Sunburn is characterised clinically by erythema due to vasodilatation and, histologically, a dermal infiltrate of neutrophils and mononuclear cells is observed (2,3) . Activation of cutaneous phospholipase A 2 by UVR is a key part of the inflammatory response, releasing membrane-esterified fatty acids, including arachidonic acid, which is subsequently metabolised by cyclo-oxygenase (COX), lipoxygenase (LOX) and cytochrome P450 isozymes to produce eicosanoids with vasodilatory and chemoattractant properties (4) . Potent pro-inflammatory mediators, PGE 2 and 12-hydroxyeicosatetraenoic acid (12-HETE), are the most abundant eicosanoids at the peak of the sunburn response, correlating with UVR upregulated expression of COX-2 and 12-LOX in human skin (4) .Polyphenols are plant-der...