[en] Full text: Exposure of the skin of mice and men to increasing doses of UV radiation causes erythema, blistering, accelerated photoageing, DNA lesions and photocarcinogenesis. Moderate exposure also suppresses T cell-mediated immune function, a defect which is a prerequisite for the promotion or outgrowth phase of the UV-initiated tumour, and which is accompanied by dysregulated cutaneous cytokine patterns. A major cutaneous photoreceptor for the immunosuppression is epidermal urocanic acid (UCA). Naturally occurring trans-UCA photoisomerises in the stratum corneum and epidermis to cis-UCA, in a direct reaction. Cis-UCA has been found to have local and systemic immunosuppressive properties. The action spectrum for the photoimmuno-suppression is maximal in the UVB (280 320nm) waveband. However longer wavelength UVA (320-400nm), which interacts with skin predominantly via oxidative reactions, is not immunosuppressive at environmental exposure doses, and unexpectedly can provide protection from UVB-immunosuppression. We find that UVA protective exposure prevents the major UVB-alterations to the cytokine array. In addition, UVA (but not UVB) exposure induces cutaneous haem oxygenase (HO) activity, an endogenous antioxidant enzyme. HO is known to be redox-regulated, and to be the major stress protein induced in cultured fibroblasts by UVA. We find that UVA-immune protection is dependent on the induced HO; that enhanced HO activity following UVA is cytokine-dependent; and that the induced HO acts by inhibiting the immunosuppressive potential of cis-UCA. Thus oxidant states resulting predominantly from UVA irradiation, while apparently immunologically innocuous, seem to actively upregulate this defensive HO response. These studies have therefore revealed interactions between different UV wavebands important for immune regulation both in the skin and systemically, which may have a critical bearing on the carcinogenic outcome in chronically exposed skin, and offer the possibility of utilising the UVA waveband for more effective photoprotection in humans

[en] Lyophilized aged garlic extract has been incorporated at concentrations of 0.1%, 1% and 4% by weight into semi purified powdered diets and fed to hairless mice. Under moderate UVB exposure conditions resulting in 58% suppression of the systemic contact hypersensitivity response in control-fed mice, a dose-responsive protection was observed in the garlic-fed mice; contact hypersensitivity in the UVB-exposed mice fed 4% garlic extract was suppressed by only 19%. If the UVB exposure was replaced by topical application of one of a series of lotions containing increasing concentrations of cis-urocanic acid, a dose-responsive suppression of contact hypersensitivity was demonstrated in control-fed mice (urocanic acid at 25, 50, 100 and 200 micrograms per mouse resulting in 22-46% suppression). Mice fed a diet containing 1% aged garlic extract were partially protected from cis-urocanic acid-induced suppression of contact hypersensitivity, with greater protection from the lower concentrations of urocanic acid. Mice fed a diet containing 4% aged garlic extract were protected from all concentrations of urocanic acid. The results indicate that aged garlic extract contains ingredient(s) that protect from UVB-induced suppression of contact hypersensitivity and suggest that the mechanism of protection is by antagonism of the cis-urocanic acid mediation of this form of immunosuppression