紫外线辐射减低表皮中谷胱甘肽的含量

DEPLETION OF CUTANEOUS GLUTATHIONE BY ULTRAVIOLET RADIATION†

Supplemental antioxidants may have a role in ameliorating or preventing the actinic damage that can lead to cutaneous disorders such as skin cancer, hyper pigmentation, premature aging. Glutathione is an ant endogenous antioxidant fulfills various protective functions in the skin. Irradiation of hairless mice with short (UVB) or long (UVA) wavelength ultraviolet radiation or with UVA combined with a photosensitizing psoralen (PUVA) can deplete skin glutathione levels. Ultraviolet B irradiation causes rapid transient fluctuations in the epidermal glutathione level the relative amount present as the oxidized form. Ultraviolet A irradiation can deplete epidermal dermal glutathione for several hours but requires much higher doses than UVB. PUVA treatments may lead to extensive prolonged depletions of epidermal dermal glutathione, the severity of which is dependent on the psoralen dose may last for several days. These transient depletions, oxidations, sometimes rapid recoveries of cutaneous glutathione levels are compatible with a role for glutathione as an endogenous photoprotective agent in the skin. erimental evidence supports such a role: for example severe skin edema develops in mice only after about 50% of the glutathione has been depleted by PUVA treatment. Although different mechanisms are involved in each case, glutathione depletion may contribute to the production of phototoxicity by UVB, UVA, by PUVA. Understing the depletion mechanisms may allow the development of strategies aimed at preventing loss of cutaneous glutathione, at reinforcing the natural protective functions of this critical cell component.