No abstract

Ultraviolet radiation damage to the skin is due, in part, to the generation of reactive oxygen species. Vitamin C (L-ascorbic acid) functions as a biological co-factor and antioxidant due to its reducing properties. Topical application of vitamin C has been shown to elevate significantly cutaneous levels of this vitamin in pigs, and this correlates with protection of the skin from UVB damage as measured by erythema and sunburn cell formation. This protection is biological and due to the reducing properties of the molecule. Further, we provide evidence that the vitamin C levels of the skin can be severely depleted after UV irradiation, which would lower this organ's innate protective mechanism as well as leaving it at risk of impaired healing after photoinduced damage. In addition, vitamin C protects porcine skin from UVA-mediated phototoxic reactions (PUVA) and therefore shows promise as a broad-spectrum photoprotectant.

No abstract

No abstract

Acute low-dose treatment of murine skin with ultra violet B (UVB) light impairs induction of contact hypersensitivity (CH) to dinitrofluorobenzene (DNFB) in certain inbred strains of mice (termed UVB-susceptible), but not in others (termed UVB-resistant), and promotes tolerance. These deleterious effects of ultraviolet radiation (UVR) are mediated in part by TNF-alpha, which is released from UVR-exposed epidermal and dermal cells. Because UVR damage to skin has also been ascribed in part to the generation of reactive oxygen intermediates (ROIs) such as superoxide anion (O2-), hydrogen peroxide (H2O2), hydroxyl radical (OH-), and singlet oxygen ((1)O2), we investigated whether vitamin C (ascorbic acid), which can nullify ROIs, prevents the deleterious effects of UVR on the cutaneous immune system. We found that epicutaneous application of vitamin C (10% L-ascorbic acid solution) abrogated the deleterious effects of acute low-dose UVR on induction of CH and prevented the induction of tolerance. Vitamin C, however, did not reverse the effects of TNF-alpha on CH induction and tolerance. These results indicate that (i) ROIs generated intracutaneously by UVR contribute to the impaired ability of exposed skin to support the induction of CH and to promote the induction of tolerance and (ii) these effects are not dependent on TNF-alpha.

No abstract

No abstract

No abstract