title: Vitamin C abrogates the deleterious effects of UVB radiation on cutaneous immunity by a mechanism that does not depend on TNF-alpha.
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.
authors.affiliation: Schepens Eye Research Institute and Department of Dermatology, Harvard Medical School, Boston, Massachusetts 02114, U.S.A.
authors.forename: T
authors.initials: T
authors.lastname: Nakamura
authors.forename: S R
authors.initials: SR
authors.lastname: Pinnell
authors.forename: D
authors.initials: D
authors.lastname: Darr
authors.forename: I
authors.initials: I
authors.lastname: Kurimoto
authors.forename: S
authors.initials: S
authors.lastname: Itami
authors.forename: K
authors.initials: K
authors.lastname: Yoshikawa
authors.forename: J W
authors.initials: JW
authors.lastname: Streilein
mesh_terms: D000818:Animals; D001205:Ascorbic Acid / Q000627:therapeutic use*; D003877:Dermatitis, Contact / Q000209:etiology / Q000517:prevention & control; D007108:Immune Tolerance / Q000187:drug effects / Q000528:radiation effects; D051379:Mice; D008809:Mice, Inbred C3H; D011833:Radiation Injuries, Experimental / Q000209:etiology* / Q000517:prevention & control*; D012867:Skin / Q000276:immunology* / Q000528:radiation effects; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology*; D014466:Ultraviolet Rays / Q000009:adverse effects*
chemical_list: D014409:Tumor Necrosis Factor-alpha; D001205:Ascorbic Acid