ascorbic-acid and Dermatitis--Contact

A multi-clinical double-blind study on therapeutic effect of combination preparation of vitamins E and C was undertaken in comparison with single preparation of vitamin E and vitamin C in the treatment of chloasma or pigmented contact dermatitis (PCD). Combination treatment resulted in significantly better clinical improvement than vitamin C alone in both diseases. Objective data compiled from color difference measurements and color photographs revealed significantly better results with combination treatment in chloasma than vitamin C alone and, in PCD, than vitamin E or C alone. Differences in skin luminosity between hyperpigmented and normal areas significantly decreased in all three groups, with the combination group producing the most significant change. The total serum lipoperoxide level and its ratio to total serum lipids tended to decline in the combination group, and decreased significantly in vitamin E group. The sebum lipoperoxide level decreased significantly only in the combination group (EC).

Topics: alpha-Tocopherol; Ascorbic Acid; Clinical Trials as Topic; Dermatitis, Contact; Double-Blind Method; Drug Therapy, Combination; Humans; Lipid Metabolism; Lipid Peroxides; Melanosis; Photography; Sebum; Skin Pigmentation; Tocopherols; Vitamin E

Topics: Aged, 80 and over; Ascorbic Acid; Dermatitis, Atopic; Dermatitis, Contact; Dietary Fats; Excipients; Glycyrrhetinic Acid; Humans; Male; Palmitates; Plant Extracts; Skin Cream

The skin sensitizer 2,4-dinitrofluorobenzene (DNFB) provokes delayed hypersensitivity responses as a result of topical application to the skin. Here, we demonstrate that DNFB modifies proteins in RAW 264.7 cells and skin tissues in NC/Nga mice; we also show the functional involvement of DNFB-induced modification of cellular proteins in the DNFB-induced macrophage inflammatory protein (MIP)-2 gene expression in RAW 264.7 cells. In addition, we demonstrate that DNFB strongly induces reactive oxygen species (ROS) production. Our RT-PCR analysis and reporter gene assays reveal that the DNFB-induced intracellular ROS production is necessary for MIP-2 gene expression by DNFB. We observed that the vitamin C and chemical oxidant scavenger N-acetyl-cysteine have an inhibitory effect on the generation of ROS, the activation of MAP kinase pathways, and the MIP-2 gene expression in DNFB-treated RAW 264.7 cells. These results provide insight into the mechanisms involved in DNFB-induced contact hypersensitivity.

Topics: Acetylcysteine; Animals; Ascorbic Acid; Cell Line; Cell Survival; Chemokine CXCL2; Dermatitis, Contact; Dinitrofluorobenzene; Free Radical Scavengers; Gene Expression; Hypersensitivity, Delayed; Mice; Mitogen-Activated Protein Kinases; Peroxidase; Proteins; Reactive Oxygen Species; Skin; Vitamins

Exposure of C3HBYB/Wq hairless (hr/hr) mice to ultra-violet radiation (UVR) for 15 days induced intense tanning of their dorsal skin. Small, dark freckles appeared first, gradually enlarging and coalescing as treatment progressed yielding a uniform tan. Histologically, the gross changes in skin color were matched initially by the appearance of scattered epidermal melanocytes that subsequently proliferated to form discrete, progressively expanding and abutting populations resulting in a uniform melanocyte network throughout the basal layer of the interfollicular epidermis. In contrast, when applied topically before each daily exposure to UVR, a cream or lotion vehicle containing both vitamins C and E (Vits C/E) inhibited UVR-induced erythema and tanning. Application of Vits C/E, both before and after irradiation, was no more effective in providing photoprotection than pre-treatment only. At the tissue level, UVR-induced proliferation and melanogenesis of melanocytes were reduced compared with irradiated controls. The density of individual melanocyte populations was reduced, as was the number of melanocyte populations achieving merger (confluence) with others. Confluence grades and cell counts, estimating the maximum density of melanocyte populations in UVR-Vits C/E-treated mice, were approximately two thirds those of UVR-vehicle-treated controls. However, tanning was only one fifth that of UVR-vehicle-treated controls, suggesting that melanogenesis was also inhibited. In addition to its inhibitory actions on irradiated melanocytes, Vits C/E also inhibited UVR-induced suppression of contact hypersensitivity (CHS) in haired (Hr/hr) and hr/hr mice of the C3HBYB/Wq strain. The common denominators for most, if not all, of the influences of topically-applied Vits C/E in muting the responses of the melanocyte and immune systems to UVR may stem from the vitamins' combined ability to suppress UVR-stimulated inflammation and its associated cascade of mediators.

Topics: Administration, Topical; Animals; Antioxidants; Ascorbic Acid; Cell Division; Dermatitis, Contact; Epidermal Cells; Epidermis; Erythema; Immunosuppression Therapy; Melanins; Melanocytes; Mice; Mice, Hairless; Mice, Inbred C3H; Ultraviolet Rays; Vitamin E

Reactive oxygen species are involved in UV-induced suppression of the immune system. Topical treatment with the antioxidant vitamins C (L-ascorbic acid, ASC) and E (D-alpha-tocopherol, TOC) can support the endogenous antioxidant defence system and prevent immunosuppression.. Mice were topically treated with a single dose of ASC, TOC or a combination and irradiated with UVB. Then systemic immunosuppression was measured using a model based on the induction of a contact hypersensitivity response to dinitrofluorobenzene. To investigate the mechanism of protection, cis-urocanic acid-induced immunosuppression was investigated in a different contact hypersensitivity model measuring local immunosuppression. The levels of ASC and TOC in the epidermis were determined by HPLC.. Both ASC and TOC prevented UV-induced suppression of the contact hypersensitivity response. TOC was effective at doses of 2.5 to 10 nmol/cm2 and ASC at 0.5 to 5 micromol/cm2. At the highest dose, the response in the ASC-treated mice was no longer significantly different from that in the positive control group. Contrary to expectations, combinations of the two compounds did not provide additional protection. The experiments with ASC or TOC against immunosuppression by cis-urocanic acid also yielded protection, but this was less efficient than against UV. The concentrations of ASC and TOC in the epidermis were so low that UVB absorption could be excluded as the cause of the protection.. ASC and TOC can be used to prevent systemic UV-induced immunosuppression. They are effective at relatively low doses after a single topical application prior to the irradiation.

Topics: Animals; Antioxidants; Ascorbic Acid; Dermatitis, Contact; Dose-Response Relationship, Drug; Immune Tolerance; Male; Mice; Mice, Inbred BALB C; Skin; Ultraviolet Rays; Urocanic Acid; Vitamin E

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.

Topics: Animals; Ascorbic Acid; Dermatitis, Contact; Immune Tolerance; Mice; Mice, Inbred C3H; Radiation Injuries, Experimental; Skin; Tumor Necrosis Factor-alpha; Ultraviolet Rays

Topics: Ascorbic Acid; Chromates; Dermatitis, Contact; Dermatitis, Occupational; Humans; Male; Middle Aged; Ointments; Potassium Dichromate; Technology, Radiologic; Workforce

Firstly we showed the reason for the choice of each product used in the preparation of this cosmetic. After this we studied "in vitro" the effect of this preparation, and "in vivo" in 25 patients sensitive to Potassium dichromate. On seeing the null effect of this preparation, owing to the oxidation of ascorbic acid, on these 25 patients, we modified the formula, substituting the ascorbic acid and EDTA, respectively, for tartaric acid and glycine. The respective tests "in vitro" and "in vivo" on 20 patients, this time showed beneficial effect of this preparation in 60% of the patients tested. Of these 60%, a 25% have continue to work exposed to the allergen (dichromate or nickel) and the other 35% have continue working with lesions controlled by habitual topic therapy. This preparation can also be used, with less effect, for nickel.

Topics: Administration, Topical; Ascorbic Acid; Chromium; Cosmetics; Dermatitis, Contact; Dermatitis, Occupational; Edetic Acid; Humans; Nickel; Silicones

A case of vitamin C allergy of the delayed type is reported. Eczematous skin lesions appeared during normal uptake of the vitamin C contained in food. After a vitamin C-free diet, the skin lesions disappeared. Patch tests and an oral exposure with vitamin C gave positive reactions. This observation of vitamin C allergy is compared with previous published cases.

Topics: Ascorbic Acid; Dermatitis, Contact; Eczema; Fluocortolone; Humans; Male; Middle Aged

Topics: Ascorbic Acid; Chromates; Dermatitis; Dermatitis, Contact; Dermatitis, Occupational; Eczema; Edetic Acid; Female; Humans; Ion Exchange; Male; Ointments; Skin Tests; Switzerland

Topics: Ascorbic Acid; Chromium; Dermatitis, Contact

Topics: Acne Vulgaris; Adolescent; Amino Acids; Ascorbic Acid; Dermatitis; Dermatitis, Contact; Dermatology; Drug Eruptions; Eczema; Erythema; Glutamates; Melanosis; Neurodermatitis; Pantothenic Acid; Polyarteritis Nodosa; Psoriasis; Tablets; Tiopronin; Toxicology; Urticaria

Topics: Aniline Compounds; Ascorbic Acid; Chromium; Coloring Agents; Dermatitis; Dermatitis, Contact; Humans; Turpentine; Vitamins

Topics: Acne Vulgaris; Ascorbic Acid; Dermatitis; Dermatitis, Contact; Humans; Oils; Sebaceous Gland Diseases; Vitamin A; Vitamins

Topics: Ascorbic Acid; Biomedical Research; Dermatitis; Dermatitis, Contact; Humans; Rhus; Toxicodendron