ascorbic-acid and Dermatitis--Allergic-Contact

Repeated topical exposure to chromium(VI) may cause an allergic contact dermatitis or the formation of chrome ulcers. Systemic toxicity may occur following the ingestion of a chromium(VI) salt, from chromium(VI)-induced skin burns, or from inhalation of chromium(VI) occurring occupationally. Soluble chromium(VI) salts are usually absorbed more easily and cross cell membranes more readily than trivalent chromium salts, and, therefore chromium(VI) is more toxic than chromium(III). In experimental studies, endogenous ascorbic acid in rat lung, liver, and kidney and human plasma, effectively reduces chromium(VI) to chromium(III). The administration of exogenous ascorbic acid has been advocated therefore in the treatment of systemic chromium poisoning and chromium dermatitis to enhance the extracellular reduction of chromium(VI) to the less bioavailable chromium(III).. In vitro experiments confirm that the addition of ascorbic acid to plasma containing chromium(VI) leads to a dose-dependent reduction of chromium(VI) to chromium(III). In animal studies, parenteral ascorbic acid 0.5-5 g/kg significantly reduced chromium-induced nephrotoxicity when administered 30 minutes before parenteral sodium dichromate and up to 1 hour after parenteral sodium chromate dosing. Parenteral ascorbic acid 0.5-5 g/kg also reduced mortality when given orally up to 2 hours after oral potassium dichromate dosing. However, the administration of parenteral ascorbic acid more than 2 hours after parenteral chromate in these experimental studies did not protect against renal damage, and parenteral ascorbic acid given 3 hours postparenteral chromate increased toxicity. In addition, there is no confirmed clinical evidence that the administration of ascorbic acid lessens morbidity or mortality in systemic chromium poisoning. A possible reason for the lack of benefit of ascorbic acid when administration is delayed, is that chromium(VI) cellular uptake has occurred prior to ascorbic acid administration. Topical 10% ascorbic acid has been claimed to reduce significantly the healing time of experimentally induced chrome ulcers in guinea pigs. The proposed mechanism is reduction on the skin surface of chromium(VI) to chromium(III). Several case reports suggest that topical ascorbic acid is effective in the management of chromium dermatitis but this has not been confirmed in controlled clinical trials and, moreover, the practical difficulties of frequent application are likely to limit its usefulness.. Based on experimental studies, substantial amounts of ascorbic acid would need to be administered, preferably parenterally, soon after exposure to prevent systemic toxicity from chromium(VI) in humans. However, as ascorbic acid is a metabolic precursor of oxalate, the administration of ascorbic acid in high dose could lead to acute oxalate nephropathy, particularly in the presence of renal failure. While smaller doses of ascorbic acid (e.g., 10 g intravenously) are not toxic, such doses probably will not reduce the mortality from systemic chromium poisoning.. There is currently insufficient evidence to advocate the use of ascorbic acid in the management of systemic chromium toxicity. Topical ascorbic acid may reduce dermal hexavalent chromium exposure, but this observation must be confirmed in controlled studies.

Topics: Animals; Antidotes; Ascorbic Acid; Chromium; Dermatitis, Allergic Contact; Humans

Topics: Ascorbic Acid; Cosmetics; Dermatitis, Allergic Contact; Humans; Patch Tests

Topics: Adult; Allergens; Ascorbic Acid; Cosmetics; Dermatitis, Allergic Contact; Female; Humans; Patch Tests

Topics: Aged; Antirheumatic Agents; Arthritis, Rheumatoid; Ascorbic Acid; Dermatitis, Allergic Contact; Erythema; Etanercept; Facial Dermatoses; Female; Humans; Immunosuppressive Agents; Methotrexate; Patch Tests; Skin Cream

Topics: Ascorbic Acid; Cosmetics; Dermatitis, Allergic Contact; Facial Dermatoses; Female; Humans; Middle Aged; Patch Tests; Skin Lightening Preparations

An allergic contact reaction is accompanied by high oxidative stress in the skin. Pretreatment of the skin with antioxidative substances could reduce the elicitation reaction.. To investigate, in a proof-of-principle study, whether pretreatment of the skin with the antioxidant ascorbic acid reduces the elicitation reaction to a p-phenylenediamine (PPD)-containing hair dye in sensitized subjects.. Twelve subjects with contact allergy to PPD, a documented skin reaction to a hair dye simulation exposure model and a history of hair dye-related skin complaints were included in this study. Skin areas on the forearms were, in a left versus right design, exposed to an emulsion with ascorbic acid and an emulsion without ascorbic acid, and then to a 2% PPD-containing hair dye testing formulation. In addition, control areas were exposed to the emulsions and to the PPD-containing hair dye formulation without pretreatment. Skin reactions were graded on day (D)2 and D3.. Pretreatment with ascorbic acid emulsion resulted in a reduction in the elicitation reaction in 7 of 12 subjects at D3 (p = 0.046). No statistically significant difference was observed at D2.. Pretreatment of the skin with the antioxidant ascorbic acid had an attenuating effect on the elicitation reaction to PPD in sensitized individuals.

Topics: Adolescent; Adult; Aged; Antioxidants; Ascorbic Acid; Coloring Agents; Dermatitis, Allergic Contact; Female; Humans; Male; Middle Aged; Oxidative Stress; Patch Tests; Phenylenediamines; Premedication; Skin; Young Adult

Hair dyes represent one of the most important causes of allergic contact dermatitis resulting from the use of cosmetic products. The principal causative chemistry is associated with oxidation products of p-phenylenediamine (PPD) and closely related substances.. To examine whether prior application of the antioxidant vitamin C to the skin was able to reduce the cutaneous allergic response to PPD.. Twenty eight volunteers with a proven history of contact allergy to PPD were recruited. Each was tested with a range of PPD doses and PPD-containing hair dye on untreated skin and skin pretreated for 10 min with a vitamin C formulation.. Pretreatment of skin sites with vitamin C led to a reduction in the intensity, or even ablation, of the cutaneous allergic reaction to PPD in ∼75% of cases as compared with untreated skin.. The results suggest that treatment of the skin adjacent to the hair-bearing area with antioxidant could form part of a strategy to reduce the burden of cosmetic allergic contact dermatitis caused by hair dyeing.

Topics: Antioxidants; Ascorbic Acid; Coloring Agents; Dermatitis, Allergic Contact; Hair Dyes; Humans; Patch Tests; Phenylenediamines; Premedication; Severity of Illness Index

Topics: Aged; Ascorbic Acid; Dermatitis, Allergic Contact; Female; Glycyrrhiza; Humans; Patch Tests; Plant Extracts; Skin Lightening Preparations

Topics: Ascorbic Acid; Dermatitis, Allergic Contact; Facial Dermatoses; Female; Humans; Middle Aged; Molecular Structure; Patch Tests; Skin Absorption; Skin Lightening Preparations

Topics: Ascorbic Acid; Dermatitis, Allergic Contact; Dermatologic Agents; Female; Humans; Middle Aged; Palmitates; Patch Tests

We investigated whether the oxidative stress (OS) caused by skin inflammation could reflect in the blood, in a 21-year-old female student sensitized to nickel, colophony and abitole with often relapsing allergic contact dermatitis (ACD). As glutathione redox ratio was increased in the blood not only during the relapse but also in the beginning of remission phase, we prescribed natural medical preparations of d-alpha-tocopherol (in the first week 100 mg three times a day followed by 100 mg/day) and ascorbic acid (200 mg/day) for 25 days to her. After using antioxidants in the remission period, one of the principal OS markers-the glutathione redox ratio reached the normal physiological level. In this report, we showed that during acute extensive ACD OS is expressed in the blood and simultaneous supplementation of d-alpha-tocopherol and ascorbic acid might reduce systemic OS.

Topics: Adult; alpha-Tocopherol; Antioxidants; Ascorbic Acid; Dermatitis, Allergic Contact; Female; Glutathione; Humans; Oxidative Stress

Topics: Aging; Antioxidants; Ascorbic Acid; Cosmetics; Dermatitis, Allergic Contact; Female; Humans; Middle Aged; Ointments; Patch Tests

A possible free radical mechanism in metal allergy was investigated in peripheral blood mononuclear cell (PBMC) cultures from 6 subjects, contact allergic to Ni2+ and Co2+, and 6 control individuals. Ni2+ and Co(2+)-mediated free radical generation was studied with electron spin resonance spectroscopy. The immune response was characterized by cellular [methyl-3H]thymidine uptake and interferon-gamma (IFN-gamma) production Ni2+ and Co2+ (10-50 microM) significantly increased lymphocyte proliferation and IFN-gamma production in PBMC cultures from contact allergic subjects in comparison with cultures from controls. Inhibition of Co(2+)-mediated free radical generation by ascorbic acid did not influence cellular [methyl-3H]thymidine uptake and IFN production. Detectable amounts of free radicals were not obtained with Ni2+. We therefore conclude that it is unlikely that free radicals are involved in contact allergy to Ni2+ and Co2+.

Topics: Adult; Ascorbic Acid; Case-Control Studies; Cell Culture Techniques; Copper; Dermatitis, Allergic Contact; Electron Spin Resonance Spectroscopy; Female; Free Radicals; Humans; Interferon-gamma; Middle Aged; Monocytes; Nickel; Patch Tests

The generation of free radicals by Ni(2+) and Co(2+) was studied at physiological pH in H(2)O(2)-containing solutions in the absence and presence of various radical-mediating ligands and in human peripheral blood mononuclear cell (PBMC) cultures. With ESR spectroscopy, free radical species were identified and quantitated by spin trapping with 5,5-dimethyl-1-pyrroline-N-oxide (DMPO). Co(2+) generated hydroxyl radicals from H(2)O(2) in PBS solutions containing glutathione (GSH) or histidine (His). Omission of GSH or His from the reaction mixture significantly reduced the ESR-signal, indicating the importance of metal-chelation in free radical generation. Carnosine did not significantly enhance the reactivity of Co(2+) toward H(2)O(2), whereas cysteine (Cys) and N-acetylcysteine (NAC) suppressed free radical generation. Under identical reaction conditions, Ni(2+) was markedly less reactive toward H(2)O(2) in comparison with Co(2+). GSH, His, Cys and NAC did not enhance free radical generation of Ni(2+) from H(2)O(2). However, in the presence of carnosine weak but significantly enhanced ESR intensities were found. Incubation of PBMC cultures from healthy subjects with Co(2+) (10-50 microM) yielded the DMPO-.OH adduct, suggesting Co(2+)-mediated hydroxyl radical generation. In contrast, incubation of PBMC cultures with Ni(2+) (10-50 microM) did not produce a detectable ESR-signal. Ascorbic acid efficiently inhibited Co(2+)-mediated free radical generation in PBS solutions and PBMC cultures. The observed difference in free radical generating capacity between Ni(2+) and Co(2+) is of interest with respect to the absence of cross-reactivity between the two metal-ions in experimental allergic contact dermatitis.

Topics: Acetylcysteine; Adult; Ascorbic Acid; Carnosine; Cells, Cultured; Cobalt; Cysteine; Dermatitis, Allergic Contact; Electron Spin Resonance Spectroscopy; Female; Free Radical Scavengers; Free Radicals; Glutathione; Histidine; Humans; Hydrogen Peroxide; Middle Aged; Monocytes; Nickel

Nickel sensitivity is a common problem, often causing significant morbidity from chronic eczematous dermatitis. The main treatment, topical steroids, usually is unable to suppress the dermatitis completely.. Our purpose was to study the effects of "barrier" ointments containing either chelating agents (clioquinol or ethylenediaminetetraacetic acid [EDTA]) or antioxidants (ascorbic acid or alpha-tocopherol) and 1% hydrocortisone on nickel-induced hypersensitivity reactions.. Nickel-sensitive subjects were challenged with nickel-containing coins coated with the desired barrier ointment and their inhibitory effects observed. Patients with bilateral hand or earring dermatitis explored the efficacy of these agents in clinical use.. Clioquinol (3%) completely abolished the allergic reaction in all 29 subjects tested. EDTA (15%), ascorbic acid (20%), and alpha-tocopherol (10%) were less effective, and 1% hydrocortisone had no significant effect. In clinical use sites treated with a commercially available preparation containing 3% clioquinol and 1% hydrocortisone showed marked clinical improvement in all 10 subjects.. Clioquinol is a potent inhibitor of nickel-induced hypersensitivity reactions and is feasible to use as a barrier ointment to block the allergenic effects of nickel in sensitive patients.

Topics: Administration, Topical; Antioxidants; Ascorbic Acid; Chelating Agents; Clioquinol; Dermatitis, Allergic Contact; Drug Eruptions; Edetic Acid; Humans; Hydrocortisone; Nickel; Pilot Projects; Vitamin E