Effect of N-Acetylcysteine, an Inhibitor of Tumor Necrosis Factor, on Irritant Contact Dermatitis in the Human

Pasche-Koo, Florence; Arechalde, Ana; Arrighi, Jean‐François; Hauser, Conrad

doi:10.1159/000424316

Cited by 5 publications

(1 citation statement)

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“…12 Although N-acetylcysteine, alpha-tocopherol and ascorbate inhibit the expression and functional activity of cutaneous lymphocyte-associated antigen (CLA) in isolated human T-lymphocytes, 13 these antioxidants do not inhibit contact dermatitis when administered in topical form. 14 In keratinocytes, cell-permeable SOD suppresses TNF-induced MMP-9; thus, SOD is thought to be an immunomodulatory agent in inflammatory skin diseases. 15 A topical PPAR-alpha activator induces antioxidant enzymes and reduces inflammation in irritant and ACD models.…”

Section: Contact Dermatitismentioning

confidence: 99%

Oxidative stress and antioxidant strategies in dermatology

2016

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Oxidative stress results from a prooxidant-antioxidant imbalance, leading to cellular damage. It is mediated by free radicals, such as reactive oxygen species or reactive nitrogen species, that are generated during physiological aerobic metabolism and pathological inflammatory processes. Skin serves as a protective organ that plays an important role in defending both external and internal toxic stimuli and maintaining homeostasis. It is becoming increasingly evident that oxidative stress is involved in numerous skin diseases and that antioxidative strategies can serve as effective and easy methods for improving these conditions. Herein, we review dysregulated antioxidant systems and antioxidative therapeutic strategies in dermatology.

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Section: Contact Dermatitismentioning

confidence: 99%

Oxidative stress and antioxidant strategies in dermatology

2016

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Characterization of the Altered Cutaneous Reactivity of Transgenic Mice Whose Keratinocytes Overexpress B7-1

Gaspari

Burns

Kondo

et al. 1998

Clinical Immunology and Immunopathology

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Annual Review of Cosmetic Ingredient Safety Assessments—2002/20031

2005

Int J Toxicol

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Niacinamide (aka nicotinamide) and Niacin (aka nicotinic acid) are heterocyclic aromatic compounds which function in cosmetics primarily as hair and skin conditioning agents. Niacinamide is used in around 30 cosmetic formulations including shampoos, hair tonics, skin moisturizers, and cleansing formulations. Niacin is used in a few similar product types. The concentration of use of Niacinamide varies from a low of 0.0001% in night preparations to a high of 3% in body and hand creams, lotions, powders and sprays. Niacin concentrations of use range from 0.01% in body and hand creams, lotions, powders and sprays to 0.1% in paste masks (mud packs). Both ingredients are accepted for use in cosmetics in Japan and the European Union. Both are GRAS direct food additives and nutrient and/or dietary supplements. Niacinamide may be used in clinical treatment of hypercholesteremia and Niacin in prevention of pellegra and treatment of certain psychological disorders. Both ingredients are readily absorbed from skin, blood, and the intestines and widely distribute throughout the body. Metabolites include N1-methylnicotinamide and N1-methyl-4-pyridone-3-carboxamide. Excretion is primarily through the urinary tract. While Niacinamide is more toxic than Niacin in acute toxicity studies, both are relatively non-toxic. Short-term oral, parenteral, or dermal toxicity studies did not identify significant irreversible effects. Niacinamide, evaluated in an in vitro test to predict ocular irritation, was not an acute ocular hazard. Animal testing of Niacinamide in rabbits in actual formulations produced mostly non-irritant reactions, with only some marginally irritating responses. Skin irritation tests of up to 2.5% Niacinamide in rabbits produced only marginal irritation. Skin sensitization tests of Niacinamide at 5% during induction and 20% during challenge were negative in guinea pigs. Neither cosmetic ingredient was mutagenic in Ames tests, with or without metabolic activation. Niacinamide and Niacin at 2 mg/ml were negative in a chromosome aberration test in Chinese hamster ovary cells, but did produce large structural chromosome aberrations at 3 mg/ml. Niacinamide induced sister chromatid exchanges in Chinese hamster ovary cells, but Niacin did not. Under certain circumstances, Niacinamide can cause an increase in unscheduled DNA synthesis in human lymphocytes treated with UV or a nitrosoguanidine compound. Niacinamide itself was not carcinogenic when administered (1%) in the drinking water of mice. No data on the carcinogenic effect of Niacin were available. Niacinamide can moderate the induction of tumors by established carcinogens. Niacinamide in combination with streptozotocin (a nitrosourea compound) or with heliotrine (a pyrrolizidine alkaloid), produced pancreatic islet tumors. On the other hand, Niacinamide reduced the renal adenomas produced by streptozotocin; and intestinal and bladder tumors induced by a preparation of bracken fern. Niacinamide evaluated in in vitro test systems did affect development, but Niacinamide re...

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Effect of N-Acetylcysteine, an Inhibitor of Tumor Necrosis Factor, on Irritant Contact Dermatitis in the Human

Cited by 5 publications

References 0 publications

Oxidative stress and antioxidant strategies in dermatology

Oxidative stress and antioxidant strategies in dermatology

Characterization of the Altered Cutaneous Reactivity of Transgenic Mice Whose Keratinocytes Overexpress B7-1

Annual Review of Cosmetic Ingredient Safety Assessments—2002/20031

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