1.
Mechanisms of Nickel-Induced Cell Damage in Allergic Contact Dermatitis and Nutritional Intervention Strategies.
Filatova, D, Cherpak, C
Endocrine, metabolic & immune disorders drug targets. 2020;(7):1010-1014
Abstract
BACKGROUND Hypersensitivity to nickel is a very common cause of allergic contact dermatitis since this metal is largely present in industrial and consumer products as well as in some commonly consumed foods, air, soil, and water. In nickel-sensitized individuals, a cell-mediated delayed hypersensitivity response results in contact to dermatitis due to mucous membranes coming in long-term contact with nickel-containing objects. This process involves the generation of reactive oxidative species and lipid peroxidation-induced oxidative damage. Immunologically, the involvement of T helper (h)-1 and Th-2 cells, as well as the reduced function of T regulatory cells, are of importance. The toxicity, mutagenicity, and carcinogenicity of nickel are attributed to the generation of reactive oxygen species and induction of oxidative damage via lipid peroxidation, which results in DNA damage. OBJECTIVE The aim of this research is to identify nutritionally actionable interventions that can intercept nickel-induced cell damage due to their antioxidant capacities. CONCLUSION Nutritional interventions may be used to modulate immune dysregulation, thereby intercepting nickel-induced cellular damage. Among these nutritional interventions are a low-nickel diet and an antioxidant-rich diet that is sufficient in iron needed to minimize nickel absorption. These dietary approaches not only reduce the likelihood of nickel toxicity by minimizing nickel exposure but also help prevent oxidative damage by supplying the body with antioxidants that neutralize free radicals.
2.
A time-lapse approach to examine chromium and nickel effects on wound healing in vitro.
Perfetto, B, Stellavato, A, Melito, A, De Gregorio, V, Cammarota, M, Giuliano, M
Journal of immunotoxicology. 2012;(4):392-400
Abstract
Chromium and nickel cause allergic contact dermatitis, a common biological skin response to sensitizing agents. This study used a conventional in vitro wounding model to study the impact of sensitizing agents on the innate immune response of human keratinocytes. Experiments were designed to evaluate the involvement of specific Toll-like receptors and metalloproteinases as effectors molecules downstream, at a molecular level. Further, keratinocytes were co-cultured with monocytes (THP-1 cells) to reproduce an inductive stimulus on monocytes made by metals. Human keratinocytes (HaCat) were grown on plates covered with collagen type I, chemically treated, and then mechanically injured with a sterile pipette tip. Restoration of the monolayer integrity was monitored by time-lapse video microscopy. Effector gene expression was evaluated by real-time PCR. The presence of chromium significantly dropped the rate of wound closure, while nickel-induced hyper-proliferation ended in an acceleration of the healing process, an event that does not occur in vivo. This latter outcome led to considering nickel as an unsuitable example for use in the experimental model. Focusing solely on the chromium aspect of this study, RNA profiles of selected molecular markers were generated to ascertain if the detrimental stimulus from chromium was eliminated or persisted both in keratinocytes alone and/or during co-cultures of keratinocytes and monocytes. Monocytes accelerated the process of wound repair. This in vitro experimental model highlighted the involvement of innate immunity in response to chromium and might be useful for test molecules of therapeutic interest for the treatment of skin lesions. However, the experience with nickel reveals that there are limitations to the utility of this wound model system after all.
3.
[Nickel dermatitis, systemic nickel allergy syndrome, immuno-genesis, immune-tolerance: an Italian study].
Cirla, AM, Cirla, PE
Giornale italiano di medicina del lavoro ed ergonomia. 2012;(3 Suppl):147-9
Abstract
Subjects with Nickel sensitization proved by patch test may suffer of contact eczema, but also of a Sistemic Nickel Allergy Syndrome (SNAS) consisting of urticaria-like troubles, itch, erythema, cutaneous rush, headache, intestinal symptoms, recurrent vesicular palmar dermatitis. 160 subjects (130 F, 30 M) were classified into three groups and underwent dosage of Nickel in urines (U-Ni) and blood (B-Ni). The two groups with SNAS showed an higher indicators of Nickel absorption, while the only-eczema group did not. 95 subjects with SNAS were enrolled for a Nickel-scanty diet: most of them improved. 24 ones again symptomatic were admitted to an experimental treatment, by a schedule of oral increasing microdose (nanograms) of Nickel sulphate: all of them improved. In conclusion Nickel pathology is changing, allergy seems to be due to different mechanism, dietary intake is important, an immune-tolerance can be induced.
4.
Prevention of nickel allergy: the case for regulation?
Lu, LK, Warshaw, EM, Dunnick, CA
Dermatologic clinics. 2009;(2):155-61, vi-vii
Abstract
Nickel is the most common allergen detected in patch-tested patients. Nickel allergy is highest among females and patients under the age of 18, affecting 35.8% of patients patch-tested in this demographic. Nickel allergic contact dermatitis is a T-cell-mediated immune reaction which most commonly presents as a skin rash in areas exposed to nickel; however, more serious reactions to nickel in medical devices and more widespread eruptions to dietary nickel can occur. In contrast to Europe, where regulations have resulted in a decreasing prevalence of nickel allergy, the incidence of nickel allergic contact dermatitis in North America is increasing. This article summarizes primary prevention strategies as well as management of patients already sensitized to nickel.