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Nickel-keratinocyte interaction: a possible role in sensitization.
M Picardo1, C Zompetta, C De Luca
1San Gallicano Dermatological Institute, Rome University, Italy.
The British Journal of Dermatology
|June 1, 1990
Summary
Nickel exposure damages skin cells and may trigger allergic reactions. Studies show nickel ions (Ni2+) inhibit keratinocyte growth and increase inflammatory markers, suggesting potential for skin sensitization.
Area of Science:
- Dermatology
- Toxicology
- Immunology
Background:
- Nickel (Ni2+) is a common environmental allergen.
- Keratinocytes are the primary cells in the epidermis.
- Understanding nickel's effects on skin cells is crucial for allergy research.
Purpose of the Study:
- To investigate the effects of nickel ions (Ni2+) on normal human keratinocytes and keratinocyte-derived cell lines.
- To determine the dose- and time-dependent toxicity of nickel on skin cells.
- To assess nickel-induced inflammatory responses and potential for sensitization.
Main Methods:
- Exposure of keratinocytes (NCTC 2544, A 431) and normal human keratinocytes to varying nickel concentrations (0.023-46.6 µg/ml) for different durations (1-5 days).
- Assessment of cell growth inhibition and viability.
- Measurement of interleukin-1 (IL-1) release from keratinocytes.
- Evaluation of lipoxygenase activation in leukocytes following short-term nickel exposure.
Main Results:
- Nickel ions (Ni2+) demonstrated a dose- and time-dependent inhibition of keratinocyte growth and viability.
- Approximately 50% cell survival was observed at 2.3 µg Ni2+/ml after 5 days.
- Increased interleukin-1 (IL-1) release was detected in keratinocytes cultured with 2.3-11.5 µg Ni2+/ml for 24 hours.
- Short incubation periods (30 min) with nickel activated lipoxygenase in leukocytes without affecting cell viability.
Conclusions:
- Percutaneous penetration of nickel (Ni2+) can cause damage to keratinocytes.
- Nickel exposure can lead to the release of inflammatory mediators like IL-1.
- These effects suggest that nickel can initiate skin sensitization and allergic contact dermatitis.