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Merck

Nickel induces apoptosis in human neutrophils.

Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine (2012-10-26)
Marisa Freitas, Pedro Barcellos-de-Souza, Christina Barja-Fidalgo, Eduarda Fernandes
RESUMEN

Nickel is an ubiquitous transition metal that is industrially applied in many forms, which inevitably leads to a high degree of occupational and environmental exposure. Over-exposure to nickel can produce a variety of adverse effects on human health, including allergy and lung and nasal cancers. In the present study, it is demonstrated, for the first time, that nickel [(Ni(II)] (as a nickel nitrate salt) at concentrations that may be attained in vivo, induces neutrophils' apoptosis by the intrinsic pathway. The use of diphenyleneiodonium, a NADPH oxidase inhibitor, delayed Ni(II)-induced apoptosis, suggesting that NADPH oxidase-derived reactive oxygen species and subsequent signaling could contribute to this event. This is an important finding since increased apoptosis mediated by nickel may disrupt the physiological activities of neutrophils, with potential impact in its immunological and antimicrobial role.

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Sigma-Aldrich
Nickel(II) nitrate hexahydrate, 99.999% trace metals basis
Sigma-Aldrich
Nickel(II) nitrate hexahydrate, purum p.a., crystallized, ≥97.0% (KT)
Sigma-Aldrich
Nickel(II) nitrate hexahydrate, crystals
Sigma-Aldrich
Nickel(II) nitrate hexahydrate, puriss. p.a., ≥98.5% (KT)