REQUIMTE, Departamento de Ciências Químicas, Faculdade de Farmácia, Universidade do Porto, Rua de Jorge Viterbo Ferreira no. 228, 4050-313, Porto, Portugal.
Biometals. 2013 Feb;26(1):13-21. doi: 10.1007/s10534-012-9590-2. Epub 2012 Oct 25.
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.
镍是一种普遍存在的过渡金属,以多种形式在工业中应用,这不可避免地导致了高度的职业和环境暴露。过度暴露于镍会对人类健康产生多种不良影响,包括过敏、肺癌和鼻癌。在本研究中,首次证明镍[(Ni(II)](作为硝酸镍盐)在体内可能达到的浓度通过内在途径诱导中性粒细胞凋亡。使用二苯乙烯碘,一种 NADPH 氧化酶抑制剂,延迟了 Ni(II)诱导的凋亡,表明 NADPH 氧化酶衍生的活性氧和随后的信号转导可能导致了这一事件。这是一个重要的发现,因为镍介导的细胞凋亡增加可能破坏中性粒细胞的生理活性,对其免疫和抗菌作用产生潜在影响。