Milnerowicz Halina, Ściskalska Milena, Dul Magdalena
Department of Biomedical and Environmental Analysis, Faculty of Pharmacy, Wroclaw Medical University, Borowska 211, 50-556 Wroclaw, Poland.
Department of Biomedical and Environmental Analysis, Faculty of Pharmacy, Wroclaw Medical University, Borowska 211, 50-556 Wroclaw, Poland.
J Trace Elem Med Biol. 2015 Jan;29:1-10. doi: 10.1016/j.jtemb.2014.04.008. Epub 2014 May 9.
Metals present in tobacco smoke have the ability to cause a pro-oxidant/antioxidant imbalance through the direct generation of free radicals in accordance with the Fenton or Haber-Weiss reaction and redox properties. Metals can also interact with antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase) and small molecular antioxidants (glutathione) through binding to SH groups or by replacement of metals ions in the catalytic center of enzymes. Excessive free radicals production can induce an inflammatory response. The aim of this study was to review the information on the induction of inflammation by metals present in tobacco smoke such as lead (Pb), cadmium (Cd), arsenic (As), aluminum (Al), nickel (Ni) and mercury (Hg). In cellular immune response, it was demonstrated that radicals induced by metals can disrupt the transcription signaling pathway mediated by the mitogen-activated protein kinase (induced by Pb), NLRP3-ASC-caspase 1 (induced by Ni), tyrosine kinase Src (induced by As) and the nuclear factor κB (induced by Pb, Ni, Hg). The result of this is a gene transcription for early inflammatory cytokines, such as Interleukine 1β, Interleukine 6, and Tumor necrosis factor α). These cytokines can cause leukocytes recruitment and secretions of other pro-inflammatory cytokines and chemokines, which intensifies the inflammatory response. Some metals, such as cadmium (Cd), can activate an inflammatory response through tissue damage induction mediated by free radicals, which also results in leukocytes recruitment and cytokines secretions. Inflammation generated by metals can be reduced by metallothionein, which has the ability to scavenge free radicals and bind toxic metals through the release of Zn and oxidation of SH groups.
烟草烟雾中的金属能够通过按照芬顿或哈伯-维伊斯反应及氧化还原特性直接生成自由基，导致促氧化剂/抗氧化剂失衡。金属还可通过与巯基结合或取代酶催化中心的金属离子，与抗氧化酶（超氧化物歧化酶、过氧化氢酶、谷胱甘肽过氧化物酶）及小分子抗氧化剂（谷胱甘肽）相互作用。自由基产生过多会引发炎症反应。本研究的目的是综述有关烟草烟雾中存在的金属如铅（Pb）、镉（Cd）、砷（As）、铝（Al）、镍（Ni）和汞（Hg）诱导炎症的信息。在细胞免疫反应中，已证实金属诱导的自由基可破坏由丝裂原活化蛋白激酶介导的转录信号通路（由铅诱导）、NLRP3-ASC-半胱天冬酶1（由镍诱导）、酪氨酸激酶Src（由砷诱导）及核因子κB（由铅、镍、汞诱导）。其结果是早期炎症细胞因子如白细胞介素1β、白细胞介素6和肿瘤坏死因子α的基因转录。这些细胞因子可导致白细胞募集及其他促炎细胞因子和趋化因子的分泌，从而加剧炎症反应。一些金属，如镉（Cd），可通过自由基介导的组织损伤诱导激活炎症反应，这也会导致白细胞募集和细胞因子分泌。金属诱导的炎症可通过金属硫蛋白减轻，金属硫蛋白有能力通过释放锌和巯基氧化来清除自由基并结合有毒金属。
