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首页> 外文期刊>Archives of Toxicology >Carcinogenic metal compounds: recent insight into molecular and cellular mechanisms.
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Carcinogenic metal compounds: recent insight into molecular and cellular mechanisms.

机译：致癌金属化合物：对分子和细胞机制的最新见解。

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摘要

Mechanisms of carcinogenicity are discussed for metals and their compounds, classified as carcinogenic to humans or considered to be carcinogenic to humans: arsenic, antimony, beryllium, cadmium, chromium, cobalt, lead, nickel and vanadium. Physicochemical properties govern uptake, intracellular distribution and binding of metal compounds. Interactions with proteins (e.g., with zinc finger structures) appear to be more relevant for metal carcinogenicity than binding to DNA. In general, metal genotoxicity is caused by indirect mechanisms. In spite of diverse physicochemical properties of metal compounds, three predominant mechanisms emerge: (1) interference with cellular redox regulation and induction of oxidative stress, which may cause oxidative DNA damage or trigger signaling cascades leading to stimulation of cell growth; (2) inhibition of major DNA repair systems resulting in genomic instability and accumulation of critical mutations; (3) deregulation of cell proliferation by induction of signalingpathways or inactivation of growth controls such as tumor suppressor genes. In addition, specific metal compounds exhibit unique mechanisms such as interruption of cell-cell adhesion by cadmium, direct DNA binding of trivalent chromium, and interaction of vanadate with phosphate binding sites of protein phosphatases.
机译：讨论了金属及其化合物的致癌机理，这些金属及其化合物被分类为对人类致癌或被认为对人类致癌：砷，锑，铍，镉，铬，钴，铅，镍和钒。物理化学特性决定着金属化合物的吸收，细胞内分布和结合。与蛋白质的相互作用（例如与锌指结构的相互作用）似乎对金属致癌性比与DNA的结合更相关。通常，金属遗传毒性是由间接机制引起的。尽管金属化合物具有不同的理化特性，但还是出现了三个主要机制：（1）干扰细胞氧化还原调节和诱导氧化应激，这可能引起氧化DNA损伤或触发信号级联，从而刺激细胞生长; （2）抑制主要的DNA修复系统，导致基因组不稳定和关键突变的积累; （3）通过诱导信号通路或灭活生长控制剂（例如肿瘤抑制基因）来使细胞增殖失调。另外，特定的金属化合物表现出独特的机理，例如镉中断细胞间粘附，三价铬的直接DNA结合以及钒酸盐与蛋白质磷酸酶的磷酸结合位点的相互作用。

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