Apostoli P, Catalani S
Dipartimento di Medicina Sperimentale e Applicata, Sezione di Medicina del Lavoro e Igiene Industriale, Università degli Studi di Brescia, Italy.
G Ital Med Lav Ergon. 2008 Oct-Dec;30(4):382-91.
In this paper we will deal with mechanism of carcinogenic action of metallic elements and their species (arsenic, beryllium, cadmium, cobalt, chromium, nickel) identified by EU as carcinogen R 45 or R 49. The carcinogenic effect depended on the ability of to penetrate the cell and interacted with the target sites, therefore the state of oxidation, charging, the solubility, type of binding, stereochemistry and the ability to interact with other xenobiotics were crucial. The carcinogenic metallic elements classified R45 or R49 are essentially weak mutagen and do not form adducts with the DNA as initial step of their carcinogenicity In spite of the wide range of metallic elements physicochemical properties, some common general mechanisms of carcinogenesis emerge:from the induction of oxidative stress, to inhibition of DNA repair, from activation of mitogenic signalling, to epigenetic modification of gene expression. However, each species lead to specific molecular interactions and were subject to different bioavailability. It has been also strongly supported the hypothesis that the metallic elements may act as a co-carcinogen with other organic compounds, for example with PAH.
在本文中,我们将探讨被欧盟认定为致癌物R45或R49的金属元素及其物种(砷、铍、镉、钴、铬、镍)的致癌作用机制。致癌作用取决于其穿透细胞并与靶位点相互作用的能力,因此氧化态、电荷、溶解度、结合类型、立体化学以及与其他异生物素相互作用的能力至关重要。被归类为R45或R49的致癌金属元素本质上是弱诱变剂,在其致癌性的初始阶段不会与DNA形成加合物。尽管金属元素具有广泛的物理化学性质,但仍出现了一些常见的致癌一般机制:从氧化应激的诱导到DNA修复的抑制,从有丝分裂信号的激活到基因表达的表观遗传修饰。然而,每种物种都会导致特定的分子相互作用,并且具有不同的生物利用度。金属元素可能与其他有机化合物(例如多环芳烃)共同致癌的假设也得到了有力支持。