Zhitkovich A, Voitkun V, Kluz T, Costa M
Nelson Institute of Environmental Medicine, New York University Medical Center, New York, New York, USA.
Environ Health Perspect. 1998 Aug;106 Suppl 4(Suppl 4):969-74. doi: 10.1289/ehp.98106s4969.
Human exposure to carcinogenic Cr(VI) compounds is found among workers in a large number of professional groups, and it can also occur through environmental pollution. A significant number of toxic waste sites contain Cr as a major contaminant. In this paper we summarize our efforts to apply measurements of DNA-protein cross-links (DPC) as test for biologically active doses of Cr(VI). DPC were found at elevated levels in lymphocytes in several human populations with low to medium Cr exposures. At high exposure to Cr(VI), exemplified by a group of Bulgarian chromeplaters, DPC plateaued and adducts' levels were similar to those found in environmentally exposed individuals. Lymphocytic DPC correlated strongly with Cr levels in erythrocytes that are indicative of Cr(VI) exposure. DPC in lymphocytes were not confounded by such variables as smoking, age, body weight, gender, or ethnicity. A new version of the cross-link assay offers improved sensitivity and requires a small amount of biologic material. Preliminary results indicate that the ability of DPC to reach detectable levels at low levels of Cr exposure could be related to a lack of repair of these lesions in lymphoid cells. Cr(III)-mediated cross-links of DNA with peptide glutathione or single amino acids were mutagenic in human cells, with a relationship of higher molecular weight of the peptide/amino acid correlating with a more potent mutagenic response. We speculate that bulky DPC could also have a significant promutagenic effect. The current methodology does not allow specific determination of Cr-induced DPC; however, demonstrated sensitivity of DPC measurements and the assay's large sample capacity may allow this assay to be used as the initial screening test for the occurrence of DNA damage in Cr(VI)-exposed populations.
在众多职业群体的工人中都发现了人类接触致癌性六价铬(Cr(VI))化合物的情况,而且这种接触也可能通过环境污染发生。大量有毒废物场地都含有铬作为主要污染物。在本文中,我们总结了我们为应用DNA - 蛋白质交联(DPC)测量作为六价铬生物活性剂量测试所做的努力。在一些低至中等铬暴露水平的人群的淋巴细胞中发现DPC水平升高。在高六价铬暴露情况下,以一组保加利亚镀铬工人为例,DPC趋于平稳,加合物水平与在环境暴露个体中发现的水平相似。淋巴细胞DPC与红细胞中的铬水平密切相关,而红细胞中的铬水平可指示六价铬暴露。淋巴细胞中的DPC不受吸烟、年龄、体重、性别或种族等变量的影响。交联测定的新版本提高了灵敏度,并且需要少量生物材料。初步结果表明,在低水平铬暴露时DPC达到可检测水平的能力可能与淋巴细胞中这些损伤缺乏修复有关。Cr(III)介导的DNA与肽谷胱甘肽或单个氨基酸的交联在人类细胞中具有致突变性,肽/氨基酸分子量越高,致突变反应越强。我们推测大分子DPC也可能具有显著的促突变作用。目前的方法无法特异性测定铬诱导的DPC;然而,已证明DPC测量的灵敏度以及该测定法的大样本容量可能使该测定法用作六价铬暴露人群中DNA损伤发生情况的初始筛查测试。