Cell-enhanced dissolution of carcinogenic lead chromate particles: the role of individual dissolution products in clastogenesis.
Cell-enhanced dissolution of carcinogenic lead chromate particles: the role of individual dissolution products in clastogenesis.
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致癌铬酸铅颗粒的细胞增强溶解：单个溶解产物在断裂发生中的作用。
DOI：
10.1093/carcin/15.10.2249
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发表时间：
1994
期刊：
影响因子：
4.7
通讯作者：
Patierno,SR
中科院分区：
文献类型：
--
作者：
WiseSr,JP;Stearns,DM;Wetterhahn,KE;Patierno,SR
铬酸铅诱导染色体损伤作为细胞外溶解产生溶解的铬和铅的结果，我们在这里表明，溶解过程大大加快了细胞的存在。我们试图确定这些离子中的哪一种参与铬酸铅诱导的致染色体断裂作用。细胞介导的参与铬酸铅的细胞外溶解导致溶解的铬和溶解的铅两者的积累，在细胞外介质中分别达到15和1.9 μ M的浓度，并且在细胞内分别达到2700和97 μM的浓度。铬在细胞外和细胞内的积累都具有时间依赖性，从低剂量到高剂量，溶解的铅和铬都成比例地增加。将细胞暴露于水溶性铬酸钠的条件下，产生类似的时间依赖性细胞内浓度的铬也产生类似的数量和光谱的染色体损伤的铬酸铅。相反，暴露于谷氨酸铅导致细胞内铅水平比铬酸铅高438倍，但没有产生染色体损伤。较高剂量的谷氨酸铅的致染色体断裂作用较弱，但它诱导的染色体畸变谱与铬酸铅不同。用维生素E预处理细胞对铬的摄取没有影响，但使铬酸钠和铬酸铅诱导的染色体断裂减少了54- 93%。维生素E预处理不影响谷氨酸铅诱导的染色体断裂。这项研究的结果表明，虽然铅（II）是弱致染色体断裂在高剂量下，六价铬是近染色体断裂剂在铬酸铅诱导的染色体断裂。此外，这是第一次报道，用维生素E预处理细胞可以阻断颗粒铬酸盐诱导的染色体断裂。
Lead chromate induces chromosomal damage as a result of extracellular dissolution producing solubilized chromium and lead and we show here that the dissolution process is greatly accelerated by the presence of cells. We have sought to determine which of these ions is involved in lead chromate-induced clastogenicity. Cell-mediated extracellular dissolution of participate lead chromate resulted in the accumulation of both solubilized chromium and solubilized lead, reaching concentrations in the extracellular medium of 15 and 1.9 μ.M respectively and reaching concentrations inside the cell of 2700 and 97 (μM respectively. Both the extracellular and intracellular accumulation of chromium was time dependent and both the solubilized lead and chromium increased proportionately from a lower dose to a higher dose. Exposing cells to water soluble sodium chromate under conditions which produced similar time-dependent intracellular concentrations of chromium also produced a similar amount and spectrum of chromosome damage as lead chromate. In contrast, exposure to lead glutamate resulted in intracellular lead levels 438-times higher than those produced by lead chromate, but produced no chromosome damage. A higher dose of lead glutamate was weakly clastogenic, but it induced a different spectrum of chromosomal aberrations than lead chromate. Pretreatment of cells with vitamin E had no effect on the uptake of chromium, but reduced both sodium chromateand lead chromate-induced clastogenesis by 54-93%. Vitamin E pretreatment did not affect lead glutamateinduced clastogenesis. The results of this study indicate that although lead(II) is weakly clastogenic at high doses, hexavalent chromium is the proximate clastogen in lead chromate-induced clastogenesis. Additionally, this is the first report that pretreatment of cells with vitamin E can block clastogenesis induced by particulate chromates.