Gambelunghe Angela, Piccinini Renza, Abbritti Giuseppe, Ambrogi Maura, Ugolini Barbara, Marchetti Cristina, Migliorati Graziella, Balducci Chiara, Muzi Giacomo
Department of Clinical and Experimental Medicine, Division of Occupational Medicine, University of Perugia, Perugia, Italy.
J Occup Environ Med. 2006 Mar;48(3):319-25. doi: 10.1097/01.jom.0000197859.46894.7d.
Hexavalent chromium compounds are well-documented human carcinogens. In vitro experiments show Cr (VI) induces cell death by apoptosis by activating p53 protein. The aim of this study was to evaluate Cr (VI)-induced apoptosis in a human bronchial epithelial cell line (BEAS-2B) and in a lymphoblastic leukemia cell line (MOLT-4). Cr (VI) caused a dose- and time-dependent increase in the apoptosis rate in both cell lines. Western blotting showed increased p53 protein expression in MOLT-4 cells, but not in BEAS-2B cells, after exposure to 0.5 and 3 muM hexavalent chromium for 12 hours and 4 hours, respectively. Apoptotic cell death induced by Cr (VI) was not decreased by pretreatment with caspase-3, -8, and -9 inhibitors. These preliminary results provide evidence of Cr (VI)-induced apoptosis, which deserves further investigation in occupationally exposed workers.
六价铬化合物是有充分文献记载的人类致癌物。体外实验表明，六价铬通过激活p53蛋白诱导细胞凋亡而导致细胞死亡。本研究的目的是评估六价铬在人支气管上皮细胞系（BEAS-2B）和淋巴细胞白血病细胞系（MOLT-4）中诱导的细胞凋亡情况。六价铬在两种细胞系中均导致凋亡率呈剂量和时间依赖性增加。蛋白质印迹法显示，分别用0.5 μM和3 μM六价铬处理MOLT-4细胞12小时和BEAS-2B细胞4小时后，MOLT-4细胞中p53蛋白表达增加，而BEAS-2B细胞中未增加。用半胱天冬酶-3、-8和-9抑制剂预处理后，六价铬诱导的凋亡细胞死亡并未减少。这些初步结果为六价铬诱导的细胞凋亡提供了证据，值得对职业暴露工人进行进一步研究。
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