Zhang Aihua, Gao Chen, Han Xue, Wang Lifang, Yu Chun, Zeng Xiaowen, Chen Liping, Li Daochuan, Chen Wen
Department of Toxicology, School of Public Health, Guiyang Medical University, Guiyang 550004, China.
Department of Toxicology, School of Public Health, Sun Yat-sen University, Guangzhou 510080, China.
Toxicol Rep. 2014 Sep 17;1:692-698. doi: 10.1016/j.toxrep.2014.08.007. eCollection 2014.
Arsenic exposure from burning high arsenic-containing coal has been associated with human skin lesion and cancer. However, the mechanisms of arsenic-related carcinogenesis are not fully understood. Inactivation of critical tumor suppression genes by epigenetic regulation or genetic modification might contribute to arsenic-induced carcinogenicity. This study aims to clarify the correlation between arsenic pollution and functional defect of gene in arsenic exposure residents from a region of Guizhou Province, China. To this end, 103 arsenic exposure residents and 105 control subjects were recruited in this study. The results showed that the exposure group exhibited higher levels of urinary and hair arsenic compared with the control group (55.28 28.87 μg/L, 5.16 1.36 μg/g). Subjects with higher arsenic concentrations are more likely to have methylation and gene deletion ( = 4.28, = 0.04 and = 4.31, = 0.04). We also found that the degree of hypermethylation and gene deletion occurred at higher incidence in the poisoning cases with skin cancer (3.7% and 14.81% in non-skin cancer group, 41.18% and 47.06 in skin cancer group), and were significantly associated with the stage of skin lesions ( = 12.82, < 0.01 and = 7.835, = 0.005). These observations indicate that inactivation of through genetic alteration or epigenetic modification is a common event that is associated with arsenic exposure and the development of arsenicosis.
燃烧高砷煤导致的砷暴露与人类皮肤病变和癌症有关。然而，砷相关致癌作用的机制尚未完全明确。通过表观遗传调控或基因修饰使关键肿瘤抑制基因失活可能会导致砷诱导的致癌性。本研究旨在阐明中国贵州省某地区砷暴露居民中砷污染与基因功能缺陷之间的相关性。为此，本研究招募了103名砷暴露居民和105名对照受试者。结果显示，与对照组相比，暴露组的尿砷和发砷水平更高（55.28±28.87μg/L，5.16±1.36μg/g）。砷浓度较高的受试者更有可能发生甲基化和基因缺失（χ² = 4.28，P = 0.04；χ² = 4.31，P = 0.04）。我们还发现，皮肤癌中毒病例中甲基化和基因缺失的发生率更高（非皮肤癌组为3.7%和14.81%，皮肤癌组为41.18%和47.06%），并且与皮肤病变的分期显著相关（χ² = 12.82，P < 0.01；χ² = 7.835，P = 0.005）。这些观察结果表明，通过基因改变或表观遗传修饰使[基因名称]失活是与砷暴露和砷中毒发展相关的常见事件。
