Wu M M, Chiou H Y, Wang T W, Hsueh Y M, Wang I H, Chen C J, Lee T C
Institute of Biomedical Sciences, Academia Sinica, 128 Academia Road, Section 2, Nankang, Taipei 11529, Taiwan, Republic of China.
Environ Health Perspect. 2001 Oct;109(10):1011-7. doi: 10.1289/ehp.011091011.
Arsenic is a notorious environmental toxicant known as both a carcinogen and an atherogen in human beings, but the pathogenic mechanisms are not completely understood. In cell culture studies, trivalent arsenic enhanced oxidative stress in a variety of mammalian cells, and this association may be closely associated with the development of arsenic-related diseases. To investigate the effect of arsenic exposure on oxidative stress in humans, we conducted a population study to determine the relationships of blood arsenic to reactive oxidants and antioxidant capacity at the individual level. We recruited 64 study subjects ages 42-75 years from residents of the Lanyang Basin on the northeast coast of Taiwan, where arsenic content in well water varies from 0 to > or = 3,000 microg/L. We used a chemiluminescence method, with lucigenin as an amplifier for measuring superoxide, to measure the plasma level of reactive oxidants. We used the azino-diethyl-benzthiazoline sulphate method to determine the antioxidant capacity level in plasma of each study subject. We determined arsenic concentration in whole blood by hydride formation with an atomic absorption spectrophotometer. The average arsenic concentration in whole blood of study subjects was 9.60 +/- 9.96 microg/L (+/- SD) with a range from 0 to 46.50 microg/L. The level of arsenic concentration in whole blood of study subjects showed a positive association with the level of reactive oxidants in plasma (r = +0.41, p = 0.001) and an inverse relationship with the level of plasma antioxidant capacity (r = -0.30, p = 0.014). However, we found no significant association (p = 0.266) between levels of plasma reactive oxidants and antioxidant capacity. Our results also show that the lower the primary arsenic methylation capability, the lower the level of plasma antioxidant capacity (p = 0.029). These results suggest that ingestion of arsenic-contaminated well water may cause deleterious effects by increasing the level of reactive oxidants and decreasing the level of antioxidant capacity in plasma of individuals. Persistent oxidative stress in peripheral blood may be a mechanism underlying the carcinogenesis and atherosclerosis induced by long-term arsenic exposure.
砷是一种臭名昭著的环境毒物,在人类中既是致癌物又是致动脉粥样硬化物,但其致病机制尚未完全明确。在细胞培养研究中,三价砷增强了多种哺乳动物细胞中的氧化应激,这种关联可能与砷相关疾病的发生密切相关。为了研究砷暴露对人体氧化应激的影响,我们开展了一项人群研究,以确定个体水平上血砷与活性氧化剂及抗氧化能力之间的关系。我们从台湾东北海岸兰阳盆地的居民中招募了64名年龄在42 - 75岁之间的研究对象,该地区井水砷含量在0至≥3000微克/升之间变化。我们采用以光泽精作为超氧化物放大器的化学发光法来测量活性氧化剂的血浆水平。我们使用硫酸氮杂二乙苯并噻唑啉法来测定每个研究对象血浆中的抗氧化能力水平。我们用原子吸收分光光度计通过氢化物形成法测定全血中的砷浓度。研究对象全血中的平均砷浓度为9.60±9.96微克/升(±标准差),范围为0至46.50微克/升。研究对象全血中的砷浓度水平与血浆中活性氧化剂水平呈正相关(r = +0.41,p = 0.001),与血浆抗氧化能力水平呈负相关(r = -0.30,p = 0.014)。然而,我们发现血浆活性氧化剂水平与抗氧化能力之间无显著关联(p = 0.266)。我们的结果还表明,初级砷甲基化能力越低,血浆抗氧化能力水平越低(p = 0.029)。这些结果表明,摄入受砷污染的井水可能通过提高个体血浆中活性氧化剂水平并降低抗氧化能力水平而产生有害影响。外周血中持续的氧化应激可能是长期砷暴露诱导致癌和动脉粥样硬化的潜在机制。