权益分类	功能权益	普通用户	{{item.name}}会员
{{category.name}}	{{benefitItem.name}}

A intervention study for improvement of decreased nitric oxide levels and oxidative stress in arsenosis patients in China

改善中国砷中毒患者一氧化氮水平下降和氧化应激的干预研究

基本信息

批准号：
15406004
负责人：
KUMAGAI Yoshito
金额：
$ 8.38万
依托单位：
University of Tsukuba
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (B)
财政年份：
2003
资助国家：
日本
起止时间：
2003 至 2005
项目状态：
已结题

项目摘要

Arsenic is a naturally occurring element that is ubiquitously present in the environment. The main source of human environmental exposure is through consumption of water containing high levels of arsenic, primarily from natural contamination. In Asia, millions of people are chronically exposed to a high level of arsenic from their drinking water, obtained from wells drilled into arsenic-rich geologic strata. Nitric oxide (NO) is a messenger molecule that plays an important role in neurotransmission, vasodilation, and immune response. In a field study in an endemic area of chronic arsenic poisoning in Inner Mongolia, China, we found that prolonged exposure of humans to arsenic results in reduction of systemic NO levels and oxidative stress. Such phenomena were also seen with rabbits chronically exposed to arsenic (18 weeks, 5μg/ml), supporting the notion that arsenic is a metalloid that causes impairment of systemic NO production and increased oxidative stress through reactive oxygen species (ROS) generation and decreased antioxidant enzyme activities.Replacement of heavily arsenic-contaminated drinking water with low-arsenic water is thought to be a potential intervention strategy for arsenosis, although the reversibility of arsenic intoxication has not been established. However, our current intervention study in the endemic area of chronic arsenic poisoning in Inner Mongolia indicated that decreased NO levels and peripheral vascular disease in arsenosis patients can be reversed by exposure cessation. These results have important implications in the public health approach to arsenic exposure. From these observations, we thought that clearance of arsenic at the cellular level is critical for decreased arsenic poisoning.

砷是一种天然存在的元素，普遍存在于环境中。人类环境接触的主要来源是饮用含有高含量砷的水，主要来自自然污染。在亚洲，数百万人长期暴露于饮用水中高含量的砷，这些饮用水是从富含砷的地质层中钻出的威尔斯井中获得的。一氧化氮（NO）是一种信使分子，在神经传递、血管舒张和免疫反应中起重要作用。在中国内蒙古慢性砷中毒流行区的一项实地研究中，我们发现人类长期暴露于砷导致全身NO水平和氧化应激降低。这种现象也见于长期接触砷的兔子（18周，5μg/ml），支持砷是一种类金属的概念，它通过活性氧（ROS）的产生和抗氧化酶活性的降低，导致系统NO产生受损和氧化应激增加。砷水被认为是一种潜在的砷中毒干预策略，尽管砷中毒的可逆性尚未确定。然而，我们目前在内蒙古慢性砷中毒病区的干预研究表明，砷中毒患者NO水平下降和外周血管疾病可以通过停止接触来逆转。这些结果对砷暴露的公共卫生方法具有重要意义。从这些观察结果，我们认为，在细胞水平上清除砷是减少砷中毒的关键。

项目成果

期刊论文数量（16）

专著数量（0）

科研奖励数量（0）

会议论文数量（0）

专利数量（0）

Sulforaphane, an activator of Nrf2, suppresses cellular accumulation of arsenic and its cytotoxicity in primary mouse hepatocytes

DOI：
10.1016/j.febslet.2006.02.031
发表时间：
2006-03-20
期刊：
FEBS LETTERS
影响因子：
3.5
作者：
Shinkai, Y;Sumi, D;Kumagai, Y
通讯作者：
Kumagai, Y

Sulforphane, an activator of Nrf2,suppresses cellular accumulation of arsenic and its cytotoxicity in primary mouse hepatocytes.

Sulforphane 是 Nrf2 的激活剂，可抑制原代小鼠肝细胞中砷的细胞积累及其细胞毒性。

DOI：
发表时间：
2006
期刊：
FEBS Letters (In press)
影响因子：
0
作者：
Shinkai Y;sumi D;Fukami I;Ishii T;Kumagai Y
通讯作者：
Kumagai Y

Diphenylarsinic acid poisoning from chemical weapons in Kamisu, Japan

DOI：
10.1002/ana.20290
发表时间：
2004-11-01
期刊：
ANNALS OF NEUROLOGY
影响因子：
11.2
作者：
Ishii, K;Tamaoka, A;Shimojo, N
通讯作者：
Shimojo, N

Vascular dysfunction in patients with chronic arsenosis can be reversed by reduction of arsenic exposure.

慢性砷病患者的血管功能障碍可以通过减少砷暴露来逆转。

DOI：
10.1289/ehp.7471
发表时间：
2005-03
期刊：
Environmental health perspectives
影响因子：
10.4
作者：
通讯作者：

Decreased enzyme activities of hepatic thioredoxin reductase and glutathione reductase in rabbits by prolonged exposure to inorganic arsenate.

长期接触无机砷酸盐会降低兔子肝脏硫氧还蛋白还原酶和谷胱甘肽还原酶的酶活性。

DOI：
发表时间：
2003
期刊：
Environmental Toxicology 18
影响因子：
0
作者：
Nikaido M;Pi JB;Kumagai Y;Yamauchi H;Taguchi K;Horiguchi S;Sun Y;Sun GF;Shimojo N
通讯作者：
Shimojo N