Non-malignant diseases associated with environmental arsenic exposure in Taiwan, Chile, and Bangladesh

Non-malignant diseases associated with environmental arsenic exposure in Taiwan, Chile, and Bangladesh
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台湾、智利和孟加拉国与环境砷暴露相关的非恶性疾病

DOI:
10.11299/metallomicsresearch.mr202109
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发表时间:
2021
期刊:
Metallomics Research
影响因子:
--
通讯作者:
K
K
中科院分区:
--
文献类型:
--
作者:
Himeno;S.;Hossain;K

文献摘要

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在台湾、智利和孟加拉国进行的广泛流行病学研究表明,长期接触砷与皮肤损伤、癌症以及非恶性疾病(如高血压、糖尿病、心血管疾病和呼吸系统疾病)的发病率和流行率增加有关。然而,砷如何促进血管疾病和糖尿病的潜在机制仍不清楚。为了了解与砷引起的非恶性疾病相关的生化机制,我们研究了孟加拉国西部地区砷污染地区与疾病相关的血液生物标志物和砷暴露水平之间的关系。在这篇综述中,我们总结了我们在孟加拉国的研究结果,并与台湾和智利的流行病学观察结果进行了比较,讨论了它们的意义。我们已经确定了砷诱导的生物标志物的变化,反映氧化应激,炎症,血脂异常,血管收缩,单核细胞粘附和血管生成,所有相关的促进动脉粥样硬化和高血压。葡萄糖耐受不良、血清胰岛素和肌酐以及瘦体重的测定表明砷诱导的骨骼肌萎缩及其与胰岛素抵抗的关系具有潜在作用。呼吸功能、血清免疫球蛋白E和细胞因子的测定表明,砷诱导的Th2优势免疫调节可能是诱发Th2高型哮喘的易感因素。因此,对疾病相关生物标志物的研究使我们能够对砷相关的非恶性疾病增加的生化机制提供新的见解。
Extensive epidemiological studies in Taiwan, Chile, and Bangladesh have shown that chronic arsenic exposure is associated with increased incidence and prevalence of skin lesions, cancers, as well as non-malignant disorders such as hypertension, diabetes mellitus, cardiovascular diseases, and respiratory diseases. However, the underlying mechanisms of how arsenic facilitates vascular disorders and diabetes remained unclear. To understand biochemical mechanisms related to arsenic-induced non-malignant diseases, we have examined the relationships between disease-related blood biomarkers and arsenic exposure levels in the arsenic-contaminated area in the western region of Bangladesh. In this review, we presented a summary of the findings of our studies in Bangladesh and discussed their significances in comparison with epidemiological observations in Taiwan and Chile. We have identified arsenic-induced changes in the biomarkers reflecting oxidative stress, inflammation, dyslipidemia, vasoconstriction, monocyte adhesion, and angiogenesis, all related to promoting atherosclerosis and hypertension. Determinations of glucose intolerance, serum insulin and creatinine, and lean body mass suggested a potential role of arsenic-induced skeletal muscle atrophy and its association with insulin resistance. Respiratory function tests and measurements of serum immunoglobulin E and cytokines showed that arsenic-induced T helper 2 (Th2)-dominant immunomodulation might predispose to developing Th2-high type asthma. Thus, the investigation of disease-related biomarkers allowed us to provide novel insight into biochemical mechanisms of arsenic-associated increases in non-malignant diseases.