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Protection of melatonin against long‐term radon exposure‐caused lung injury
Environmental Toxicology ( IF 4.5 ) Pub Date : 2020-10-27 , DOI: 10.1002/tox.23052
Qianqian Wu 1 , Lijun Fang 2 , Youjing Yang 1 , Aiqing Wang 3 , Xiaoyu Chen 1 , Jiaojiao Sun 1 , Jianmei Wan 3 , Chengjiao Hong 3 , Jian Tong 1 , Shasha Tao 1, 4 , Hailin Tian 1, 4
Affiliation  

Radon is one of the major pathogenic factors worldwide. Recently, epidemiological studies have suggested that radon exposure plays an important role in lung injury, which could further cause cancer. However, the toxic effects and underlying mechanism on lung injury are still not clear. Here, we identified the detailed toxic effects of long-term radon exposure. Specifically, the manifestations were inflammatory response and cell apoptosis in dose- and time-dependent manners. In detail, it caused the mitochondrial dysfunction and oxidative stress as determined by the abnormal levels of mitochondrial DNA copy number, adenosine triphosphate, mitochondrial membrane potential, superoxide dismutase, and cycloxygenase-2. Furthermore, we found that melatonin treatment ameliorated mitochondrial dysfunction and attenuated the levels of oxidative stress caused by long-term radon exposure, which could further inhibit the lung tissue apoptosis as determined by the decreased levels of cleaved caspase 3. Our study would provide potential therapeutic application of melatonin on lung tissue injury caused by long-term radon exposure.

中文翻译:

褪黑激素对长期氡暴露所致肺损伤的保护作用

氡是世界范围内的主要致病因素之一。最近,流行病学研究表明,氡暴露在肺损伤中起重要作用,肺损伤可能进一步导致癌症。然而,肺损伤的毒性作用和潜在机制尚不清楚。在这里,我们确定了长期氡暴露的详细毒性影响。具体表现为呈剂量和时间依赖性的炎症反应和细胞凋亡。具体而言,它导致线粒体功能障碍和氧化应激,这是由线粒体 DNA 拷贝数、三磷酸腺苷、线粒体膜电位、超氧化物歧化酶和环加氧酶-2 的异常水平决定的。此外,
更新日期:2020-10-27
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