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Protection of melatonin against long‐term radon exposure‐caused lung injury
Author(s) -
Wu Qianqian,
Fang Lijun,
Yang Youjing,
Wang Aiqing,
Chen Xiaoyu,
Sun Jiaojiao,
Wan Jianmei,
Hong Chengjiao,
Tong Jian,
Tao Shasha,
Tian Hailin
Publication year - 2021
Publication title -
environmental toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.813
H-Index - 77
eISSN - 1522-7278
pISSN - 1520-4081
DOI - 10.1002/tox.23052
Subject(s) - oxidative stress , melatonin , superoxide dismutase , lung , radon exposure , apoptosis , reactive oxygen species , dna damage , pharmacology , mitochondrion , radon , chemistry , medicine , lung cancer , toxicology , biology , pathology , biochemistry , dna , physics , quantum mechanics
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.