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Arsenic exposure and pulmonary function decline: Potential mediating role of TRAIL in chronic obstructive pulmonary disease patients
Journal of Trace Elements in Medicine and Biology ( IF 3.5 ) Pub Date : 2024-02-17 , DOI: 10.1016/j.jtemb.2024.127415
Ying Liu , Feng-Min Zhu , Juan Xu , You-Peng Deng , Jing Sun , Qi-Yuan He , Zhen-Yu Cheng , Min-Min Tang , Jin Yang , Lin Fu , Hui Zhao

Environmental arsenic (As) exposure is strongly related to the progression of chronic obstructive pulmonary disease (COPD). Pulmonary epithelial cells apoptosis is implicated in the pathophysiological mechanisms of COPD. However, the role of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), one biomarker of apoptosis, remains unclear in As-mediated pulmonary function alternations in COPD patients. This study included 239 COPD patients. The serum level of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) was measured by enzyme-linked immunosorbent assay (ELISA). The blood As level was determined through inductively coupled plasma mass spectrometry (ICP-MS). Blood As levels exhibited a negative and dose-dependent correlation with pulmonary function. Per unit elevation of blood arsenic concentrations was related to reductions of 0.339 L in FEV1, 0.311 L in FVC, 1.171% in FEV1/FVC%, and 7.999% in FEV1% in COPD subjects. Additionally, a positive dose-response correlation of blood As with serum TRAIL was found in COPD subjects. Additionally, the level of serum TRAIL was negatively linked to lung function. Elevated TRAIL significantly mediated As-induced decreases of 11.05%, 13.35%, and 31.78% in FVC, FEV1, and FEV1%, respectively among the COPD patients. Blood As level is positively correlated with pulmonary function decline and serum TRAIL increase in individuals with COPD. Our findings suggest that elevated TRAIL levels may serve as a mediating mechanism through which As contributes to declining lung function in COPD patients.

中文翻译:

砷暴露与肺功能下降:TRAIL 在慢性阻塞性肺疾病患者中的潜在中介作用

环境砷(As)暴露与慢性阻塞性肺病(COPD)的进展密切相关。肺上皮细胞凋亡与COPD的病理生理机制有关。然而,肿瘤坏死因子相关凋亡诱导配体 (TRAIL)(细胞凋亡的生物标志物之一)在 As 介导的 COPD 患者肺功能改变中的作用仍不清楚。这项研究包括 239 名慢性阻塞性肺病患者。采用酶联免疫吸附试验(ELISA)测定血清肿瘤坏死因子相关凋亡诱导配体(TRAIL)水平。通过电感耦合等离子体质谱法 (ICP-MS) 测定血液砷水平。血液砷水平与肺功能呈负相关且呈剂量依赖性相关。COPD 受试者中,血砷浓度每单位升高与 FEV1 降低 0.339 L、FVC 降低 0.311 L、FEV1/FVC% 降低 1.171%、FEV1% 降低 7.999% 相关。此外,在 COPD 受试者中发现血液 As 与血清 TRAIL 呈正剂量反应相关性。此外,血清 TRAIL 水平与肺功能呈负相关。TRAIL 升高显着介导 As 诱导的 COPD 患者 FVC、FEV1 和 FEV1% 分别降低 11.05%、13.35% 和 31.78%。COPD 患者的血液 As 水平与肺功能下降和血清 TRAIL 升高呈正相关。我们的研究结果表明,TRAIL 水平升高可能是 As 导致 COPD 患者肺功能下降的一种介导机制。
更新日期:2024-02-17
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