Organic extracts from African dust storms stimulate oxidative stress and induce inflammatory responses in human lung cells through Nrf2 but not NF-κB

被引:31
|
作者
Rodriguez-Cotto, Rosa I. [1 ,2 ]
Ortiz-Martinez, Mario G. [1 ,2 ]
Jimenez-Velez, Braulio D. [1 ,2 ]
机构
[1] Univ Puerto Rico, Dept Biochem, San Juan, PR 00936 USA
[2] Ctr Environm & Toxicol Res, San Juan, PR 00936 USA
基金
美国国家卫生研究院;
关键词
African dust; Metals; ROS; Oxidative stress; Nrf2; Particulate matter; AIRBORNE PARTICULATE MATTER; DIESEL EXHAUST PARTICLE; EPITHELIAL-CELLS; TRANSCRIPTION FACTOR; SIGNALING PATHWAY; AMBIENT; ACTIVATION; TOXICITY; AIRWAY; EXPRESSION;
D O I
10.1016/j.etap.2015.02.015
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
The health impact of the global African dust event (ADE) phenomenon in the Caribbean has been vaguely investigated. Heavy metals in ADE and non-ADE extracts were evaluated for the formation of reactive oxygen species (ROS) and antioxidant capacity by cells using, deferoxamine mesylate (DF) and N-acetyl-L-cysteine (NAC). Results show that ADE particulate matter 2.5 (PM2.5) induces ROS and stimulates oxidative stress. Pre-treatment with DF reduces ROS in ADE and Non-ADE extracts and in lung cells demonstrating that heavy metals are of utmost importance. Glutathione-S-transferase and Heme Oxygenase 1 mRNA levels are induced with ADE PM and reduced by DF and NAC. ADE extracts induced Nrf2 activity and IL-8 mRNA levels significantly more than Non-ADE. NF-kappa B activity was not detected in any sample. Trace elements and organic constituents in ADE PM2.5 enrich the local environment load, inducing ROS formation and activating antioxidant-signaling pathways increasing pro-inflammatory mediator expressions in lung cells. (C) 2015 Elsevier B.V. All rights reserved.
引用
收藏
页码:845 / 856
页数:12
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