N-acetylcysteineamide (NACA) prevents inflammation and oxidative stress in animals exposed to diesel engine exhaust
N-acetylcysteineamide (NACA) prevents inflammation and oxidative stress in animals exposed to diesel engine exhaust
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DOI：
10.1016/j.toxlet.2009.02.022
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发表时间：
2009-06-22
影响因子：
3.5
通讯作者：
Ercal, Nuran
中科院分区：
文献类型：
--
作者：
Banerjee, Atrayee;Trueblood, Max B.;Ercal, Nuran
柴油机排气颗粒物（DEPs）是柴油机排气的副产物，是城市大气颗粒物（PM）的主要组成部分。DEP由烟灰、多环芳烃（PAH）、氧化还原活性半醌和过渡金属组成，已知其产生促氧化和促炎作用，从而导致肺中氧化应激诱导的损伤。本研究的目的是确定N-乙酰半胱氨酸酰胺（NACA），一种新的巯基抗氧化剂，赋予保护暴露于DEP的动物免受氧化应激诱导的肺损伤。为了研究这一点，雄性C57 BL/6小鼠，用NACA（250 mg/kg体重）或盐水预处理，暴露于DEP（15 mg/m3）或过滤空气（1.5-3小时/天）连续9天。最后一次暴露后24小时处死动物。与仅暴露于DEP的动物相比，暴露于DEP的NACA处理的动物的巨噬细胞数量和肺中粘液栓形成量显著减少。此外，DEP暴露的动物，NACA预处理，也经历了显着低于未处理组的氧化应激，所示的谷胱甘肽（GSH），丙二醛（MDA）水平和过氧化氢酶（CAT）活性。此外，DEP诱导的肺毒性在NACA处理的动物中逆转，如乳酸脱氢酶水平所示。总之，这些数据表明，硫醇抗氧化剂NACA可以保护肺免受DEP诱导的炎症和氧化应激相关的损伤。(C)2009爱思唯尔爱尔兰有限公司保留所有权利。
Diesel exhaust particles (DEPs), a by-product of diesel engine exhaust (DEE), are one of the major components of air borne particulate matter (PM) in the urban environment. DEPs are composed of soot, polycyclic aromatic hydrocarbons (PAHs), redox active semi-quinones, and transition metals, which are known to produce pro-oxidative and pro-inflammatory effects, thereby leading to oxidative stress-induced damage in the lungs. The objective of this study was to determine if N-acetylcysteineamide (NACA), a novel thiol antioxidant, confers protection to animals exposed to DEPs from oxidative stress-induced damage to the lung. To study this, male C57BL/6 mice, pretreated with either NACA (250 mg/kg body weight) or saline, were exposed to DEPs (15 mg/m(3)) or filtered air (1.5-3 h/day) for nine consecutive days. The animals were sacrificed 24 h after the last exposure. NACA-treated animals exposed to DEP had significant decreases in the number of macrophages and the amount of mucus plug formation in the lungs, as compared to the DEP-only exposed animals. In addition, DEP-exposed animals, pretreated with NACA, also experienced significantly lower oxidative stress than the untreated group, as indicated by the glutathione (GSH), and malondialdehyde (MDA) levels and catalase (CAT) activity. Further, DEP-induced toxicity in the lungs was reversed in NACA-treated animals, as indicated by the lactate dehydrogenase levels. Taken together, these data suggest that the thiol-antioxidant, NACA, can protect the lungs from DEP-induced inflammation and oxidative stress related damage. (C) 2009 Elsevier Ireland Ltd. All rights reserved.