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空气污染颗粒物介导的肺泡巨噬细胞氧化应激分析

Analysis of air pollution particulate-mediated oxidant stress in alveolar macrophages.

作者信息

Goldsmith C A, Imrich A, Danaee H, Ning Y Y, Kobzik L

机构信息

Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts 02115, USA.

出版信息

J Toxicol Environ Health A. 1998 Aug 7;54(7):529-45. doi: 10.1080/009841098158683.

DOI:10.1080/009841098158683
PMID:9726778
Abstract

Adverse health effects of urban air pollution particulates may be attributable to particle-mediated oxidant stress and inflammation. Intracellular oxidant production in normal hamster alveolar macrophages (AMs) was measured upon exposure to concentrated ambient particulates (CAPs), residual oil fly ash (ROFA), and their water-soluble and particulate fractions. ROFA and CAPs caused increases in dichlorofluorescin (DCFH) oxidation, a fluorescent measure of intracellular reactive oxygen species (ROS) production, comparable to the positive control, phorbol myristate acetate (PMA). The water-soluble component of both CAPs and ROFA (CAPs, S and ROFA, S) significantly increased AM oxidant production over negative control. CAPs samples and components showed substantial day-to-day variability in their oxidant effects. Metal chelation by desferrioxamine (DF, 1 mM) caused significant inhibition of particulate-induced AM oxidant production. ROFA exposure resulted in increased macrophage inflammatory protein-2 (MIP-2) message in AMs and in increased tumor necrosis factor alpha (TNF-alpha) production by the monocyte-macrophage cell line, RAW 264.7. TNF-alpha production was inhibitable by the antioxidant N-acetylcysteine (NAC). The data suggest that metal components adsorbed to urban air pollution particulates can significantly contribute to particulate ability to cause oxidant stress and cytokine production in AMs.

摘要

城市空气污染颗粒物对健康的不良影响可能归因于颗粒物介导的氧化应激和炎症。在暴露于浓缩环境颗粒物(CAPs)、残油飞灰(ROFA)及其水溶性和颗粒部分后,测量了正常仓鼠肺泡巨噬细胞(AMs)中的细胞内氧化剂生成。ROFA和CAPs导致二氯荧光素(DCFH)氧化增加,这是一种测量细胞内活性氧(ROS)生成的荧光指标,与阳性对照佛波酯肉豆蔻酸酯乙酸酯(PMA)相当。CAPs和ROFA的水溶性成分(CAPs,S和ROFA,S)与阴性对照相比,显著增加了AMs中的氧化剂生成。CAPs样品及其成分在其氧化作用方面表现出显著的每日变化。去铁胺(DF,1 mM)进行金属螯合可显著抑制颗粒物诱导的AMs氧化剂生成。暴露于ROFA导致AMs中巨噬细胞炎性蛋白-2(MIP-2)信使增加,单核巨噬细胞系RAW 264.7中肿瘤坏死因子α(TNF-α)生成增加。抗氧化剂N-乙酰半胱氨酸(NAC)可抑制TNF-α的生成。数据表明,吸附在城市空气污染颗粒物上的金属成分可显著促进颗粒物在AMs中引起氧化应激和细胞因子生成的能力。

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