Zhang Yuexia, Yang Zhenhua, Feng Yan, Li Ruijin, Zhang Quanxi, Geng Hong, Dong Chuan
Institute of Environmental Science, Shanxi University, No. 92 Wucheng Road, Taiyuan, 030006, Shanxi Province, People's Republic of China.
Environ Sci Pollut Res Int. 2015 Aug;22(16):12450-7. doi: 10.1007/s11356-015-4437-3. Epub 2015 Apr 24.
The main aim of the present study was to examine in vitro responses of rat alveolar macrophages (AMs) exposed to coarse chalk dust particles (particulate matter in the size range 2.5-10 μm, PM(coarse)) by respiratory burst and oxidative stress. Chalk PM(coarse)-induced respiratory burst in AMs was measured by using a luminol-dependent chemiluminescence (CL) method. Also, the cell viability; lactate dehydrogenase (LDH) release; levels of cellular superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), malondialdehyde (MDA), and acid phosphatase (ACP); plasma membrane ATPase; and extracellular nitric oxide (NO) level were determined 4 h following the treatment with the different dosages of chalk PM(coarse). The results showed that chalk PM(coarse) initiated the respiratory burst of AMs as indicated by strong CL, which was inhibited by diphenyleneiodonium chloride and L-N-nitro-L-arginine methyl ester hydrochloride. It suggested that chalk PM(coarse) induced the production of reactive oxygen species (ROS) and reactive nitrogen species (RNS) in AMs. This hypothesis was confirmed by the fact that chalk PM(coarse) resulted in a significant decrease of intracellular SOD, GSH, ACP, and ATPase levels and a notable increase of intracellular CAT, MDA content, and extracellular NO level, consequently leading to a decrease of the cell viability and a increase of LDH release. It was concluded that AMs exposed to chalk PM(coarse) can suffer from cytotoxicity which may be mediated by generation of excessive ROS/RNS. Graphical Abstract The possible mechanism of coarse chalk particles-induced adverse effects in AMs.
本研究的主要目的是通过呼吸爆发和氧化应激来检测暴露于粗粉笔尘颗粒（粒径范围为2.5 - 10μm的颗粒物，PM(粗)）的大鼠肺泡巨噬细胞（AMs）的体外反应。使用鲁米诺依赖性化学发光（CL）方法测量粉笔PM(粗)诱导的AMs呼吸爆发。此外，在不同剂量的粉笔PM(粗)处理4小时后，测定细胞活力；乳酸脱氢酶（LDH）释放；细胞超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、谷胱甘肽（GSH）、丙二醛（MDA）和酸性磷酸酶（ACP）的水平；质膜ATP酶；以及细胞外一氧化氮（NO）水平。结果表明，如强CL所示，粉笔PM(粗)引发了AMs的呼吸爆发，而这种爆发受到二苯基碘鎓氯化物和L - N - 硝基 - L - 精氨酸甲酯盐酸盐的抑制。这表明粉笔PM(粗)诱导了AMs中活性氧（ROS）和活性氮（RNS）的产生。这一假设通过以下事实得到证实：粉笔PM(粗)导致细胞内SOD、GSH、ACP和ATP酶水平显著降低，细胞内CAT、MDA含量和细胞外NO水平显著升高，从而导致细胞活力下降和LDH释放增加。得出的结论是，暴露于粉笔PM(粗)的AMs可能会遭受细胞毒性，这可能是由过量ROS/RNS的产生介导的。图形摘要 粗粉笔颗粒对AMs产生不良影响的可能机制。
