Effects of blowing sand fine particles on plasma membrane permeability and fluidity, and intracellular calcium levels of rat alveolar macrophages.
Ambient fine particulate matter (PM2.5, particulates with an aerodynamic diameter < or = 2.5 microm) can suppress alveolar macrophage (AM) functions, but the data concerning the effects of blowing sand PM2.5 on AMs remain limited. The aim of the present study is to investigate the influences of blowing sand PM2.5 on AM plasma membranes and intracellular calcium ion concentration ([Ca2+]i), and explore the mechanisms of the observed toxicological effects. The samples of normal PM2.5 (collected on sunshiny and non-blowing sand days) and blowing sand PM2.5 were collected in Wuwei city, Gansu Province, China. After AMs from rat bronchoalveolar lavage fluid (BALF) were treated in vitro for 4 h with the suspensions of these samples, the cell viability, plasma membrane permeability and fluidity, cytosolic free Ca2+ levels, and oxidative stress were examined. It was observed a dose-dependent decrease in cell viability, plasma membrane Ca2+Mg2+-dependent adenosinetriphosphatase (Ca2+Mg2+-ATPase) and Na+K+-dependent adenosinetriphosphatase (Na+K+-ATPase) activities, cellular glutathione (GSH) levels, fluorescence intensities of lipid probe 8-anilino-1-naphthalene-sulfonic acid (ANS) and fluorescence polarization of lipid probe 1,6-diphenyl-1,3,5-hexatriene (DPH) combined with cell membranes in the treatment groups of normal and blowing sand PM2.5 as compared to the control (saline group); and also observed a dose-dependent increase in the leakage of lactate dehydrogenase (LDH) and acid phosphatase (ACP), and intracellular [Ca2+]i and malondialdehyde (MDA) levels. These observations indicate blowing sand PM2.5, as similar to urban normal ones, could induce oxidative stress on AMs, enlarge plasma membrane permeability and membrane lipid fluidity, and elevate intracellular [Ca2+]i levels, resulting in cytotoxicity. A two-way ANOVA showed the toxic effects of normal and blowing sand PM2.5 on AMs were only relative to treatment dosages but not to dust types, suggesting the blowing sand PM2.5 whose airborne mass concentrations were much higher should be more harmful.
Geng
Hong
H
Institute of Environmental Medicine and Toxicology, Shanxi University, Wucheng Road 36, Taiyuan 030006, PR China. genghong2004@126.com
Meng
Ziqiang
Z
Zhang
Quanxi
Q
D000388:Air / Q000032:analysis; D000393:Air Pollutants / Q000493:pharmacokinetics / Q000633:toxicity*; D000818:Animals; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology; D002118:Calcium / Q000378:metabolism*; D002463:Cell Membrane Permeability / Q000187:drug effects*; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D002681:China; D003600:Cytosol / Q000187:drug effects / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D016676:Macrophages, Alveolar / Q000187:drug effects* / Q000378:metabolism; D008560:Membrane Fluidity / Q000187:drug effects*; D018384:Oxidative Stress; D010316:Particle Size; D051381:Rats; D012822:Silicon Dioxide / Q000493:pharmacokinetics / Q000633:toxicity*
D000393:Air Pollutants; D012822:Silicon Dioxide; D002118:Calcium