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Query: UMLS:C0037116 (silicosis)
 1,822 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rat alveolar macrophages were exposed to silica dust (quartz) suspended in culture medium (SiO2, dry particle size less than 5 microns in diameter) and fluctuation in their cytosolic free calcium content ([Ca2+]i) was detected in cell monolayers with a fluorescent calcium probe (Indo-1AM). Cytosolic free calcium content was correlated with lactate dehydrogenase (LDH) release, an index of cell damage. SiO2 induced a concentration- and time-dependent increase of cytosolic free Ca2+ ion concentration and LDH release. [Ca2+]i was increased about fivefold when cells were exposed to 200 micrograms of SiO2 per milliliter (3 ml per dish) for 2 hr. [Ca2+]i changed within 15 min of SiO2 treatment, whereas LDH release was measurably increased only after 30 min. Chelation of extracellular Ca2+ by 2 mM ethylene glycol bis(beta-aminoethyl ether) N,N'-tetraacetate did not prevent SiO2-induced fluctuation of macrophage [Ca2+]i, but did partially prevent the SiO2-induced increase in LDH release (p less than 0.01). We conclude that a very early event in SiO2-induced damage of alveolar macrophages involves mobilization of intracellular calcium pools to increase [Ca2+]i. These results suggest that SiO2-induced macrophage damage, a key event in the development of silicosis, may involve perturbation of intracellular calcium homeostasis.
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PMID:Silica increases cytosolic free calcium ion concentration of alveolar macrophages in vitro. 165 54

Historical studies report that cellular injury and silicosis are related to cytosolic free calcium (Ca2+). Moreover, reactive oxygen species (ROS) have been linked to cellular injury. However, the detail mechanism of the increase in [Ca2+]i and the relationship between [Ca2+]i and ROS production remains unknown. Quartz particle has been found to increase [Ca2+]i and activate the generation of ROS. Our hypothesis is that [Ca2+]i increase induced by quartz particle is from extracellular Ca2+ through the Ca2+ channel, and [Ca2+]i increase is believed to activate ROS production. In order to examine this hypothesis, we treated rat alveolar macrophages with quartz (SiO2) particles and used laser scanning confocal microscopy to measure [Ca2+]i and the fluorescence intensity of ROS. Time- and dose-dependent increases in [Ca2+]I and ROS in macrophages as well as cell viability were observed. Through chelating extracellular Ca2+ with ethylene glycol tetraacetic acid and releasing intracellular Ca2+ with thapsigargin, we found that 72.7% of the [Ca2+]i increase was due to the influx of Ca2+ from the extracellular environment, via Ca2+ channels in the plasma membrane. By adding mannitol to scavenge hydroxyl radicals (OH(.)), and removing surface iron from the quartz particles to reduce OH(.) generation, we observed a reduced level of ROS generation, whereas the increase in [Ca2+]i was unaffected. When using EGTA to reduce [Ca2+]i, we observed a decrease in ROS production. This study suggests that the [Ca2+]i influx was independent of OH(.) production, and the [Ca2+]i increase resulted in ROS production. These results further indicate that there is a strong relationship between cytosolic free Ca2+ content and cellular injury as well as silica exposure.
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PMID:Intracellular influx of calcium induced by quartz particles in alveolar macrophages. 1983