Increased calcium influx in a monocytic cell line on exposure to ultrafine carbon black

Ultrafine particles have been shown to induce pro-inflammatory effects both in vivo and in vitro. Increased expression of pro-inflammatory genes probably requires the activation of specific transcription factors such as nuclear factor kappa B (NF-kappaB) via a number of possible pathways including Ca2+ and reactive oxygen species. The fluorescent dye fura 2, was used to measure cytosolic Ca2+ in the human monocytic cell line, Monomac 6 on exposure to 66 microg x mL(-1) of either ultrafine carbon black (ufCB; diameter 14 nm), carbon black (CB; diameter 260 nm), quartz (diameter 1.45 microm), or medium alone. UfCB but not fine CB induced a 1.6-fold increase (p<0.01) in the resting cytosolic Ca2+ concentration of Monomac 6 cells. In addition ufCB induced a 2.6-fold increase (p<0.001) in the response to the endoplasmic reticulum Ca2+- adenosine triphosphatase (ATPase) inhibitor, thapsigargin, suggesting the Ca2+ release-activated Ca2+ current across the plasma membrane was enhanced. This response was inhibited by the removal of extracellular Ca2+ and by the Ca2+ channel blocker, verapamil. In addition, ufCB stimulated the entry of extracellular Mn2+. Finally, the antioxidants mannitol and nacystelin both inhibited the effects of ufCB on the response to thapsigargin. These data suggest that ultrafine carbon black particles stimulated an increase in cytosolic Ca2+, possibly through the entry of extracellular Ca2+ via Ca2+ channels in the plasma membrane. The particles may in part activate the opening of Ca2+ channels via a mechanism involving reactive oxygen species.

This article has been cited by other articles:

				J. Schwartz, S. K. Park, M. S. O'Neill, P. S. Vokonas, D. Sparrow, S. Weiss, and K. Kelsey Glutathione-S-Transferase M1, Obesity, Statins, and Autonomic Effects of Particles: Gene-by-Drug-by-Environment Interaction Am. J. Respir. Crit. Care Med., December 15, 2005; 172(12): 1529 - 1533. [Abstract] [Full Text] [PDF]

				T. P. J. Hofer, E. Bitterle, I. Beck-Speier, K. L. Maier, M. Frankenberger, J. Heyder, and L. Ziegler-Heitbrock Diesel exhaust particles increase LPS-stimulated COX-2 expression and PGE2 production in human monocytes J. Leukoc. Biol., May 1, 2004; 75(5): 856 - 864. [Abstract] [Full Text] [PDF]

				D. M. Brown, K. Donaldson, P. J. Borm, R. P. Schins, M. Dehnhardt, P. Gilmour, L. A. Jimenez, and V. Stone Calcium and ROS-mediated activation of transcription factors and TNF-{alpha} cytokine gene expression in macrophages exposed to ultrafine particles Am J Physiol Lung Cell Mol Physiol, February 1, 2004; 286(2): L344 - L353. [Abstract] [Full Text] [PDF]

				W. MacNee and K. Donaldson Mechanism of lung injury caused by PM10 and ultrafine particles with special reference to COPD Eur. Respir. J., May 1, 2003; 21(40_suppl): 47S - 51s. [Abstract] [Full Text] [PDF]

				H. Kim, X. Liu, T. Kobayashi, T. Kohyama, F.-Q. Wen, D. J. Romberger, H. Conner, P. S. Gilmour, K. Donaldson, W. MacNee, et al. Ultrafine Carbon Black Particles Inhibit Human Lung Fibroblast-Mediated Collagen Gel Contraction Am. J. Respir. Cell Mol. Biol., January 1, 2003; 28(1): 111 - 121. [Abstract] [Full Text] [PDF]

				P. S. Gilmour, I. Rahman, S. Hayashi, J. C. Hogg, K. Donaldson, and W. MacNee Adenoviral E1A primes alveolar epithelial cells to PM10-induced transcription of interleukin-8 Am J Physiol Lung Cell Mol Physiol, September 1, 2001; 281(3): L598 - L606. [Abstract] [Full Text] [PDF]

				A M Knaapen, G J den Hartog, A Bast, and P J. Borm Ambient particulate matter induces relaxation of rat aortic rings in vitro Human and Experimental Toxicology, May 1, 2001; 20(5): 259 - 265. [Abstract] [PDF]

				K Donaldson, V Stone, A Clouter, L Renwick, and W MacNee Ultrafine particles Occup. Environ. Med., March 1, 2001; 58(3): 211 - 216. [Full Text]

				D M Brown, V Stone, P Findlay, W MacNee, and K Donaldson Increased inflammation and intracellular calcium caused by ultrafine carbon black is independent of transition metals or other soluble components Occup. Environ. Med., October 1, 2000; 57(10): 685 - 691. [Abstract] [Full Text]

				W. MacNee and K. Donaldson Exacerbations of COPD : Environmental Mechanisms Chest, May 1, 2000; 117 (2009): 390S - 397S. [Abstract] [Full Text] [PDF]