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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Gentamicin-induced increases in cytosolic calcium in pig kidney cells (LLC-PK1).

LLC-PK1 cells, an established epithelial cell line derived from pig kidney, were tested as a model system for assessing the role of calcium in gentamicin-induced nephrotoxicity. Cell viability was evaluated by a vital dye exclusion procedure, and intracellular free calcium [Ca2+]i was measured employing Fura-2 fluorescence. Exposing cell suspensions (10(6)/ml) to concentrations of the drug, which had no apparent effect on viability, produced a rapid and prolonged increase in intracellular [Ca2+]. The perturbation of calcium homeostasis could be blocked by the addition of mepiperphenidol, an inhibitor of the organic cation transport system. We propose that LLC-PK1 cells are an appropriate model to study drug-induced nephrotoxicity. Gentamicin disrupts calcium homeostasis and causes plasma membrane alterations. Since mepiperphenidol blocked the gentamicin-induced Ca2+ increases, the data suggest that aminoglycosides enter the cell via the organic cation transporter.[1]


  1. Gentamicin-induced increases in cytosolic calcium in pig kidney cells (LLC-PK1). Holohan, P.D., Sokol, P.P., Ross, C.R., Coulson, R., Trimble, M.E., Laska, D.A., Williams, P.D. J. Pharmacol. Exp. Ther. (1988) [Pubmed]
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