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Colistin is a polycation antibiotic used for the treatment of multidrug-resistance (MDR) gram-negative infections; nevertheless, its use is often limited by the high incidence of renal damage. The mechanism underlying colistin-induced nephrotoxicity is not known, but perhaps related to its accumulation in the renal cortex upon extensive reabsorption from the nascent urine. Because little is known about the membrane transport of colistin, the purpose of the present study was to characterize better the transport system involved in colistin renal handling by using HEK293 cells stably transfected with the main organic cation transporters expressed at the apical membrane of the proximal tubule. [ 14 C]Colistin was transported by the carnitine/organic cation transporter 2 (OCTN2, SLC22A5) but not by the organic cation transporter 1 (OCT1) and N1 (OCTN1). Non-labeled colistin inhibited the OCTN2-mediated transport of [ 3 H]L-carnitine in a non-competitive manner and that of [ 14 C]tetraethylammonium bromide ([ 14 C]TEA) in a competitive manner. Unlike that of [ 3 H]L-carnitine, the [ 14 C]colistin OCTN2-mediated uptake was Na + -independent. When endogenous OCTN2-mediated colistin transport was inhibited by co-incubation with L-carnitine, primary mouse proximal tubular cells were fully protected from colistin toxicity, suggesting that colistin toxicity occurred upon intracellular accumulation.

Colistin is Substrate of the Carnitine/Organic Cation Transporter 2 (OCTN2, SLC22A5)