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Monocarboxylate Transporters are not Responsible for Cr3+ Transport from Endosomes

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Abstract

Cr3+, similar to Fe3+, is transported into cells primarily via endocytosis as the metal-transferrin complex. As Cr3+ ions are not readily reduced under biological conditions, the ion cannot be transported from endosomes by the same mechanism as iron that utilized divalent metal ion transporters. Cr3+ has been hypothesized to potentially be transported as small ligand complexes with a free carboxylate functionality by monocarboxylate transporters (MCT), in a similar fashion to that proposed for Al3+. Consequently, mouse C2C12 muscle cells were utilized to determine if Cr3+ is potentially transported by MCT by examining the effects of MCT inhibitors on Cr and Fe transport and subcellular distribution when the metals are added as their transferrin complexes. The results suggest that Cr is not primarily transported by MCT from the endosomes to the cytosol, and that another mechanism for this transport needs to be identified.

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Acknowledgments

This work was supported by the National Research Initiative grant 2009-35200-05200 from the USDA Cooperative State, Research, Educational, and Extension Service to JBV and JFR. Kristin R. Di Bona assisted in working out conditions for the cell homogenization.

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The authors have no conflicts of interest to declare.

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Correspondence to John B. Vincent.

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Rhodes, N.R., LeBlanc, P.A., Rasco, J.F. et al. Monocarboxylate Transporters are not Responsible for Cr3+ Transport from Endosomes. Biol Trace Elem Res 148, 409–414 (2012). https://doi.org/10.1007/s12011-012-9381-1

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  • DOI: https://doi.org/10.1007/s12011-012-9381-1

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