Abstract
Cr(3+), similar to Fe(3+), is transported into cells primarily via endocytosis as the metal-transferrin complex. As Cr(3+) 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. Cr(3+) 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 Al(3+). Consequently, mouse C2C12 muscle cells were utilized to determine if Cr(3+) 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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