Please use this identifier to cite or link to this item:
|Title:||Quinacrine attenuates increases in divalent metal transporter-1 and iron levels in the rat hippocampus, after kainate-induced neuronal injury|
|Authors:||Wang, X.S. |
Divalent metal transporter-1
|Citation:||Wang, X.S., Ong, W.Y., Connor, J.R. (2003). Quinacrine attenuates increases in divalent metal transporter-1 and iron levels in the rat hippocampus, after kainate-induced neuronal injury. Neuroscience 120 (1) : 21-29. ScholarBank@NUS Repository. https://doi.org/10.1016/S0306-4522(03)00293-8|
|Abstract:||The present investigation was carried out to elucidate the effect of the antimalarial drug quinacrine on levels of expression of the non-heme iron transporter, divalent metal transporter-1 (DMT1) and iron, in the hippocampus of rats after kainate treatment. The untreated hippocampus was lightly stained for DMT1, while an increase in DMT1 staining in astrocytes in the degenerating cornu ammonis (CA) fields, after kainate lesions. The increased DMT1 immunoreactivity was correlated with increased levels of Fe3+ and Fe2+ staining in the CA fields, as demonstrated by iron histochemistry (Perl's and Turnbull's blue stain for Fe3+ and Fe2+). The increases in DMT1 and iron staining were significantly attenuated by quinacrine. Rats injected with kainate and daily i.p. injections of quinacrine (5 mg/kg) for 7 days or 2 weeks showed significantly lower levels of DMT1 immunoreactivity and iron staining, compared with rats injected with kainate and saline. These results show that DMT1 expression is closely linked to iron levels, and provide further support for a crucial role that DMT1 plays in iron accumulation in the degenerating hippocampus. © 2003 IBRO. Published by Elsevier Science Ltd. All rights reserved.|
|Appears in Collections:||Staff Publications|
Show full item record
Files in This Item:
There are no files associated with this item.
checked on Jul 20, 2018
WEB OF SCIENCETM
checked on Jun 5, 2018
checked on May 5, 2018
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.