View : 10 Download: 0

Cadmium-induced astroglial death proceeds via glutathione depletion

Title
Cadmium-induced astroglial death proceeds via glutathione depletion
Authors
Im J.-Y.Paik S.-G.Han P.-L.
Ewha Authors
한평림
SCOPUS Author ID
한평림scopus
Issue Date
2006
Journal Title
Journal of Neuroscience Research
ISSN
0360-4012JCR Link
Citation
vol. 83, no. 2, pp. 301 - 308
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Cadmium is a heavy metal that accumulates in the body, and its accumulation in the brain damages both neurons and glial cells. In the current study, we explored the mechanism underlying cadmium toxicity in primary cortical astroglia cultures. Chronic treatment with 10 μM cadmium was sufficient to cause 90% cell death in 18 hr. However, unlike that observed in neurons, cadmium-induced astroglial toxicity was not attenuated by the antioxidants trolox (100 μM), caffeic acid (1 mM), and vitamin C (1 mM). In contrast, extracellular 100 μM glutathione (GSH; 7-Glu-CyS-Gly) or 100 μM cysteine almost completely blocked cadmium-induced astroglial death, whereas 300 μM oxidized GSH (GSSG) or 300 μM cystine, which do not have the free thiol group, were ineffective. In addition, cadmium toxicity was noticeably inhibited or enhanced when intracellular GSH was, respectively, increased by using the cell-permeable glutathione ethyl ester (GSH-EE) or depleted by using buthionine sulfoximine (BSO), an inhibitor of γ-glutamylcysteine synthetase. In agreement with these data, intracellular GSH levels were found to be depressed in cadmium-treated astrocytes. These results suggest that the toxic effect of cadmium on primary astroglial cells involves GSH depletion and, furthermore, that GSH administration can potentially be used to counteract cadmium-induced astroglial cell death therapeutically. © 2005 Wiley-Liss, Inc.
DOI
10.1002/jnr.20722
Appears in Collections:
일반대학원 > 뇌·인지과학과 > Journal papers
Files in This Item:
There are no files associated with this item.
Export
RIS (EndNote)
XLS (Excel)
XML


qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

BROWSE