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An aluminum-induced increase in GFAP is attenuated by some chelators.

Authors
Yokel-RA; O'Callaghan-JP
Source
Neurotoxicol Teratol 1998 Jan-Feb; 20(1):55-60
NIOSHTIC No.
20025503
Abstract
Enhanced expression of glial fibrillary acidic protein (GFAP) has been shown to be associated with gliosis, a generic response of the CNS to neural injury. The effects of aluminum (Al) on regional GFAP concentrations were evaluated to determine potential sites of Al-induced neural injury. Rabbits received 20 Al (100 mumol/kg) or sodium lactate injections over 1 month. Frontal cortical GFAP increased (approximately twofold above control) in Al-loaded rabbits; whereas hippocampal and cerebellar GFAP concentrations were not affected. Frontal cortical synaptophysin, neurofilament 68, and myelin basic protein concentrations were then examined in an attempt to determine cell-specific targets of Al neurotoxicity. These proteins were not affected by Al. The ability of chelators to influence brain Al concentrations and the Al effect on GFAP were assessed. Desferrioxamine (DFO) and six 3-hydroxypyridin-4-ones (CPs) were given 12 times, over 1 month, to Al-loaded rabbits. CP24 significantly reduced brain Al. CP93, CP52, and CP24 significantly reduced frontal cortical GFAP. The data suggest an Al-induced gliosis consequent to subtle damage in the frontal cortex and a protective role of some chelators against this CNS injury.
Keywords
Aluminum-compounds; Neurotoxicity; Neurotoxic-effects; Laboratory-animals; Animals; Animal-studies; Central-nervous-system
CODEN
NETEEC
CAS No.
7429-90-5
Publication Date
19980101
Document Type
Journal Article
Fiscal Year
1998
NTIS Accession No.
NTIS Price
Issue of Publication
1
ISSN
0892-0362
NIOSH Division
HELD
Source Name
Neurotoxicology and Teratology
State
WV; KY
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