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Lithium inhibits aluminum‐induced apoptosis in rabbit hippocampus, by preventing cytochrome c translocation, Bcl‐2 decrease, Bax elevation and caspase‐3 activation
Author(s) -
Ghribi Othman,
Herman Mary M.,
Spaulding Natalie K.,
Savory John
Publication year - 2002
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.2002.00957.x
Subject(s) - neuroprotection , cytochrome c , dna fragmentation , apoptosis , microbiology and biotechnology , caspase 3 , endoplasmic reticulum , biology , tunel assay , bcl 2 associated x protein , mitochondrion , chemistry , programmed cell death , biochemistry , pharmacology
A variety of studies on neuronal death models suggest that lithium has neuroprotective properties. In the present investigation, we have examined the effect of chronic lithium treatment on hippocampus, as monitored by changes at the subcellular level of apoptosis‐regulatory proteins which have been induced by the neurotoxin, aluminum maltolate. Intracisternal administration of aluminum into rabbit brain induces cytochrome c release, decreases levels of the anti‐apoptotic proteins Bcl‐2 and Bcl‐X L , increases levels of the pro‐apoptotic Bax, activates caspase‐3, and causes DNA fragmentation as measured by the TUNEL assay. Pretreatment for 14 days with 7 m m of lithium carbonate in drinking water prevents aluminum‐induced translocation of cytochrome c , and up‐regulates Bcl‐2 and Bcl‐X L, down‐regulates Bax, abolishes caspase‐3 activity and reduces DNA damage. The regulatory effect of lithium on the apoptosis‐controlling proteins occurs in both the mitochondria and endoplasmic reticulum. We propose that the neuroprotective effect of lithium involves the modulation of apoptosis‐regulatory proteins present in the subcellular organelles of rabbit brain.