Multiple pathways of neuroprotection against oxidative stress and excitotoxic injury in immature primary hippocampal neurons

Almli, LM; Hamrick, SE; Koshy, AA; Täuber, MG; Ferriero, DM (2001). Multiple pathways of neuroprotection against oxidative stress and excitotoxic injury in immature primary hippocampal neurons. Developmental brain research, 132(2), pp. 121-9. Amsterdam: Elsevier 10.1016/S0165-3806(01)00302-9

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In the immature brain hydrogen peroxide accumulates after excitotoxic hypoxia-ischemia and is neurotoxic. Immature hippocampal neurons were exposed to N-methyl-D-aspartate (NMDA), a glutamate agonist, and hydrogen peroxide (H(2)O(2)) and the effects of free radical scavenging and transition metal chelation on neurotoxicity were studied. alpha-Phenyl-N-tert.-butylnitrone (PBN), a known superoxide scavenger, attenuated both H(2)O(2) and NMDA mediated toxicity. Treatment with desferrioxamine (DFX), an iron chelator, at the time of exposure to H(2)O(2) was ineffective, but pretreatment was protective. DFX also protected against NMDA toxicity. TPEN, a metal chelator with higher affinities for a broad spectrum of transition metal ions, also protected against H(2)O(2) toxicity but was ineffective against NMDA induced toxicity. These data suggest that during exposure to free radical and glutamate agonists, the presence of iron and other free metal ions contribute to neuronal cell death. In the immature nervous system this neuronal injury can be attenuated by free radical scavengers and metal chelators.

Item Type:	Journal Article (Original Article)
Division/Institute:	04 Faculty of Medicine > Service Sector > Institute for Infectious Diseases
UniBE Contributor:	Täuber, Martin G.
ISSN:	0165-3806
ISBN:	11744116
Publisher:	Elsevier
Language:	English
Submitter:	Factscience Import
Date Deposited:	04 Oct 2013 15:00
Last Modified:	05 Dec 2022 14:18
Publisher DOI:	10.1016/S0165-3806(01)00302-9
PubMed ID:	11744116
Web of Science ID:	000173120100002
URI:	https://boris.unibe.ch/id/eprint/25737 (FactScience: 60842)