69 243

Cited 23 times in

NT-4/5 exacerbates free radical-induced neuronal necrosis in vitro and in vivo.

Authors
Won, SJ; Park, EC; Ryu, BR; Ko, HW; Sohn, S; Kwon, HJ; Gwag, BJ
Citation
Neurobiology of disease, 7(4):251-259, 2000
Journal Title
Neurobiology of disease
ISSN
0969-99611095-953X
Abstract
Neurotrophins render neurons highly vulnerable to certain injuries. We examined the possibility that NT-4/5 would enhance free radical neurotoxicity in vivo as well as in vitro. Striatal neurons exposed to 10 microM Fe(2+) or 1 mM l-buthionine-[S, R]-sulfoximine (BSO) underwent mild degeneration within 24 h. With concurrent addition of 10-100 ng/ml NT-4/5, neuronal death following exposure to Fe(2+) or BSO was significantly increased and suppressed by addition of 100 microM trolox, an antioxidant. In the adult brain, the intrastriatal injections of 20 nmol Fe(2+) revealed features of neuronal necrosis such as swelling cell body and mitochondria, fenestration of plasma membrane prior to nuclear membrane, and scattering condensation of nuclear chromatin. Cotreatment with 1.8 microg NT-4/5 augmented the striatal damage 24 h following the injections of Fe(2+). This study implies that free radicals produce necrotic degeneration in vivo as well as in vitro that becomes more sensitive in the presence of neurotrophins.
MeSH terms
AnimalsCell Death/*drug effects/physiologyCells, CulturedCorpus StriatumEmbryo, MammalianFree Radicals/pharmacologyNecrosisNerve Degeneration/chemically inducedNerve Growth Factors/*pharmacologyNeurons/*drug effects/pathologyNeuroprotective Agents/*pharmacologyRats
DOI
10.1006/nbdi.2000.0284
PMID
10964597
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Pharmacology
Journal Papers > School of Medicine / Graduate School of Medicine > Microbiology
AJOU Authors
손, 성향곽, 병주
Full Text Link
Files in This Item:
Full-Text Not Available.txtDownload
Export
RIS (EndNote)
XLS (Excel)
XML

qrcode

해당 아이템을 이메일로 공유하기 원하시면 인증을 거치시기 바랍니다.

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

Browse