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Titolo:
MITOCHONDRIAL TOXINS IN MODELS OF NEURODEGENERATIVE DISEASES .1. IN-VIVO BRAIN HYDROXYL RADICAL PRODUCTION DURING SYSTEMIC MPTP TREATMENT OR FOLLOWING MICRODIALYSIS INFUSION OF METHYLPYRIDINIUM OR AZIDE IONS
Autore:
SMITH TS; BENNETT JP;
Indirizzi:
UNIV VIRGINIA,HLTH SCI CTR,SCH MED,CTR STUDY NEURODEGENERAT DIS,DEPT NEUROL,BOX 394 CHARLOTTESVILLE VA 22908 UNIV VIRGINIA,HLTH SCI CTR,SCH MED,CTR STUDY NEURODEGENERAT DIS,DEPT NEUROL CHARLOTTESVILLE VA 22908 UNIV VIRGINIA,HLTH SCI CTR,CTR STUDY NEURODEGENERAT DIS,DEPT PSYCHIATMED CHARLOTTESVILLE VA 22908 UNIV VIRGINIA,HLTH SCI CTR,CTR STUDY NEURODEGENERAT DIS,DEPT PHARMACOL CHARLOTTESVILLE VA 22908
Titolo Testata:
Brain research
fascicolo: 2, volume: 765, anno: 1997,
pagine: 183 - 188
SICI:
0006-8993(1997)765:2<183:MTIMON>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
NITRIC-OXIDE SYNTHASE; COMPLEX-I DEFICIENCY; PARKINSONISM-INDUCING NEUROTOXIN; ELECTRON-TRANSPORT CHAIN; ALZHEIMERS-DISEASE; CYTOCHROME-OXIDASE; RESPIRATORY-CHAIN; 1-METHYL-4-PHENYLPYRIDINIUM MPP+; SUBMITOCHONDRIAL PARTICLES; SKELETAL-MUSCLE;
Keywords:
BRAIN DIALYSIS; OXYGEN FREE RADICAL; METHYLPYRIDINIUM; AZIDE; NMDA CHANNEL; NITRIC OXIDE SYNTHASE PARKINSONS DISEASE; ALZHEIMERS DISEASE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
49
Recensione:
Indirizzi per estratti:
Citazione:
T.S. Smith e J.P. Bennett, "MITOCHONDRIAL TOXINS IN MODELS OF NEURODEGENERATIVE DISEASES .1. IN-VIVO BRAIN HYDROXYL RADICAL PRODUCTION DURING SYSTEMIC MPTP TREATMENT OR FOLLOWING MICRODIALYSIS INFUSION OF METHYLPYRIDINIUM OR AZIDE IONS", Brain research, 765(2), 1997, pp. 183-188

Abstract

Mitochondrial electron transport chain (ETC) function is selectively reduced in multiple tissues, including brain, from patients with Parkinson's disease (PD) and Alzheimer's disease (AD). The ETC defects are specific to each illness, involve complex I in PD and complex IV in AD, are transferable with mitochondrial DNA (mtDNA) and lead to increased production of reactive oxygen species (ROS) in mtDNA-deficient clonal neuronal cells hybridized with mtDNA ('cybrids') from PD or AD patients. C57BL/6 mice treated with MPTP developed elevated tissue hydroxylradical ((OH)-O-.) levels in striatum and ventral midbrain but not cerebellum. In brain microdialysis in awake rats, striatal (OH)-O-. output increased 3-5-fold after infusion of methylpyridinium ion (MPP+), acomplex I inhibitor, or sodium azide, a complex IV inhibitor. Elevated (OH)-O-. after MPP+ was blocked stereospecifically by infusion of the nitric oxide synthase (NOS) inhibitor nitro-L-arginine or by the NMDA channel blocker MK801. Neither NOS inhibition nos NMDA blockade altered azide-induced (OH)-O-. production. ETC inhibition in vivo increases production of toxic (OH)-O-., but the underlying mechanisms vary as a function of which ETC complex is inhibited. These results support the concept of developing oxygen free radical scavengers for both AD andPD and further suggest that inhibition of NOS and blockade of NMDA receptor function may alter progression of idiopathic PD. (C) 1997 Elsevier Science B.V.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 09/04/20 alle ore 13:29:24