Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Activation of murine microglial cell lines by lipopolysaccharide and interferon-gamma causes NO-mediated decreases in mitochondrial and cellular function
Autore:
Moss, DW; Bates, TE;
Indirizzi:
Univ Coll London, Inst Neurol, Dept Neurochem, London WC1N 3BG, England Univ Coll London London England WC1N 3BG ochem, London WC1N 3BG, England
Titolo Testata:
EUROPEAN JOURNAL OF NEUROSCIENCE
fascicolo: 3, volume: 13, anno: 2001,
pagine: 529 - 538
SICI:
0953-816X(200102)13:3<529:AOMMCL>2.0.ZU;2-X
Fonte:
ISI
Lingua:
ENG
Soggetto:
NITRIC-OXIDE SYNTHASE; RAT-BRAIN MITOCHONDRIA; PRIMARY GLIAL CULTURES; ELECTRON-TRANSPORT CHAIN; CENTRAL-NERVOUS-SYSTEM; IN-VITRO; PARKINSONS-DISEASE; ALZHEIMERS-DISEASE; MULTIPLE-SCLEROSIS; OXIDATIVE STRESS;
Keywords:
ATP; glutathione; murine; neurodegeneration; oxidative stress;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
73
Recensione:
Indirizzi per estratti:
Indirizzo: Moss, DW Univ Coll London, Wolfson Inst Biomed Res, Dept Cell & Mol Biol, CruciformBldg,Gower St, London WC1E 6AU, England Univ Coll London CruciformBldg,Gower St London England WC1E 6AU
Citazione:
D.W. Moss e T.E. Bates, "Activation of murine microglial cell lines by lipopolysaccharide and interferon-gamma causes NO-mediated decreases in mitochondrial and cellular function", EUR J NEURO, 13(3), 2001, pp. 529-538

Abstract

Activation of murine microglial and macrophage cell lines with lipopolysaccharide (LPS) and interferon-gamma (IFN-gamma) resulted in the induction ofthe inducible form of nitric oxide synthase (NOS) and the release of micromolar amounts of NO into the surrounding medium. The synthesis of NO was associated with increased cellular membrane damage as assessed by trypan bluedye exclusion and the leakage of lactate dehydrogenase into the cell culture medium. However, the synthesis and release of cytokines was largely unaffected. NO-mediated cell damage was also accompanied by a marked decrease in the intracellular levels of reduced glutathione and ATP. In addition, significant inhibition of mitochondrial respiratory chain enzyme activities was seen following cellular activation. However, citrate synthase activity (amitochondrial matrix enzyme) was not detectable in the extracellular supernatants, suggesting preservation of the integrity of the mitochondrial inner membrane following activation. These effects were largely prevented by the addition of the NOS inhibitor, N-guanidino monomethyl L-arginine during the activation period. Our observations demonstrate that induction of NOS activity in microglia results in damage to the plasma membrane leading to a loss of glutathione, complex-specific inhibition of the mitochondrial electron transport chain and depletion of cellular ATP. Our data suggest that pharmacological modulation of NOS activity in activated microglia in vivo may prevent cellular damage to bystander cells such as neurons, astrocytes and oligodendrocytes, as well as to microglia themselves.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/01/20 alle ore 19:01:34