Abstract:
:The features of neuronal damage induced by the mitochondrial toxin NaN(3) were investigated in rat primary cortical neuron cultures. Cell viability (MTT colorimetric determination) and transmembrane mitochondrial potential (J-C1 fluorescence) were concentration-dependently reduced 24 h after NaN(3); neither nuclear fragmentation by DAPI, nor Annexin V positivity by flow cytometry were detected, ruling out the occurrence of apoptosis. The loss in cell viability (to 54 +/- 2%) observed 24 h after a 10-min treatment with 3 mM NaN(3) was prevented by the NMDA glutamate receptor antagonist MK801 (1 microM), by the antioxidants trolox (100 microM) and acetyl-L-carnitine (1 mM) and by the nitric oxide synthase inhibitor, L-NAME (100 microM), but not by the guanylylcyclase inhibitor ODQ, 10 microM. The mitochondrial dysfunction induced by NaN(3) provides a common platform for investigating the mechanisms of both ischemic and degenerative neuronal injury, useful for screening potential protective agents against neuronal death.
journal_name
Neurochem Resjournal_title
Neurochemical researchauthors
Selvatici R,Previati M,Marino S,Marani L,Falzarano S,Lanzoni I,Siniscalchi Adoi
10.1007/s11064-008-9852-0subject
Has Abstractpub_date
2009-05-01 00:00:00pages
909-16issue
5eissn
0364-3190issn
1573-6903journal_volume
34pub_type
杂志文章abstract::Convulsions and brain levels of amino acids and 5-hydroxytryptamine (5-HT) in E1 mice were examined after oral administration of a 1% guanidinoethane sulfonate (GES) solution. The incidence of convulsions increased 3 days after starting GES administration, and this effect continued throughout the 6 months of drug admi...
journal_title:Neurochemical research
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