Abstract
The features of neuronal damage induced by the mitochondrial toxin NaN3 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 NaN3; 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 NaN3 was prevented by the NMDA glutamate receptor antagonist MK801 (1 μM), by the antioxidants trolox (100 μM) and acetyl-l-carnitine (1 mM) and by the nitric oxide synthase inhibitor, L-NAME (100 μM), but not by the guanylylcyclase inhibitor ODQ, 10 μM. The mitochondrial dysfunction induced by NaN3 provides a common platform for investigating the mechanisms of both ischemic and degenerative neuronal injury, useful for screening potential protective agents against neuronal death.
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Acknowledgments
This work was supported by Grants from University of Ferrara, Italy, from Associazione Emma e Ernesto Rulfo per la Genetica Medica, Parma, Italy and from Fondazione Cassa di Risparmio di Ferrara. We are grateful to Dr. Amanda Neville for the English revision of the text.
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Rita Selvatici and Maurizio Previati equally contributed to the work.
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Selvatici, R., Previati, M., Marino, S. et al. Sodium Azide Induced Neuronal Damage In Vitro: Evidence for Non-Apoptotic Cell Death. Neurochem Res 34, 909–916 (2009). https://doi.org/10.1007/s11064-008-9852-0
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DOI: https://doi.org/10.1007/s11064-008-9852-0