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 lM), by the antioxidants trolox (100 lM) and acetyl-L-carnitine (1 mM) and by the nitric oxide synthase inhibitor, L-NAME (100 lM), but not by the guanylylcyclase inhibitor ODQ, 10 lM. 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.
Sodium Azide Induced Neuronal Damage In Vitro: Evidence for Non-Apoptotic Cell Death
SELVATICI, Rita;PREVIATI, Maurizio;MARINO, Silvia;MARANI, Luca;FALZARANO, Maria Sofia;LANZONI, Irene;SINISCALCHI, Anna
2009
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 lM), by the antioxidants trolox (100 lM) and acetyl-L-carnitine (1 mM) and by the nitric oxide synthase inhibitor, L-NAME (100 lM), but not by the guanylylcyclase inhibitor ODQ, 10 lM. 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.I documenti in SFERA sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
