[Effect of sodium azide on mitochondrial membrane potential in SH-SY5Y human neuroblastoma cells].
OBJECTIVE
To study the role of mitochondrial deficiency in the pathogenesis of neurodegenerative disease by investigating the energy metabolism in a sodium azide inhibited cytochrome-c oxidase SH-SY5Y Cell model.


METHODS
Human neuroblastoma SH-SY5Y Cells were exposed to sodium azide, then mitochondrial complex IV activity was assayed by microassay method; cell viability was measured by Thiazolyl blue(MTT) method; mitochondrial membrane potential (MMP) was detected by confocal microscopy and flow cytometry.


RESULTS
Cultured SH-SY5Y cells were exposed to 16-64 mmol/L sodium azide for 1 hour, the mitochondrial complex IV activity decreased dose-dependently. MTT absorbance decreased does- and time-dependently in cultured nerve cells treated by 16-128 mmol/L sodium azide for 1-8 hours. After the treatment of 16 mmol/L sodium azide for 1 hour, both the fluorescence intensity of MMP and normal cell events reduced. Decrease of MMP was significant especially in cell processes.


CONCLUSIONS
Sodium azide induced the impairment of mitochondrial energy synthesis in the cultured nerve cells which is an important cause in cell death.
Zhang
L
L
Department of Pharmacology, Xuan-Wu Hospital, Capital University of Medical Sciences, Beijing Key Laboratory for Brain Aging, Beijing 100053, China. lanizhg@hotmail.com
Li
L
L
Ban
L
L
An
W
W
Liu
S
S
Li
X
X
Xue
B
B
Xu
Y
Y
D016923:Cell Death / Q000187:drug effects; D003576:Electron Transport Complex IV / Q000187:drug effects / Q000378:metabolism*; D006801:Humans; D008564:Membrane Potentials / Q000187:drug effects; D008928:Mitochondria / Q000187:drug effects / Q000502:physiology*; D009447:Neuroblastoma / Q000473:pathology / Q000503:physiopathology*; D019810:Sodium Azide / Q000494:pharmacology*; D014407:Tumor Cells, Cultured
D019810:Sodium Azide; D003576:Electron Transport Complex IV