[Effect of sodium azide on mitochondrial membrane potential in SH-SY5Y human neuroblastoma cells].

Abstract

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.

CONCLUSION:

Sodium azide induced the impairment of mitochondrial energy synthesis in the cultured nerve cells which is an important cause in cell death.

• Authors: L Zhang, L Li, L Ban, W An, S Liu, X Li, B Xue, Y Xu
• Journal: Zhongguo yi xue ke xue yuan xue bao. Acta Academiae Medicinae Sinicae (Zhongguo Yi Xue Ke Xue Yuan Xue Bao) Vol. 22 Issue 5 Pg. 436-9 (Oct 2000) ISSN: 1000-503X [Print] China
• PMID: 12903423 (Publication Type: English Abstract, Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Sodium Azide
• Electron Transport Complex IV

Topics

• Cell Death (drug effects)
• Electron Transport Complex IV (drug effects, metabolism)
• Humans
• Membrane Potentials (drug effects)
• Mitochondria (drug effects, physiology)
• Neuroblastoma (pathology, physiopathology)
• Sodium Azide (pharmacology)
• Tumor Cells, Cultured