| Name | Cytochrome c oxidase (protein family or complex) |
|---|---|
| Synonyms | COX; cytochrome c oxidase; cytochrome c oxidases |
| Name | sodium azide |
|---|---|
| CAS | sodium azide |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 8632188 | Bennett MC, Mlady GW, Kwon YH, Rose GM: Chronic in vivo sodium azide infusion induces selective and stable inhibition of cytochrome c oxidase. J Neurochem. 1996 Jun;66(6):2606-11. |
82(1,1,1,2) | Details |
| 12903423 | Zhang L, Li L, Ban L, An W, Liu S, Li X, Xue B, Xu Y: [Effect of sodium azide on mitochondrial membrane potential in SH-SY5Y human neuroblastoma cells]. Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 2000 Oct;22(5):436-9. 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. |
81(1,1,1,1) | Details |
| 7622786 | Goyal N, Srivastava VM: Oxidation and reduction of cytochrome c by mitochondrial enzymes of Setaria cervi. J Helminthol. 1995 Mar;69(1):13-7. A mitochondria-rich fraction isolated from the cuticle-hypodermis-muscle system of Setaria cervi, a bovine filarial parasite, possessed substrate-coupled cytochrome c reductases and cytochrome c oxidase in appreciable activities. Sodium azide activated the reductases but substantially inhibited the oxidase activity. |
2(0,0,0,2) | Details |
| 15133893 | Zou Y, Gao J, Zhang TT, Xu L, Xu JY, Lu SY: [Changes of thioredoxin mRNA level in neurons with mitochondrial dysfunction insulted by H2O2]. Shi Yan Sheng Wu Xue Bao. 2004 Feb;37(1):15-21. Sodium azide (NaN3) is a special inhibitor of mitochondrion cytochrome c oxidase (COX), which can be used to mimic neuronal damage induced by mitochondrial deficiency. |
81(1,1,1,1) | Details |
| 9291153 | Gasparini L, Racchi M, Benussi L, Curti D, Binetti G, Bianchetti A, Trabucchi M, Govoni S: Effect of energy shortage and oxidative stress on amyloid precursor protein metabolism in COS cells. Neurosci Lett. 1997 Aug 8;231(2):113-7. Sodium azide (NaN3), an inhibitor of cytochrome c oxidase (complex IV of the mitochondrial electron transfer chain) decreased sAPP release in a concentration dependent way (maximum -75%). |
81(1,1,1,1) | Details |
| 15344313 | Qin Y, Gao J, Zhang TT, Zhao L, Wu HW, Xu L, Xu JY, Lu SY: [Changes of thioredoxin mRNA level in neurons insulted by sodium azide] . Shi Yan Sheng Wu Xue Bao. 2002 Mar;35(1):26-30. Sodium azide (NaN3) is a specific inhibitor of mitochondrial cytochrome c oxidase (COX), which can be used to mimic neuronal damage induced by mitochondrial deficiency. |
81(1,1,1,1) | Details |
| 14872239 | Karu TI, Pyatibrat LV, Kalendo GS: Photobiological modulation of cell attachment via cytochrome c oxidase. . Photochem Photobiol Sci. 2004 Feb;3(2):211-6. Epub 2003 Nov 12. Treating the cell suspension with ouabain (a Na (+), K (+)-ATPase inhibitor), amiloride (an inhibitor of N (+)/H (+) exchangers), or sodium azide (a cytochrome c oxidase inhibitor) prior to irradiation significantly modifies the action spectrum of cell attachment enhancement. |
33(0,1,1,3) | Details |
| 10699469 | Alemany C, Noe V, Ciudad CJ: Identification by RNA-based arbitrarily primed PCR of the involvement of cytochrome c oxidase in the development of resistance to methotrexate. Biochim Biophys Acta. 2000 Feb 28;1495(3):319-26. Incubation of cells with sodium azide, a specific cytochrome c oxidase inhibitor, decreased the number of resistant colonies after methotrexate treatment. |
32(0,1,1,2) | Details |
| 15362946 | Karu TI, Pyatibrat LV, Afanasyeva NI: A novel mitochondrial signaling pathway activated by visible-to-near infrared radiation. Photochem Photobiol. 2004 Sep-Oct;80(2):366-72. Treating of cell suspension with sodium azide (2 x 10 (-5) M), sodium nitroprusside (5 x 10 (-5) M), ouabain (1 x 10 (-6) M) or amiloride (1.7 x 10 (-5) M) before irradiation significantly modifies the spectrum of cell attachment enhancement. A light-induced mitochondrial signaling pathway can be regulated by small ligands directly binding to the catalytic center of cytochrome c oxidase (N (3), NO) as well as by chemicals specifically binding to plasma membrane enzymes (ouabain, amiloride). |
2(0,0,0,2) | Details |
| 11500038 | Das N, Gupta S, Mazumdar S: Direct observation of release of cytochrome c from lipid-encapsulated protein by peroxide and a possible mechanism for drug-induced apoptosis. Biochem Biophys Res Commun. 2001 Aug 17;286(2):311-4. Release of cytochrome c from inside lipid vesicles and from inside proteoliposomes formed by cytochrome c oxidase has been studied by spectrophotometric methods. The protein encapsulated inside vesicles did not form complex with sodium azide solution added externally. |
2(0,0,0,2) | Details |
| 17074421 | Gao J, Zhu ZR, Ding HQ, Qian Z, Zhu L, Ke Y: Vulnerability of neurons with mitochondrial dysfunction to oxidative stress is associated with down-regulation of thioredoxin. Neurochem Int. 2007 Jan;50(2):379-85. Epub 2006 Oct 30. In this study, we first developed an in vitro model of neuron with mitochondrial dysfunction, based on sodium azide (NaN (3))-induced inhibition of cytochrome c oxidase (complex IV) that is reduced in post-mortem AD brains, and then investigated the role of Trx expression in response of neurons with mitochondrial dysfunction to oxidative stress. |
81(1,1,1,1) | Details |
| 15853766 | Ferguson M, Mockett RJ, Shen Y, Orr WC, Sohal RS: Age-associated decline in mitochondrial respiration and electron transport in Drosophila melanogaster. Biochem J. 2005 Sep 1;390(Pt 2):501-11. Exposure of mitochondria isolated from young flies to low doses of KCN or NaAz (sodium azide), complex IV inhibitors, decreased cytochrome c oxidase activity and increased the production of H2O2. |
81(1,1,1,1) | Details |
| 17025185 | Shelemekh OV, Geidebrekht OV, Plakunov VK, Beliaev SS: regulation" of the respiratory chain composition in the yeast Debaryomyces hansenii under multiple stress]. Mikrobiologiia. 2006 Jul-Aug;75(4):562-9. Studies of the effects of respiration inhibitors (sodium azide and salicyl hydroxamic acid, SHA) and of the pattern of changes in the composition of the respiratory chain of Debaryomyces hansenii under the stated stress conditions led to the suggestion of three (or four) chains of electron transfer functioning simultaneously in the cell: the classical respiratory chain involving cytochrome-c oxidase, an alternative respiratory chain involving a - and azide-resistant oxidase, and additional respiratory chains involving oxidases resistant to salt, azide and SHA. |
31(0,1,1,1) | Details |
| 10213169 | Gasparini L, Benussi L, Bianchetti A, Binetti G, Curti D, Govoni S, Moraschi S, Racchi M, Trabucchi M: Energy metabolism inhibition impairs amyloid precursor protein secretion from Alzheimer's fibroblasts. Neurosci Lett. 1999 Mar 26;263(2-3):197-200. The present study investigates the influence of aglycemia and sodium azide (a Cytochrome c Oxidase inhibitor) on sAPP secretion from skin fibroblasts derived from sporadic AD patients and control subjects. |
31(0,1,1,1) | Details |
| 17428446 | Liu X, Zhou B, Mi S, Xue L, Shih J, Lee J, Chau J, Un F, Yen Y: An increase of cytochrome C oxidase mediated disruption of gemcitabine incorporation into DNA in a resistant KB clone. Biochem Pharmacol. 2007 Jun 15;73(12):1927-38. Epub 2007 Mar 20. Furthermore, the sensitivity to Gem could be reversed by sodium azide, a CCOX inhibitor. |
2(0,0,0,2) | Details |
| 8161207 | Partridge RS, Monroe SM, Parks JK, Johnson K, Parker WD Jr, Eaton GR, Eaton SS: Spin trapping of azidyl and in azide-inhibited rat brain submitochondrial particles. Arch Biochem Biophys. 1994 Apr;310(1):210-7. It is proposed that azide inhibition of cytochrome c oxidase results in increased production of which is efficiently converted to peroxide by membrane-bound superoxide dismutase. |
2(0,0,0,2) | Details |
| 20006572 | Unitt DC, Hollis VS, Palacios-Callender M, Frakich N, Moncada S: Inactivation of by cytochrome c oxidase under steady-state conditions. Biochim Biophys Acta. 2010 Mar;1797(3):371-7. Epub 2009 Dec 16. At both high and low O (2) concentrations the inactivation of NO is decreased when sodium azide is used to inhibit cytochrome c oxidase and decrease electron turnover. |
1(0,0,0,1) | Details |
| 15562629 | Steverding D, Scory S: Trypanosoma brucei: unexpected azide sensitivity of bloodstream forms. J Parasitol. 2004 Oct;90(5):1188-90. Azide is a toxic anion that bears chemical and biological properties in common with and may act in a similar way by inhibition of cytochrome c oxidase. |
1(0,0,0,1) | Details |
| 7814333 | Cunningham L, Williams HD: Isolation and characterization of mutants defective in the -insensitive respiratory pathway of Pseudomonas aeruginosa. J Bacteriol. 1995 Jan;177(2):432-8. One of these, cytochrome co, is a cytochrome c oxidase which is completely inhibited by concentrations of the respiratory inhibitor as low as 100 microM. The second oxidase, the -insensitive oxidase, is resistant to concentrations in excess of 1 mM as well as to sodium azide. |
1(0,0,0,1) | Details |
| 19861415 | Chowanadisai W, Bauerly KA, Tchaparian E, Wong A, Cortopassi GA, Rucker RB: Pyrroloquinoline stimulates mitochondrial biogenesis through cAMP response element-binding protein phosphorylation and increased PGC-1alpha expression. J Biol Chem. 2010 Jan 1;285(1):142-52. Epub 2009 Oct 27. Moreover, PQQ protected cells from mitochondrial inhibition by rotenone, 3-nitropropionic acid, antimycin A, and sodium azide. Exposure of mouse Hepa1-6 cells to 10-30 microm PQQ for 24-48 h resulted in increased citrate synthase and cytochrome c oxidase activity, Mitotracker staining, mitochondrial DNA content, and cellular respiration. |
1(0,0,0,1) | Details |
| 10913362 | Hedin HL, Eriksson S, Fowler CJ: Rapid inhibition by sodium azide of the phosphoinositide-mediated response to stimulation in human platelets: preservation in Alzheimer's disease. Biochem Biophys Res Commun. 2000 Aug 2;274(2):472-6. |
0(0,0,0,0) | Details |
| 7857522 | Smith RP, Wilcox DE: Toxicology of selected -donating xenobiotics, with particular reference to azide. Crit Rev Toxicol. 1994;24(4):355-77. However, it is by no means clear whether or not the NO generated in vivo from sodium azide contributes in a major way to its toxicity. |
0(0,0,0,0) | Details |