Protein Information

Name complex I
Synonyms 39kD; CI 39kD; Complex I; Complex I 39kD; NADH dehydrogenase (ubiquinone) Fe S protein 2 like; NADH ubiquinone oxidoreductase 39 kDa subunit mitochondrial; NADH ubiquinone oxidoreductase 39 kDa subunit; NDUFA 9…

Compound Information

Name sodium azide
CAS sodium azide

Reference List

PubMed Abstract RScore(About this table)
17533645 Annunen-Rasila J, Ohlmeier S, Tuokko H, Veijola J, Majamaa K: Proteome and cytoskeleton responses in osteosarcoma cells with reduced OXPHOS activity. Proteomics. 2007 Jun;7(13):2189-200.


We describe here the cellular responses to OXPHOS deficiency in osteosarcoma cells upon complex I (CI) and complex IV (CIV) inhibition, and upon the lack of mitochondrial DNA (rho0 cells).
1(0,0,0,1) Details
19488053 Torres S, Salgado-Ceballos H, Guizar-Sahagun G, Torres JL, Orozco-Suarez S, Diaz-Ruiz A, Vazquez ME, Collado C, Rios C: Deleterious versus neuroprotective effect of metabolic inhibition after traumatic spinal cord injury. Spinal Cord. 2009 Oct;47(10):745-50. Epub 2009 Jun 2.


METHODS: Animals were divided into five groups: one sham and four with TSCI, including no treatment, rotenone (inhibitor of mitochondrial complex I), sodium azide (inhibitor of mitochondrial complex IV) and pyrophosphate of thiamine or non-degradable cocarboxylase as a metabolic reactivator.
0(0,0,0,0) Details
7806513 Karnauchov I, Cai D, Schmidt I, Herrmann RG, Klosgen RB: The thylakoid translocation of subunit 3 of photosystem I, the psaF gene product, depends on a bipartite transit peptide and proceeds along an azide-sensitive pathway. J Biol Chem. 1994 Dec 30;269(52):32871-8.


Thylakoid translocation of PSI-3 is, however, impaired in the presence of sodium azide, which indicates that a homolog to the bacterial SecA protein might be involved in this process suggesting, thus, a prokaryote-like translocation pathway.
0(0,0,0,0) Details
11569921 Ishiguro H, Yasuda K, Ishii N, Ihara K, Ohkubo T, Hiyoshi M, Ono K, Senoo-Matsuda N, Shinohara O, Yosshii F, Murakami M, Hartman PS, Tsuda M: Enhancement of oxidative damage to cultured cells and Caenorhabditis elegans by mitochondrial electron transport inhibitors. IUBMB Life. 2001 Apr;51(4):263-8.


Oxygen loading enhanced the damage of PC 12 cells by thenoyltrifluoroacetone (TTFA, a complex II inhibitor), but did not by rotenone (a complex I inhibitor), antimycin (a complex III inhibitor), and sodium azide (a complex IV inhibitor).
0(0,0,0,0) Details
16034640 Baby SM, Roy A, Lahiri S: Role of mitochondria in the regulation of hypoxia-inducible factor-1alpha in the rat carotid body glomus cells. Histochem Cell Biol. 2005 Jul;124(1):69-76. Epub 2005 Jul 22.

To test this hypothesis in the CB glomus cells, we studied the effect of mitochondrial electron transport chain (ETC) inhibitors: rotenone (complex I; 1 microM), malonate (complex II; 0.5 M), antimycin A (complex III; 1 microg/ml), sodium azide (complex IV; 5 mM), and uncoupler of oxidative phosphorylation: carbonyl cyanide p-trifluoromethoxyphenylhydrazone (FCCP; 1 mM) on HIF-1alpha expression during normoxia and hypoxia.
81(1,1,1,1) Details
18298370 Isaev NK, Stelmashook EV, Dirnagl U, Plotnikov EY, Kuvshinova EA, Zorov DB: Mitochondrial free radical production induced by glucose deprivation in cerebellar granule neurons. Biochemistry. 2008 Feb;73(2):149-55.

Inhibitors of mitochondrial electron transport, i.e. rotenone (complex I), antimycin A (complex III), or sodium azide (complex IV), an inhibitor of mitochondrial ATP synthase--oligomycin, an uncoupler of oxidative phosphorylation--CCCP, a chelator of intracellular Ca2+--BAPTA, an inhibitor of electrogenic mitochondrial Ca2+ transport--ruthenium red, as well as pyruvate significantly decreased neuronal ROS production induced by GD.
81(1,1,1,1) Details
17429617 Xiong K, Cai H, Luo XG, Struble RG, Clough RW, Yan XX: Mitochondrial respiratory inhibition and oxidative stress elevate beta-secretase (BACE1) proteins and activity in vivo in the rat retina. Exp Brain Res. 2007 Aug;181(3):435-46. Epub 2007 Apr 12.

Retinas were analyzed biochemically and anatomically 48 h following intraocular applications of mitochondrial complex I, II and IV inhibitors including rotenone, 3-nitropropionic acid and sodium azide, and plaque-containing oxidants including Fe (3+) and Abeta42 fibrils (Abeta42f).
81(1,1,1,1) Details
9313890 Smith TS, Bennett JP Jr: Mitochondrial toxins in models of neurodegenerative diseases. Brain Res. 1997 Aug 15;765(2):183-8.

In brain microdialysis in awake rats, striatal 'OH output increased 3-5-fold after infusion of methylpyridinium ion (MPP+), a complex I inhibitor, or sodium azide, a complex IV inhibitor.
33(0,1,1,3) Details
15371739 Isaev NK, Stelmashook EV, Ruscher K, Andreeva NA, Zorov DB: Menadione reduces rotenone-induced cell death in cerebellar granule neurons. Neuroreport. 2004 Oct 5;15(14):2227-31.

Chemical hypoxia (term defining the simulation by using respiratory inhibitors) chosen as in vitro ischemic model, was induced in primary cultures of rat cerebellar granule neurons by inhibitors of mitochondrial electron transport such as rotenone or paraquat (complex I), 3-nitropropionic acid (3-NPA, complex II), antimycin A (complex III), or sodium azide (complex IV).
31(0,1,1,1) Details
11080215 Talpade DJ, Greene JG, Higgins DS Jr, Greenamyre JT: In vivo labeling of mitochondrial complex I (NADH:ubiquinone oxidoreductase) in rat brain using [(3) H] dihydrorotenone. J Neurochem. 2000 Dec;75(6):2611-21.

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12783190 Appanna VD, Hamel RD, Levasseur R: The metabolism of aluminum citrate and biosynthesis of oxalic acid in Pseudomonas fluorescens. Curr Microbiol. 2003 Jul;47(1):32-9.

Thus, it appears that after the uptake of Al-citrate, this complex is metabolized intracellularly.
The transport of Al-citrate was sensitive to p-dinitrophenol and sodium azide, but not to dicyclohexylcarbodiimide.
1(0,0,0,1) Details
9056250 Tatarko M, Bumpus JA: Further studies on the inactivation by sodium azide of lignin peroxidase from Phanerochaete chrysosporium. Arch Biochem Biophys. 1997 Mar 1;339(1):200-9.

Reversion is accelerated if the complex is chromatographed on a PD-10 (Sephadex G-25) column or if veratryl alcohol is added.
1(0,0,0,1) Details
15691332 Steiner JM, Berghofer J, Yusa F, Pompe JA, Klosgen RB, Loffelhardt W: Conservative sorting in a primitive plastid. FEBS J. 2005 Feb;272(4):987-98.


In the absence of data on cyanobacterial protein translocation, the cyanelles of the glaucocystophyte alga Cyanophora paradoxa for which in vitro systems for protein import and intraorganellar sorting were elaborated can serve as a model: the cyanelles are surrounded by a peptidoglycan wall, their thylakoids are covered with phycobilisomes and the composition of their oxygen-evolving complex is another feature shared with cyanobacteria.
1(0,0,0,1) Details
16239214 Ved R, Saha S, Westlund B, Perier C, Burnam L, Sluder A, Hoener M, Rodrigues CM, Alfonso A, Steer C, Liu L, Przedborski S, Wolozin B: Similar patterns of mitochondrial vulnerability and rescue induced by genetic modification of alpha-synuclein, parkin, and DJ-1 in Caenorhabditis elegans. J Biol Chem. 2005 Dec 30;280(52):42655-68. Epub 2005 Oct 19.

C. elegans lines with these genetic changes were more vulnerable than nontransgenic nematodes to mitochondrial complex I inhibitors, including rotenone, fenperoximate, pyridaben, or stigmatellin.
In contrast, the genetic manipulations did not increase sensitivity to paraquat, sodium azide, divalent metal ions (Fe (II) or Cu (II)), or etoposide compared with the nontransgenic nematodes.
1(0,0,0,1) Details
11527152 Monti E, Supino R, Colleoni M, Costa B, Ravizza R, Gariboldi MB: Nitroxide TEMPOL impairs mitochondrial function and induces apoptosis in HL60 cells. J Cell Biochem. 2001;82(2):271-6.


In addition, TEMPOL was found to specifically target complex I of the respiratory chain, with minor effects on complexes II and IV, suggesting that mitochondrial effects might play a role in TEMPOL-induced oxidative stress and apoptosis, and that TEMPOL might sensitize tumor cells to the pro-apoptotic effects of cytotoxic agents.
1(0,0,0,1) Details
11526115 Molik S, Karnauchov I, Weidlich C, Herrmann RG, Klosgen RB: The Rieske Fe/S protein of the cytochrome b6/f complex in chloroplasts: missing link in the evolution of protein transport pathways in chloroplasts?. J Biol Chem. 2001 Nov 16;276(46):42761-6. Epub 2001 Aug 28.

Furthermore, transport is affected by sodium azide as well as by competitor proteins for the Sec pathway in chloroplasts, demonstrating for the first time some cross-talk of the two pathways.
This might take place in the stroma where the Rieske protein accumulates after import in several complexes of high molecular mass, among which the cpn60 complex is the most prominent.
1(0,0,0,1) Details
9726993 Vasilyeva E, Forgac M: Interaction of the clathrin-coated vesicle V-ATPase with ADP and sodium azide. J Biol Chem. 1998 Sep 11;273(37):23823-9.

The second effect is observed at ADP concentrations as low as 0.1-0.2 microM, indicating that a high affinity inhibitory complex is formed between ADP and the V-ATPase and is only slowly dissociated after the addition of ATP.
1(0,0,0,1) Details
16363866 Sauaia MG, de Lima RG, Tedesco AC, da Silva RS: Nitric oxide production by visible light irradiation of aqueous solution of nitrosyl ruthenium complexes. Inorg Chem. 2005 Dec 26;44(26):9946-51.

[Ru (II) L (NH (3))(4)(pz) Ru (II)(bpy)(2)(NO)](PF (6))(5) (L is NH (3), py, or 4-acpy) was prepared with good yields in a straightforward way by mixing an equimolar ratio of cis-[Ru (NO (2))(bpy)(2)(NO)](PF (6))(2), sodium azide (NaN (3)), and trans-[RuL (NH (3))(4)(pz)] (PF (6))(2) in acetone.
Flash photolysis of the [Ru (II) L (NH (3))(4)(pz) Ru (II)(bpy)(2)(NO)](5+) complex is capable of releasing nitric oxide (NO) upon irradiation at 355 and 532 nm.
1(0,0,0,1) Details
10597238 Suzuki S, Higuchi M, Proske RJ, Oridate N, Hong WK, Lotan R: Implication of mitochondria-derived reactive oxygen species, cytochrome C and caspase-3 in N-(4-hydroxyphenyl) retinamide-induced apoptosis in cervical carcinoma cells. Oncogene. 1999 Nov 4;18(46):6380-7.


Rotenone, an MRC complex I inhibitor was less effective and azide, an MRC complex IV inhibitor, exhibited a marginal effect.
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