| Name | brains |
|---|---|
| Synonyms | BPG dependent PGAM 1; Brain; CDABP0006; PGAM 1; PGAM B; PGAM1; PGAM1 protein; PGAMA… |
| Name | sodium azide |
|---|---|
| CAS | sodium azide |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 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. |
31(0,1,1,1) | Details |
| 9309319 | Hamby-Mason R, Chen JJ, Schenker S, Perez A, Henderson GI: Catalase mediates formation from in fetal and neonatal rat brain. Alcohol Clin Exp Res. 1997 Sep;21(6):1063-72. The current studies present evidence that homogenates of immature rat brains can generate AcHO via a catalase (CAT)-mediated reaction and that AcHO may be produced in vivo by this system. When incubated with CAT inhibitors (sodium azide or 3-aminotriazole), AcHO formation was blocked, whereas neither the alcohol dehydrogenase inhibitor, 4-methylpyrazole, nor P-450 inhibitors decreased AcHO production. |
4(0,0,0,4) | Details |
| 11053240 | Farber SA, Slack BE, Blusztajn JK: Acceleration of synthesis and breakdown by inhibitors of mitochondrial function in neuronal cells: a model of the membrane defect of Alzheimer's disease. FASEB J. 2000 Nov;14(14):2198-206. We show that when PC12 cells are exposed to inhibitors of mitochondrial bioenergetics, the turnover of their major membrane phospholipid, is accelerated, producing a pattern of metabolic changes that mimics that observed in brains of AD patients. |
1(0,0,0,1) | Details |
| 18316212 | Riha PD, Rojas JC, Colorado RA, Gonzalez-Lima F: Animal model of posterior cingulate cortex hypometabolism implicated in amnestic MCI and AD. Neurobiol Learn Mem. 2008 Jul;90(1):112-24. Epub 2008 Mar 7. Learning and memory were examined in a spatial holeboard task and brains were analyzed using quantitative histochemical, morphological and biochemical techniques. Behavioral results showed that sodium azide-treated rats were impaired in their memory of the baited pattern in probe trials as compared to their training scores before treatment, without non-specific behavioral differences. |
1(0,0,0,1) | Details |
| 16930212 | Zimatkin SM, Pronko SP, Vasiliou V, Gonzalez FJ, Deitrich RA: Enzymatic mechanisms of oxidation in the brain. . Alcohol Clin Exp Res. 2006 Sep;30(9):1500-5. CYP2E1 plays an important role in oxidation in the rodent brains. RESULTS: The catalase inhibitors sodium azide (5 mM) and aminotriazole (5 mM) as well as CYP2E1 inhibitors diallyl sulfide (2 mM) and beta-phenethyl isothiocyanate (0.1 mM) lowered significantly the accumulation of the -derived AC and in brain homogenates. |
1(0,0,0,1) | Details |
| 15302108 | Szabados T, Dul C, Majtenyi K, Hargitai J, Penzes Z, Urbanics R: A chronic Alzheimer's model evoked by mitochondrial poison sodium azide for pharmacological investigations. Behav Brain Res. 2004 Sep 23;154(1):31-40. Selective reduction of complex IV activity is present in post-mortem AD brains. |
1(0,0,0,1) | Details |
| 9675105 | Cassarino DS, Swerdlow RH, Parks JK, Parker WD Jr, Bennett JP Jr: Cyclosporin A increases resting mitochondrial membrane potential in SY5Y cells and reverses the depressed mitochondrial membrane potential of Alzheimer's disease cybrids. Biochem Biophys Res Commun. 1998 Jul 9;248(1):168-73. Alzheimer's disease (AD) brains exhibit oxidative stress and a biochemical defect of complex IV (cytochrome oxidase, COX) of the mitochondrial electron transport chain (ETC). |
1(0,0,0,1) | Details |
| 12383965 | Dai J, Buijs RM, Kamphorst W, Swaab DF: Impaired axonal transport of cortical neurons in Alzheimer's disease is associated with neuropathological changes. Brain Res. 2002 Sep 6;948(1-2):138-44. The present study provides, for the first time, direct evidence of the presence of impaired axonal transport in AD brains. |
1(0,0,0,1) | Details |