| Name | lactate dehydrogenase (protein family or complex) |
|---|---|
| Synonyms | LDH; lactate dehydrogenase; lactate dehydrogenases |
| Name | sodium azide |
|---|---|
| CAS | sodium azide |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 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. RESULTS: After TSCI, the metabolic inhibition with sodium azide treatment diminished the lipid peroxidation process (malondialdehyde levels by spectrophotometric procedures) and the damage to the spinal cord tissue (morphometric analysis), and increased the activity of kinase and lactate dehydrogenase enzymes (P <0.05) (measured by spectrophotometric procedures 24 h after TSCI as well as after the functional recovery of the hind limb (evaluated weekly for 2 months by the BBB (Basso, Beattie and Bresnahan) scale)) when compared with the TSCI group without treatment. |
81(1,1,1,1) | Details |
| 9244537 | Artiukhova VG, Nakvasina MA, Lysenko IuA: [Active forms of and the degree of UV modification of the structural and functional properties of lactate dehydrogenase]. Radiats Biol Radioecol. 1997 May-Jun;37(3):453-60. The spectrophotometry and photofluorescence techniques were used in the studies on photochemical transformations of lactate dehydrogenase exposed to UV irradiation with a dose of 2.25 kJ/m2, in the native state and in the presence of exogenous modifiers: sodium azide, and tret-butanol. |
15(0,0,2,5) | Details |
| 10872053 | Artiukhov VG, Lysenko IuA, Nakvasina MA: [Regularities in the kinetic of photoactivation of lactate dehydrogenase by the action of UV light in different microenvironment]. Biofizika. 2000 May-Jun;45(3):427-31. The kinetics of photoinactivation of cardiac (H4) and muscular (M4) isoforms of lactate dehydrogenase irradiated by UV light (240-390 nm) in the free form and in the presence of sodium azide, and was studied. |
8(0,0,1,3) | Details |
| 9826039 | Lofgren S, Soderberg PG: Histochemical determination of lactate dehydrogenase activity in rat lens; influence of different parameters. Acta Ophthalmol Scand. 1998 Oct;76(5):555-60. The influence of incubation time, pH, the concentration of dye, lactate, phenazine methosulfate, sodium azide, hydrazine and polyvinyl on the enzyme histochemical reaction was investigated. |
6(0,0,0,6) | Details |
| 17880998 | Yitzhaki S, Hochhauser E, Porat E, Shainberg A: -5'- (UTP) maintains cardiac mitochondrial function following chemical and hypoxic stress. J Mol Cell Cardiol. 2007 Nov;43(5):653-62. Epub 2007 Aug 7. In the in vitro model, cultured cardiomyocytes were pretreated with 50 microM UTP prior to hypoxic and/or chemical stress with rotenone or sodium azide. Pretreatment with UTP maintained increased ATP levels as well as mitochondrial membrane potential and reduced lactate dehydrogenase (LDH) release. |
1(0,0,0,1) | Details |
| 19002967 | Haslam G, Wyatt D, Kitos PA: Estimating the number of viable animal cells in multi-well cultures based on their lactate dehydrogenase activities. Cytotechnology. 2000 Jan;32(1):63-75. The effects on cell growth of four metabolicinhibitors, sodium azide, actinomycin D,cycloheximide, and taxol, were determined using theLDH/INT assay and direct cell counting. |
2(0,0,0,2) | Details |
| 15637335 | De Witt Hamer PC, Jonker A, Leenstra S, Ruijter JM, Van Noorden CJ: Quantification of viability in organotypic multicellular spheroids of human malignant glioma using lactate dehydrogenase activity: a rapid and reliable automated assay. J Histochem Cytochem. 2005 Jan;53(1):23-34. Sodium azide incubation of spheroids induced reduction in VI to almost zero. |
2(0,0,0,2) | Details |
| 18769046 | Brinkkoetter PT, Song H, Losel R, Schnetzke U, Gottmann U, Feng Y, Hanusch C, Beck GC, Schnuelle P, Wehling M, van der Woude FJ, Yard BA: Hypothermic injury: the mitochondrial ATP and ROS love-hate triangle out of balance. Cell Physiol Biochem. 2008;22(1-4):195-204. Epub 2008 Jul 25. METHODS: Lactate dehydrogenase assay, intracellular ATP, reactive species and reduced thio-group measurement, intracellular measurement and mitochondrial staining were performed in the study. The protective effect of was abrogated by ionomycin and sodium azide and partly by oligomycin and CCCP. |
1(0,0,0,1) | Details |
| 19056363 | Zhu M, Li MW, Tian XS, Ou XM, Zhu CQ, Guo JC: Neuroprotective role of delta-opioid receptors against mitochondrial respiratory chain injury. Brain Res. 2009 Feb 3;1252:183-91. Epub 2008 Nov 19. In this study we tested the effects of DOR activation and inhibition on cultured cortical neurons after inhibiting mitochondrial respiratory chain with sodium azide (NaN (3)) in days 8 cultures. Neuronal injury was assessed by lactate dehydrogenase release. |
1(0,0,0,1) | Details |
| 9928684 | Hsu CH, Quistad GB, Casida JE: Phosphine-induced oxidative stress in Hepa 1c1c7 cells. Toxicol Sci. 1998 Nov;46(1):204-10. This level causes 31% cell death at 6 h, measured by lactate dehydrogenase leakage, with appropriate dependence on concentration and time. Antioxidants significantly attenuate the PH3-induced ROS formation, lipid peroxidation, 8-OH-Gua formation in DNA, and cell death, with the general order for effectiveness of GSH (5 mM) and (10 mM) scavengers), then Tempol (2.5 mM) and sodium azide (3 mM) and singlet scavengers, respectively). |
1(0,0,0,1) | Details |
| 18721805 | Hessel MH, Michielsen EC, Atsma DE, Schalij MJ, van der Valk EJ, Bax WH, Hermens WT, van Dieijen-Visser MP, van der Laarse A: Release kinetics of intact and degraded troponin I and T after irreversible cell damage. Exp Mol Pathol. 2008 Oct;85(2):90-5. Epub 2008 Aug 5. PURPOSE: We characterized the release kinetics of cardiac troponin I and T in relation to lactate dehydrogenase (LDH) from cardiomyocytes before and after the transition from reversible to irreversible cell damage. METHODS: Cardiomyocytes were exposed to mild metabolic inhibition (1 mmol/L sodium azide) to induce a necrotic cell death process that is characterized by a reversible (0-12 h) and irreversible phase (12-30 h). |
1(0,0,0,1) | Details |
| 10889343 | Hedin HL, Fowler CJ: Effects of sodium azide on the secretion of soluble amyloid-beta precursor protein and the accumulation of beta-amyloid (1-40) in cultured chick neurons. Neurosci Lett. 2000 Jul 21;288(3):203-6. |
0(0,0,0,0) | Details |
| 7823323 | Rikans LE, Cai Y, Hornbrook KR: Allyl cytotoxicity in isolated rat hepatocytes: effects of azide, fasting, and J Toxicol Environ Health. 1995 Jan;44(1):1-11. ATP, ADP, AMP, and viability loss (leakage of lactate dehydrogenase into the medium) were measured in isolated hepatocytes of fed or fasted rats exposed to 0.5 mM allyl mononucleotides and cytotoxicity were determined also in hepatocytes incubated with allyl in the presence of 4 mM sodium azide or 15 mM |
1(0,0,0,1) | Details |
| 10198341 | Ma TY, Nguyen D, Bui V, Nguyen H, Hoa N: modulation of intestinal epithelial tight junction barrier. Am J Physiol. 1999 Apr;276(4 Pt 1):G965-74. Consistent with these findings, metabolic inhibitors sodium azide and 2,4-dinitrophenol significantly prevented -induced increase in Caco-2 TJ permeability, whereas cycloheximide or actinomycin D had no effect. |
0(0,0,0,0) | Details |
| 9029274 | Leeder RG, Rafeiro E, Brien JF, Mandin CC, Massey TE: Evaluation of reactive species involvement in amiodarone pulmonary toxicity in vivo and in vitro. J Biochem Toxicol. 1996;11(3):147-60. Incubation of macrophages with AM (73 or 146 microM) for 1 hour, with or without the catalase inhibitor sodium azide (1 mM), did not result in DCF formation. |
0(0,0,0,0) | Details |