Disease relevance of 2,4-dinitrophenol

• Antigen receptors on murine T lymphocytes in contact sensitivity. I. Functional inhibition of effector T cells by monovalent 2,4-dinitrophenol: implication for a two-receptor model [1].
• Inhibiting oxidative metabolism with hypoxia, dinitrophenol (10(-5)M), or Na-azide (10(-3)M) caused marked suppression of tension (by 73 +/- 5, 65 +/- 8, and 50 +/- 14%, respectively) and a small increase in [K+]0 (0.8 +/- 0.4, 0.5 +/- 0.25, and 0.4 +/- 0.2 mM, respectively) after 10 min [2].
• Treatment of developing colonies of Podocoryne carnea, a hydractiniid hydroid, with dilute solutions of 2,4-dinitrophenol (DNP), an uncoupler of oxidative phosphorylation, accelerates the usual ontogenetic trajectory of polyp and stolon production [3].
• Although Jeggo's Chinese hamster ovary cells were more responsive to mAMSA, novo still abrogated mAMSA toxicity in the mutant cells as well as in the parental Chinese hamster ovary cells 2,4-Dinitrophenol acted similarly to novo with respect to mAMSA killing, but neither compound reduced the ATP content of V79 cells [4].
• Effects of 2,4-dinitrophenol and other metabolic inhibitors on the thermograms of Ehrlich ascites carcinoma cells registered with a microcalorimeter [5].

Psychiatry related information on 2,4-dinitrophenol

• 0. It also showed a fast response time (t95% < 1.5 min) when the sensor was applied to 2,4-dinitrophenol solution at concentration levels of 5.26 x 10(-6) and 2.10 x 10(-5) mol L(-1) alternatively [6].

High impact information on 2,4-dinitrophenol

• Mild mitochondrial uncoupling by 2,4-dinitrophenol (DNP) reduced neuronal death, and UCP-2 activity was enhanced by palmitic acid in isolated mitochondria [7].
• Another well-characterized B-cell factor is T-cell replacing factor (TRF), which, when secreted by the murine T-cell hybridoma B151K12, is defined by two activities: induction of IgM secretion by BCL1 leukaemic B-cell line; and induction of secondary anti-dinitrophenol (DNP) immunoglobulin G (IgG) synthesis in vitro by DNP-prime B cells [8].
• Human immunoglobulin was detected in some chimeras, and a human antibody response to dinitrophenol could be generated after primary and secondary immunization [9].
• Therefore, the response to DNP distinguished between inhibition of transport and metabolism; this approach may be useful for the investigation of factors that regulate active transport [10].
• LN cells or purified T cells were treated in vitro with monovalent or different multivalent 2,4-dinitrophenol (DNP) ligands [1].

Chemical compound and disease context of 2,4-dinitrophenol

• Sodium thiocyanate (6 x 10(-2) M, serosal side) inhibited spontaneous acid secretion revealing net alkalinization (0.83 +/- 0.05 mumol . cm-2 . h-1, n = 58) that was completely inhibited by anoxia and potassium cyanide (10(-2) M) and markedly reduced by 2,4-dinitrophenol (10(-4) M) [11].
• Injury to calcium-free hearts is also associated with contracture caused by anoxia, 2,4-dinitrophenol (DNP), or caffeine [12].
• We used 2,4-dinitrophenol (DNP), an uncoupler of oxidative phosphorylation, as a model to mimic hypoxia and gain insight into the signaling pathway underlying metabolic stress-induced glucose uptake in primary cultures of rat adult cardiomyocytes [13].
• Therefore, cultured porcine aortic endothelial cells (PAEC) were exposed to hypoxia (1-10% O(2)) or inhibitors of cellular energy metabolism including rotenone, 2, 4 dinitrophenol (DNP) and 2-deoxyglucose for 6 to 24 h [14].
• M14659 was taken up markedly into bacterial cells in the presence of transferrin, and its uptake was inhibited by the protonophore dinitrophenol, which inhibits active-transport systems coupled to an energized membrane such as the iron transport systems of E. coli [15].

Biological context of 2,4-dinitrophenol

• The results indicated that the progenitors for 2,4-dinitrophenol (DNP)-specific B cells are present as early as 14 d of gestation in liver and possibly as early as 15 d in spleen [16].
• This finding suggested that the 24-h induction period was insufficient for affecting the DNP-specific precursors in livers and spleens from the earlier gestational ages, and that a proportion of precursors could subsequently form DNP clones in the splenic focus assay after the removal of tolerogen [16].
• Metabolic inhibition with glucose-free, dinitrophenol-containing solution activated sarcK(ATP) current and shortened the action potential duration in ventricular cells isolated from wild-type (WT) but not KO mice [17].
• Antimycin A, dinitrophenol, oligomycin, and anaerobiosis (N2) inhibited the conversion, whereas sodium flouride and cycloheximide had no effect [18].
• Anaphase is reversibly blocked at any point by azide or dinitrophenol, with chromosome motion ceasing 1-10 min after application of the drugs [19].

Anatomical context of 2,4-dinitrophenol

• Because fetal DNP precursors from spleens and livers that had been incubated in organ culture resulted in a greater proportion of clones secreting IgG compared with age-matched uncultured controls, it was concluded that the maturation with regard to the ability to secrete IgG can occur in vitro [16].
• This alteration in the cell membrane responsiveness was reversible upon further incubation in the absence of DNP [20].
• The separated junctional membranes, expected to be highly impermeable, contain particles regularly and tightly packed as in hypoxic or DNP-treated junctions [21].
• Electron microscope examination of dividing guard mother cells fixed during azide and dinitrophenol treatment reveals that spindle microtubules are still present [19].
• Intact erythrocytes become immediately crenated upon addition of 2,4-dinitrophenol (DNP) or pyrenebutyric acid (PBA) [20].

Associations of 2,4-dinitrophenol with other chemical compounds

• Dinitrophenol- (DNP) or trinitrophenol-modified mouse spleen cells (SC) induced suppressors in donors able to transfer suppression to normal recipients [22].
• Secretion of IL-1 beta is blocked by methylamine, low temperature or serum free medium, and is increased by raising the culture temperature to 42 degrees C or by the presence of calcium ionophores, brefeldin A, monensin, dinitrophenol or carbonyl cyanide chlorophenylhydrazone [23].
• The uncoupling is produced by in vitro treatment of crayfish abdominal cords either with a Ca++, Mg++-free solution containing EDTA, followed by return to normal saline (Van Harreveld's solution), or with VAn Harreveld's solution containing dinitrophenol (DNP) [24].
• In contrast, uptake of unilamellar dipalmitoyl lecithin vesicles and multilamellar dipalmitoyl lecithin liposomes is only partially inhibited at 4 degrees C, by dinitrophenol and by prior fixation of the amoebae with glutaraldehyde, each of which inhibits pinocytosis [25].
• It is reduced to zero by the mitochondrial uncoupler 2,4-dinitrophenol but is relatively unaffected by ouabain, which inhibits the Na+/K+-pump located on the apical membrane of this epithelium [26].

Gene context of 2,4-dinitrophenol

• The results obtained with the control bcy strain, the RAS2(Val-19) strain under conditions in which RAS1 is expressed, and with dinitrophenol show that the inability of the oncogene product to mediate the cAMP signal is not due to feedback inhibition by the high protein kinase activity in strains containing the RAS2(Val-19) oncogene [27].
• In strains carrying the cif1 mutation the intracellular concentration of ATP decreased immediately after addition of glucose while the intracellular concentration of cAMP did not increase. cAMP concentration increased in response to galactose or 2,4-dinitrophenol [28].
• Subcellular fractionation studies revealed that the amount of mature caspase-8 but not pro-caspase at the membrane was increased following CD95-stimulation in the presence of DNP [29].
• Other antioxidants such as catalase, Cu/Zn-SOD and GSHPx were not activated by DNP treatment [30].
• Although DNP slightly elevated Mn-SOD activity, the rate of increase in Mn-SOD (1.3-fold) was smaller than that in MT (3.7-fold) [30].

Analytical, diagnostic and therapeutic context of 2,4-dinitrophenol

• Recently we demonstrated that low-pH compartments can be visualized with the electron microscope using a basic congener of dinitrophenol, 3-(2,4-dinitroanilino)-3'-amino-N-methyldipropylamine (DAMP), which concentrates in acidic compartments and can be detected by immunocytochemistry with a monoclonal anti-dinitrophenol antibody [31].
• However, if tolerogen were present for 3--5 d during organ culture there was near total elimination of potential DNP clones [16].
• Perfusion with partially calcium-loaded nitrophen often caused a loading transient--slow secretion for up to 1 min due to displacement of Ca2+ by cytoplasmic Mg2+ [32].
• Treatment of Fao cells with 2,4-dinitrophenol for 45 min depleted cellular ATP by 80% and equally inhibited insulin-stimulated receptor autophosphorylation, as determined by immunoprecipitation of surface-iodinated or [32P]phosphate-labeled cells with anti-phosphotyrosine antibody [33].
• Normal saline, when administered in a similar manner, did not increase either ventilation or cardiac output, and simple denervation without previous infusions of DNP also had no effect [34].

References