Disease relevance of DETA

• Efficacy of treatment with the iron (III) complex of diethylenetriamine pentaacetic acid in mice and primates inoculated with live lethal dose 100 Escherichia coli [1].
• Magnetic resonance imaging of acute myocardial infarction: gadolinium diethylenetriamine pentaacetic acid as a marker of reperfusion [2].
• Radioimmunotherapy using 90Y-labeled diethylenetriamine pentaacetic acid-antibody conjugates was studied in Rauscher erythroleukemia virus-infected mice [3].
• To examine the influence of hypoxia on NO*-mediated apoptosis, we exposed bovine aortic endothelial cells (BAEC) to (Z)-1-[N-(2-aminoethyl)-N-(2-ammonioethyl) amino]diazen-1-ium-1,2-diolate (diethylenetriamine NONOate, DETA-NO) (1 mmol/liter) under normoxic or hypoxic conditions (pO2 = 35 mm of Hg) and measured the indices of apoptotic cell death [4].
• Moreover, we have developed a model using 99mTc-DTPA (diethylenetriamine pentaacetic acid), which can be used, as an alternative to adenovirus, to determine the profile of lung deposition of the vector [5].

High impact information on DETA

• The iron (III) complex of diethylenetriamine pentaacetic acid (DTPA iron [III]) protected mice and baboons from the lethal effects of an infusion with live LD100 Escherichia coli [1].
• Although loss of reactive lysine groups could be due to either oxidative modification or nonenzymatic glycation of apolipoprotein B-100, inhibition of lipid peroxidation by the metal chelator, diethylenetriamine pentaacetic acid, blocked the changes in free lysines [6].
• Other less traditional probes include 99m Tc diethylenetriamine pentaacetic acid-galactosyl-human serum albumin for evaluation of functional liver volume and 99m Tc-labeled tetrofosmin and methoxisobutylisonitrile for detecting drug resistance [7].
• Interestingly, Fancc(-/-) hematopoietic cells also exhibited increased growth inhibition on exposure to 2 distinct NO-generating agents, S-nitroso-N-acetyl-D, L-penicillamine (SNAP) and diethylenetriamine nitric oxide adduct (DETA/NO) [8].
• The pharmacokinetics of the C110 anti-carcinoembryonic antigen antibody radiolabeled with 111In via a novel benzylisothiocyanate derivative of diethylenetriamine pentaacetic acid have been determined in 12 patients [9].

Chemical compound and disease context of DETA

• Using a monoclonal antibody specific for the Mr 70,000 glycoprotein of Rauscher erythroleukemia virus, we have determined the optimal conditions for conjugation with the cyclic anhydride of diethylene triamine pentaacetic acid and subsequent labeling with 46Sc [10].
• To understand the mechanisms of NO-induced cell stress, we studied the effects of the NO donors diethylenetriamine and spermine NONOate and the peroxynitrite donor 5-amino-3-(4-morpholinyl)-1,2,3-oxadiazolium chloride (SIN-1) in SH-SY5Y and NG108-15 neuroblastoma cells [11].
• The rate of clearance from the lungs of inhaled technetium-99m labelled diethylene triamine penta-acetic acid (99mTc-DTPA) is often increased in interstitial lung disease as well as in smoking [12].
• Optimising technetium 99m diethylene triamine penta-acetate lung clearance in patients with the acquired immunodeficiency syndrome [13].
• Bleomycin lung toxicity detected by technetium-99m diethylene triamine penta-acetic acid aerosol scintigraphy [14].

Biological context of DETA

• Plasma volume was measured with 125I-albumin (human) and extracellular volume measured with either 99mTc diethylenetriamine pentaacetic acid or [14C]sucrose [15].
• Treatment of rat mesangial cells (MC) with the NO donors diethylenetriamine NO (DETA-NO) or spermine-NONOate resulted in a time- and dose-dependent upregulation of PDGF receptor alpha (PDGFRalpha) but not PDGFRbeta mRNA levels [16].
• The animals became hypoxic, and airway resistance, tissue resistance, lung elastance, and static compliance all deteriorated well before any change in alveolar neutrophils, macrophages, lung fluid (99mTc-labeled diethylenetriamine pentaacetic acid), or 125I-albumin flux, which were only appreciably increased at 8.5 hours [17].
• Renal function, measured by serum creatinine and technecium-99m diethylenetriamine pentaacetic acid glomerular filtration rate, was not altered and no adverse events were attributed to NEO [18].
• We hypothesized that a nebulized DETA/NO (half-time of NO release > 20 h) would stay in the lower airways and continuously supply sufficient NO to achieve sustained vasodilation in chronic pulmonary hypertension [19].

Anatomical context of DETA

• At millimolar concentrations, the chelators EDTA and diethylene triamine penta-acetic acid inhibited O2-. production by smooth muscle cells [20].
• Cultured rat cortical neurons were exposed to the NO(*) generator, diethylenetriamine/nitric oxide adduct, and were examined for signs of cell death, mitochondrial membrane potential changes (Deltapsi(m)), and the induction of a mitochondrial permeability transition (MPT) [21].
• The Abs were conjugated with biotin and 111In-benzyl diethylenetriamine pentaacetic acid, and, at various times after injection, were cleared by intraperitoneal injection of galactosylated streptavidin, which delivers the complexes to hepatocytes [22].
• Nitric oxide (NO; 1 microM) or an NO donor (500 microM diethylenetriamine-nitric oxide, DETA-NONOate) caused rapid glutamate and ATP release from cultured rat cortical astrocytes [23].
• Thus mice were administered the NO donor diethylenetriamine (DETA)/NO (4 doses of 0.1 mg/kg i.v. each) 24 h before 30 min of coronary artery occlusion followed by 24 h of reperfusion [24].

Associations of DETA with other chemical compounds

• Similarly, the survival-promoting agents aurintricarboxylic acid, N-acetylcysteine, the nitric oxide generator diethylenetriamine nitric oxide, 8-bromo-cGMP, and 8-(4-chlorophenylthio)-cAMP act upstream to inhibit JNK activation [25].
• Cell death in response to OGD, alone or in combination with hydrogen peroxide, lipopolysaccharides, interleukin-1beta, tissue necrosis factor-alpha, or nitric oxide (NO) donor diethylenetriamine/nitric oxide adduct (DETA/NO) was quantified as the ratio of propidium iodide to calcein AM-positive cells [26].
• BACKGROUND: Increased pulmonary epithelial permeability evaluated by the rate of clearance from lung to blood of the radioaerosol solute technetium-99m labelled diethylenetriamine pentaacetate (99mTc-DTPA) has been reported in smokers and in workers exposed to silica dust [27].
• BACKGROUND: The permeability of the alveolar-capillary barrier to technetium-99m labelled diethylenetriamine pentaacetate (99mTc DTPA) is known to be greatly increased in smokers, but the underlying mechanism is poorly understood [28].
• A role for haem metabolites in modulating HO-1 expression by NO was assessed by exposing cells to SNAP, SNP or DETA/NO in medium derived from cells treated with haemin, which contained increased bilirubin levels [29].

Gene context of DETA

• Two NO donors upregulated VSMC surface TNF-R1, and exogenous TNF-alpha induced VSMC apoptosis synergistically with the NO donor diethylenetriamine/NO, indicating that NO sensitizes VSMCs to TNF-alpha [30].
• Employing this approach, biglycan expression turned out to be down-regulated time- and dose-dependently either by interleukin-1beta-stimulated endogenous nitric oxide production or by direct application of the exogenous nitric oxide donor, diethylenetriamine nitric oxide [31].
• Treatment with the nitric oxide (NO) donor diethylenetriamine NONOate increased BrdU incorporation and cell counts in eNOS(-/-) cardiomyocytes (P < 0.05) [32].
• The NO donors S-nitroso-N-acetyl-penicillamine and diethylenetriamine/NO further reduced SPARC expression in cytokine-treated MC as well as in controls [33].
• Kinetic modeling of 99mTc-labeled diethylenetriamine pentaacetic acid-galactosyl-human serum albumin (TcGSA) time-activity data yields estimates of ASGP-R concentration [R]o and amount R0, which are directly related to functional liver mass [34].

Analytical, diagnostic and therapeutic context of DETA

• The particulate fraction of PKCeta rose from 66+/-5% in the control group to 86+/-3% after ischemic PC (P<0.05), to 88+/-2% after SNAP (P<0.05) and to 85+/-1% after DETA/NO (P<0.05) [35].
• Perfusates contained 99mTc-DTPA (diethylenetriamine pentaacetic acid) and volumes of the right colon were determined by two plane scintigraphy using gamma cameras [36].
• The pulmonary perfusion pressure-flow curves were shifted downwards by DETA/NO treatment, indicating improved resistive properties of the pulmonary vasculature [19].
• METHODS: In 48 women, with either idiopathic (n = 36) or acquired (n = 12) STC, 111In-radiolabelled diethylene-triamine penta-acetic acid colonic scintigraphy was performed to determine patterns of delay (generalized or left sided), the 'severity' of transit disturbance between subgroups, and the association with age or duration of symptoms [37].
• The effect of hydration on the dose to the urinary bladder wall during technetium-99m diethylene triamine penta-acetic acid renography [38].

References