Disease relevance of DIMERCAPROL

• Late onset of gold-induced thrombocytopenia. With a practical note on the injections of dimercaprol [1].
• Mercury poisoning from home gold ore processing. Use of penicillamine and dimercaprol [2].
• In 1951 Denny-Brown and Porter described the successful treatment of Wilson's disease using the chelating agent British antilewisite [3].
• Under treatment with modified British Anti-Lewisite (BAL; "Dimaval") his polyneuropathy slowly, but incompletely, subsided over three years at which time another sural nerve biopsy specimen showed regenerative proliferation of myelinated and unmyelinated axons but no signs of Wallerian degeneration [4].
• Bismuth dimercaprol (BisBAL) at 1 ppm of Bi3+ repressed Klebsiella pneumoniae capsule expression in defined medium by nearly 90%, which exposed subsurface structures [5].

High impact information on DIMERCAPROL

• Simultaneous addition of [gamma32P]ATP and 2,3-dimercaptopropanol permitted a comparison between recovery of secretion and phosphorylation of intracellular components [6].
• Pretreatment of unstimulated neutrophils with PAO inactivated cytosolic protein kinase C (PKC); the inactivation was reversed with DMP [7].
• Herein, we report that sulfur-containing antioxidants such as N-acetylcysteine and dimercaptopropanol induced apoptosis in several transformed cell lines and transformed primary cultures but not in normal cells [8].
• Conversely, the reducing reagent BAL (British anti-Lewisite, also known as 2,3-dimercapto-1-propanol) inhibits S6K1 phosphorylation and stabilizes the interaction of mTOR and raptor to mimic the state of the complex under nutrient-deprived conditions [9].
• Since both dithiothreitol and dimercaptopropanol reversed the inhibitory effect of PAO, critical sulfhydryl groups in the PTPase must be involved in NF-kappa B activation by TNF [10].

Chemical compound and disease context of DIMERCAPROL

• These oral chelators, meso-2,3-dimercaptosuccinic acid and sodium 2,3-dimercapto-1-propanesulfonate, have numerous advantages over dimercaprol, including less toxicity [11].
• Effect of canavanine and 2,3-dimercapto-1-propanol (British antilewisite) on the proliferation of Novikoff hepatoma cells in the presence of concanavalin A [12].
• Melarsoprol toxicity in the treatment of human African trypanosomiasis. Ten cases treated with dimercaprol [13].

Biological context of DIMERCAPROL

• NO action on I(K,out) was consistent with oxidative stress and was suppressed by several reducing agents, the most effective being British anti-Lewisite (2,3-dimercapto-1-propanol) [14].
• PhAsO inhibition of IgG-aggregate-stimulated hepatic vasoconstriction and glycogenolysis was reversed significantly by infusion of 2,3-dimercaptopropan-1-ol at 3-fold molar excess, whereas 2-mercaptoethanol at 40-fold molar excess was ineffective [15].
• Influence of dimercaprol (2,3-dimercapto-1-propanol) on the pharmacokinetics of 111In-bleomycin in the P-1798 lymphoma-bearing BALB/c mouse [16].
• When Pseudomonas aeruginosa ERC1 biofilms were treated continuously with 1 x MIC of bismuth dimercaprol (BisBAL), biofilm density determined by both total cell counts and viable cell counts increased during the first 30 h period then decreased thereafter [17].
• Massive arsenic poisoning--effect of hemodialysis and dimercaprol on arsenic kinetics [18].

Anatomical context of DIMERCAPROL

• Consistent with this, several other reducing agents, the most effective of which was 2,3-dimercaptopropanol, mimicked NAC in blocking DNA synthesis and suppressing death of PC12 cells and sympathetic neurons [19].
• Calcium disodium EDTA, penicillamine, and dimercaprol significantly reduced lead uptake, although only incubation with dimercaprol resulted in a net removal of lead from erythrocytes [20].
• 2,3-Dimercaptopropanol inhibits Ca2+ transport in microsomes from brain but not from fast-skeletal muscle [21].
• The ROL displayed on the yeast cell wall exhibited activity toward soluble 2,3-dimercaptopropan-1-ol tributyl ester (BALB) and insoluble triolein [22].
• Paroxetine and dimercaptopropanol limited Abeta peptide secretion from lens epithelial cells (B3 cells) [23].

Associations of DIMERCAPROL with other chemical compounds

• Since swelling induced by the latter is relieved by the dithiol 2,3-dimercaptopropanol (BAL), it is inferred that the effect of pyruvate might be mediated by the reduction of lipoic acid [24].
• Intravenous injections of equimolar doses of 2,3-dimercaptopropanol, 2-mercaptoethanesulfonic acid, N-2-mercaptopropionylglycine, D-penicillamine, or cysteamine did not lead to any significant change in liver, kidney, spleen or lung glutathione contents 2 hr after administration [25].
• Chelation and removal of cadmium from rats which were exposed to cadmium by multiple injections were studied in vivo after injection of two different compounds, 2,3-dimercaptopropanol (BAL) and diethylenetriamine pentaacetic acid (DTPA) [26].
• Both HgCl2 and 2,3-dimercaptopropanol (BAL) are inducers of QR in these cells, and paradoxically BAL (which is about 30 times less potent than HgCl2) enhances the inducer potency of HgCl2 substantially [27].
• Evaluation of the effect of BAL (2,3-dimercaptopropanol) on arsenite-induced teratogenesis in mice [28].

Gene context of DIMERCAPROL

• In this report, we show that paroxetine (serotonin reuptake blocker) and dimercaptopropanol (Hg chelator) exerted significant effects on APP expression (steady-state levels of APP), whereas Azithromycin altered APP processing [29].
• The observed induction was inhibited by monoclonal anti-Tat antibodies and 2,3-dimercapto-1-propanol [30].
• Finally, dithiol 2,3-dimercaptopropanol was over 100 times more effective than monothiol 2-mercaptoethanol in reversing the PAO-dependent inhibition of Ah receptor DNA binding activity [31].
• Preincubation of cells with 2,3-dimercaptopropanol (DMP) or dithiothreitol (DTT), compounds containing sulfhydryls, prevented PAO-stimulated [3H]PBut formation, indicating that PAO-stimulated PLD through interacting with vicinal thiol groups [32].
• Dimercaptopropanol (DMP), which is well known to antagonize PAO effects, inhibited the abolishment of PAO effect on the inhibitory effect of insulin and IGF-1 regarding insulin release [33].

Analytical, diagnostic and therapeutic context of DIMERCAPROL

• The time course of cadmium-metallothionein synthesis was studied in non-parenchymal and parenchymal cells, isolated by a cell-separation technique from the livers of rats after the simultaneous injection of CdCl2 (0.05 mg of Cd/kg) and a 10-fold molar excess of 2,3-dimercaptopropanol [34].
• He died within 37 hours despite intensive treatment that included intramuscular dimercaprol and hemodialysis [35].
• All four suffered respiratory failure and subsequent death despite chelation therapy with dimercaprol [36].
• Inhibition of bacterial adherence on the surface of stents and bacterial growth in bile by bismuth dimercaprol [37].
• The bacterial growth in the media and the bacterial adherence on the surface of stents were tested when different concentrations of bismuth dimercaprol were used in the perfusion media [37].

References