Disease relevance of Pseudotropanol

• Growth of Pseudomonas AT3 on the alkaloid atropine as its sole source of carbon and nitrogen is nitrogen-limited and proceeds by degradation of the tropic acid part of the molecule, with the metabolism of the tropine being limited to the point of release of its nitrogen [1].
• The recombinant TRII protein expressed in Escherichia coli catalyzes pseudotropine formation from tropinone with a Km value, a pH optimum, substrate and co-substrate preferences similar to those reported for the TRII enzymes from other Solanaceae species [2].
• Pseudotropine, the major alkaloid, is known to affect motility and might represent a causative agent for the observed cases of equine intestinal fibrosis [3].
• Metabolism of the tropine indole-3-carboxylate ICS 205-930 by differentiated rat and human hepatoma cells [4].

Psychiatry related information on Pseudotropanol

• Of these, the benzofurane-3-carboxylic ester of tropine (1) was found powerfully to increase the pain threshold, with a cholinergic mechanism of action [5].

High impact information on Pseudotropanol

• Structure-activity relationships among derivatives of dicarboxylic acid esters of tropine [6].
• The substrate binding site displays a complementarity to the bound substrate (psi-tropine) in its correct orientation [7].
• The order of potencies followed that which is known for various tropine and pseudotropine esters; that is, the 3alpha configuration is more potent than the 3beta configuration, and the quaternary analogues are more potent than the tertiary ones [8].
• An acyltransferase activity that can acetylate tropine using acetylcoenzyme A as cosubstrate has been found in transformed root cultures of Datura stramonium [9].
• An isocratic HPLC method was designed using a C8 column to determine the relative lipophilicity for two sets of 5-HT3 receptor antagonists, including tropine and quinolizine analogues [10].

Biological context of Pseudotropanol

• The pharmacokinetics of atropine and its primary metabolite, tropine, were determined simultaneously [11].
• Quantitative structure-activity relationship (QSAR) studies were also performed, and good characterization could be obtained for the soft anticholinergics containing at least 1 tropine moiety in their structure [12].

Anatomical context of Pseudotropanol

• These and earlier results suggest a possible form of metabolic dependence of myelin on tropine substances from the axon [13].
• Whereas vagal stimulation caused a muscarinic receptor-mediated increase in tracheal smooth muscle tone (as indicated by a 9.6 +/- 1.1 mmHg increase in endotracheal cuff pressure), the increase in cuff pressure (1.8 +/- 0.4 mmHg) was attenuated after intrapericardial tropine (4 mg) [14].
• The metabolism of the tropine indole-3-carboxylate ICS 205-930 (ICS), a highly potent and selective antagonist of 5-HT3 receptors, was investigated in continuous cell lines derived from rat or human liver and compared to the in vivo metabolism in rat and human [4].

Associations of Pseudotropanol with other chemical compounds

• Our findings indicate that endothelial receptors are characterised by a high affinity for scopolamine, which possesses a scopine base, and that muscle binding sites have a high affinity for antagonists possessing a tropine base (atropine, homatropine) [15].
• (Solanaceae) roots (RB-1), whereas, other precursors (ornithine, arginine, and tropine) increased the content of scopolamine only slightly or not at all [16].
• In Solanaceae, tropine is incorporated into hyoscyamine and scopolamine; pseudotropine is the first specific metabolite on the way to the calystegines [17].
• The report of cochlearine, the 3-hydroxybenzoate ester of tropine found in Cochlearia officinalis, Brassicaceae, initiated a screening for tropane alkaloids in Cochlearia species and for calystegines in further Brassicaceae [18].

Gene context of Pseudotropanol

• Intrathecal administration of the 5-HT3 receptor antagonist tropine (200 microg) produced allodynia, reduced the threshold, decreased the latency, and increased the number of spikes in the late component of the nociceptive flexion reflex [19].
• Poisoning with tropine alkaloids from cultivated plants and pharmaceuticals is an uncommon cause of delirium and coma [20].
• The tropine-forming reductase (TR I, EC 1.1.1.206) was purified 108-fold, the pseudotropine-forming enzyme (TR II, EC 1.1.1.236) was purified 3410-fold to homogeneity [21].

References