Topic
Theobromine
About: Theobromine is a research topic. Over the lifetime, 1137 publications have been published within this topic receiving 29723 citations. The topic is also known as: 3,7-Dimethylxanthine & Theobromin.
Papers published on a yearly basis
Papers
More filters
Journal Article•
TL;DR: The present results indicate that the CNS action of theobromine may be received through consumption of the Obromine-containing foodstuffs or beverages in the authors' every day life.
Abstract: Effects of cocoa and its main CNS active constituent methylxanthine theobromine as well as caffeine were evaluated by ambulatory activity, and discrete lever-press and shuttle avoidance in mice. Cocoa (1 g/kg p.o.) and theobromine (10 mg/kg p.o.) significantly increased ambulatory activity. However, the other doses of cocoa and theobromine had no effect on the ambulatory activity. Caffeine increased ambulatory activity with the maximum action at 30 mg/kg p.o. Furthermore, cocoa (0.1, 0.3 and 1 g/kg), theobromine (3, 10, 30 and 100 mg/kg) and caffeine (3, 10, 30 and 100 mg/kg) enhanced the ambulation-increasing effect of methamphetamine (2 mg/kg s.c.). The ambulation-increasing effect of cocaine (20 mg/kg s.c.) was also enhanced by cocoa (1 g/kg), theobromine (10, 30 and 100 mg/kg) and caffeine (10, 30 and 100 mg/kg). On the other hand, comparatively higher doses of theobromine and caffeine disrupted the well established avoidance response. Thus, the avoidance rate was significantly decreased by theobromine (100 mg/kg and more) and caffeine (30 mg/kg and more) under the lever-press situation, and by theobromine (100 mg/kg and more) and caffeine (100 mg/kg) under the shuttle situation. These dose effect relationships revealed that cocoa contains about 1% theobromine. The present results indicate that we may receive the CNS action of theobromine through consumption of theobromine-containing foodstuffs or beverages in our every day life.
6 citations
TL;DR: Using a combination of spectroscopic techniques and quantum mechanical calculations, it is shown that moving the methyl group from N1 in theophylline to N7 in theobromine causes significant differences in their excited state properties, i.e., it produces pyramidalization in the excited state of the latter.
Abstract: We explore the influence of the relative position of the methyl substituent on the photophysics of theophylline and theobromine, two molecules that are structurally related to the DNA bases. Using a combination of spectroscopic techniques and quantum mechanical calculations, we show that moving the methyl group from N1 in theophylline to N7 in theobromine causes significant differences in their excited state properties, i.e., it produces pyramidalization of N7 in the excited state of the latter. Paradoxically, this modification seems to have little effect on the structural properties of the cation and the ionization process. It is suggested that similar effects may exist in the excited state properties of DNA bases.
6 citations
Journal Article•
TL;DR: It is suggested that CAF and its primary metabolites compete with ACM for biotransformation by the cytochrome P-450 mixed function oxidase system, thereby reducing the rate of formation of the hepatotoxic ACM metabolite.
Abstract: Administration of caffeine (CAF) to mice as early as 6 hr prior to injection of a hepatotoxic but nonlethal dose of acetaminophen (ACM) significantly antagonized the hepatotoxic action of ACM as judged by serum levels of alanine aminotransferase (ALT) activity. Administration of CAF after ACM produced complete antagonism only when CAF was given no later than 1 hr after ACM. Administration of CAF daily for 3 days prior to injection of ACM enhanced ACM toxicity markedly, but little or no toxicity ensued when CAF-pretreated mice received ACM followed immediately by CAF. The four primary metabolites of CAF, 1,3-dimethylxanthine (theophylline), 3,7-dimethylxanthine (theobromine), 1,7-dimethylxanthine (paraxanthine), and 1,3,7-trimethyluric acid were effective and virtually complete antagonists of ACM-induced hepatotoxicity when given immediately after ACM, as were the secondary metabolites, 1-methylxanthine and 1,3-dimethyluric acid. Allopurinol, which reduces theophylline clearance, increases the rate of oxidative N-demethylation of theophylline to 1-methylxanthine, and inhibits conversion of 1-methylxanthine to 1-methyluric acid, was also a dose-dependent antagonist of ACM-induced hepatotoxicity. The hepatotoxic response of mice to ACM is exaggerated by a brief period of diethyl ether anesthesia; CAF given immediately after ACM to previously anesthetized mice suppressed this response and maintained serum ALT levels at control values. It is suggested that CAF and its primary metabolites compete with ACM for biotransformation by the cytochrome P-450 mixed function oxidase system, thereby reducing the rate of formation of the hepatotoxic ACM metabolite.
6 citations
TL;DR: The case very well describes an episode of tachycardia precipitated by large amount of chocolate consumption in a patient with underlying substrate, and any association between amount of daily caffeine consumption and risk of arrhythmia is not found.
Abstract: Conflicting studies have been published concerning the association between chocolate and cardiovascular diseases. Fewer articles have described the potential arrhythmogenic risk related to chocolate intake. We present a case of paroxysmal supraventricular tachycardia in a woman after consumption of large quantity of chocolate. A 53-year-old woman with no significant medical history presented to us with complaints of palpitations and shortness of breath after consuming large amounts of chocolate. Electrocardiogram showed supraventricular tachycardia at 165 beats per minute, which was restored to sinus rhythm after adenosine bolus injection. Electrophysiology studies showed atrioventricular nodal reentry tachycardia, which was treated with radiofrequency ablation. Chocolate contains caffeine and theobromine, which are methylxanthines and are competitive antagonists of adenosine and can have arrhythmogenic potential. Our case very well describes an episode of tachycardia precipitated by large amount of chocolate consumption in a patient with underlying substrate. There are occasional case reports describing association between chocolate, caffeine, and arrhythmias. A large Danish study, however, did not find any association between amount of daily caffeine consumption and risk of arrhythmia.
6 citations
TL;DR: Pregnandiol is a potent inhibitor of microsomal drug metabolism, specifically of cytochrome P450 IA, which could explain the immaturity of some metabolic pathways of caffeine in neonates, consistent with the hypothesis that C-8 hydroxylation and demethylation of caffeine are mediated by different isoenzymes.
Abstract: Three groups of six 5-week-old Sprague Dawley female rats received i.p. injections of pregnandiol, 1.25, 2.50 or 5 mg/kg, respectively, in triolein daily for 7 days. Caffeine metabolism was studied in liver slices on day 8 by HPLC. Only primary metabolites were formed. N-1 demethylation was the most important pathway (theobromine represented 51% of total dimethylxanthines). Unlike in human in vitro or in vivo, 1,3,7-DAU (6-amino-5-(N-formylmethylamino)-1,3-dimethyluracil) was an important metabolite (9.7% of total caffeine metabolites). Pregnandiol inhibited N-1, N-3 and N-7 demethylation in vitro (-33%, -33% and -28%, respectively, at 5 mg/kg/day), but it had no effect on N-1 demethylation at 1.25 or 2.50 mg/kg/day. Pregnandiol at all doses had no effect on 1,3,7-trimethyluric acid and 1,3,7-DAU formation. These results are consistent with the hypothesis that C-8 hydroxylation and demethylation of caffeine are mediated by different isoenzymes. They indicate that pregnandiol is a potent inhibitor of microsomal drug metabolism, specifically of cytochrome P450 IA, which could explain the immaturity of some metabolic pathways of caffeine in neonates.
6 citations