Theobromine

About: Theobromine is a(n) research topic. Over the lifetime, 1137 publication(s) have been published within this topic receiving 29723 citation(s). The topic is also known as: 3,7-Dimethylxanthine & Theobromin.

Green tea composition, consumption, and polyphenol chemistry.

Abstract: Tea is grown in about 30 countries but is consumed worldwide, although at greatly varying levels. It is the most widely consumed beverage aside from water with a per capita worldwide consumption of approximately 0.12 liter per year. Tea is manufactured in three basic forms. Green tea is prepared in such a way as to preclude the oxidation of green leaf polyphenols. During black tea production oxidation is promoted so that most of these substances are oxidized. Oolong tea is a partially oxidized product. Of the approximately 2.5 million metric tons of dried tea manufactured, only 20% is green tea and less than 2% is oolong tea. Green tea is consumed primarily in China, Japan, and a few countries in North Africa and the Middle East. Fresh tea leaf is unusually rich in the flavanol group of polyphenols known as catechins which may constitute up to 30% of the dry leaf weight. Other polyphenols include flavanols and their glycosides, and depsides such as chlorogenic acid, coumarylquinic acid, and one unique to tea, theogallin (3-galloylquinic acid). Caffeine is present at an average level of 3% along with very small amounts of the other common methylxanthines, theobromine and theophylline. The amino acid theanine (5-N-ethylglutamine) is also unique to tea. Tea accumulates aluminum and manganese. In addition to the normal complement of plant cell enzymes, tea leaf contains an active polyphenol oxidase which catalyzes the aerobic oxidation of the catechins when the leaf cell structure is disrupted during black tea manufacture. The various quinones produced by the enzymatic oxidations undergo condensation reactions which result in a series of compounds, including bisflavanols, theaflavins, epitheaflavic acids, and thearubigens, which impart the characteristic taste and color properties of black tea. Most of these compounds readily form complexes with caffeine. There is no tannic acid in tea. Thearubigens constitute the largest mass of the extractable matter in black tea but their composition is not well known. Proanthocyanidins make up part of the complex. Tea peroxidase may be involved in their generation. The catechin quinones also initiate the formation of many of the hundreds of volatile compounds found in the black tea aroma fraction. Green tea composition is very similar to that of the fresh leaf except for a few enzymatically catalyzed changes which occur extremely rapidly following plucking. New volatile substances are produced during the drying stage. Oolong tea is intermediate in composition between green and black teas.

Subclasses of adenosine receptors in the central nervous system: interaction with caffeine and related methylxanthines.

Abstract: 1. The potencies of caffeine and related methylxanthines as adenosine antagonists were assessed with respect to three apparent subtypes of adenosine receptors in rat brain preparations: (i) the A1-adenosine receptor which binds with a very high affinity the ligand [3H]cyclohexyladenosine (KD, 1 nM) in rat brain membranes; (ii) a ubiquitous low-affinity A2-adenosine receptor which activates cyclic AMP accumulation in rat brain slices—this A2-adenosine system exhibits an EC50 for 2-chloroadenosine of about 20µM; and (iii) a relatively high-affinity A2-adenosine receptor which activates adenylate cyclase in rat striatal membranes—this A2-adenosine system exhibits an EC50 for 2-chloroadenosine of about 0.5µM and is present in striatal but not in cerebral cortical membranes. 2. The rank order of potency for methylxanthines versus binding of 1 nM [3H]cyclohexyladenosine in membranes from eight rat brain regions is theophylline (IC50, 20–30µM) > paraxanthine (IC50, 40–65µM) > caffeine (IC50, 90–110µM) > theobromine (IC50, 210–280µM). There thus appears to be little difference in A1-receptors in different brain regions in terms of interaction with these methylxanthines. 1-Methylxanthine is more potent than caffeine in rat cerebral cortical membranes, while 3-methylxanthine and 7-methylxanthine are less potent than caffeine. 3. The rank order of potency for methylxanthines versus activation of cyclic AMP accumulation by 50µM 2-chloroadenosine in rat striatal slices is theophylline (IC50, 60µM) > paraxanthine (IC50, 90µM) > caffeine (IC50, 120µM) » theobromine (IC50, > 1000µM). Similar potencies pertain in cerebral cortical slices. 4. The rank order of potency of methylxanthines versus activation of adenylate cyclase by 1µM 2-chloroadenosine in rat striatal membranes is theophylline (IC50, 20µM) > paraxanthine (IC50, 40µM) > caffeine (IC50, 80µM) » theobromine (IC50, > 1000µM). 5. Caffeine and other methylxanthines, thus, antagonize effectively both A1- and A2-adenosine receptors in brain perparations. Theobromine appears less effective versus A2-receptors than versus A1-receptors. Caffeine exhibits aKi value of about 50µM at the very high-affinity A1-binding sites, aKi value of about 30µM at the low-affinity A2-adenosine site in brain slices, and aKi value of about 27µM at the high-affinity A2-adenosine site in striatal membranes. The functional significance of antagonism of such adenosine receptors by caffeinein situ will depend both on the local levels of adenosine and on the affinity for adenosine for the receptor, since antagonism by xanthines is competitive in nature. In addition, the functional significance of xanthine action will depend on the degree of inhibition of adenosine input which is required to alter the output signal. For a stimulatory input to adenylate cyclase via an A2-adenosine receptor, profound antagonism by methylxanthines is probably required to alter the cyclic AMP-mediated output signal, while for inhibitory input to adenylate cyclase via an A1-adenosine receptor, presumably a lesser degree of antagonism by methylxanthines may be required to alter the cyclic AMP-mediated output signal.

Effects of cocoa powder and dark chocolate on LDL oxidative susceptibility and prostaglandin concentrations in humans

Abstract: Background Flavonoids are polyphenolic compounds of plant origin with antioxidant effects. Flavonoids inhibit LDL oxidation and reduce thrombotic tendency in vitro. Little is known about how cocoa powder and dark chocolate, rich sources of polyphenols, affect these cardiovascular disease risk factors. Objective We evaluated the effects of a diet high in cocoa powder and dark chocolate (CP-DC diet) on LDL oxidative susceptibility, serum total antioxidant capacity, and urinary prostaglandin concentrations. Design We conducted a randomized, 2-period, crossover study in 23 healthy subjects fed 2 diets: an average American diet (AAD) controlled for fiber, caffeine, and theobromine and an AAD supplemented with 22 g cocoa powder and 16 g dark chocolate (CP-DC diet), providing approximately 466 mg procyanidins/d. Results LDL oxidation lag time was approximately 8% greater (P = 0.01) after the CP-DC diet than after the AAD. Serum total antioxidant capacity measured by oxygen radical absorbance capacity was approximately 4% greater (P = 0.04) after the CP-DC diet than after the AAD and was positively correlated with LDL oxidation lag time (r = 0.32, P = 0.03). HDL cholesterol was 4% greater after the CP-DC diet (P = 0.02) than after the AAD; however, LDL-HDL ratios were not significantly different. Twenty-four-hour urinary excretion of thromboxane B(2) and 6-keto-prostaglandin F(1)(alpha) and the ratio of the 2 compounds were not significantly different between the 2 diets. Conclusion Cocoa powder and dark chocolate may favorably affect cardiovascular disease risk status by modestly reducing LDL oxidation susceptibility, increasing serum total antioxidant capacity and HDL-cholesterol concentrations, and not adversely affecting prostaglandins.

A study of the metabolism of theobromine, theophylline, and caffeine in man.

Abstract: Previous studies (1, 2) have shown that after the ingestion of caffeine or theophylline by man there was an increased urinary excretion of material which gave a blue color with the alkaline arsenophosphotungstate reagents used in the determination of uric acid. Myers and Wardell (3) and Buchanan, Christman, and Block (1) presented evidence that this extra color was caused by methyluric acids rather than by an increase in true uric acid excretion. When similar amounts of theobromine were taken, there was no increase in the excretion of chromogenic material. Subsequent work (2) demonstrated the presence of l-methyl and 1,3dimethyluric acids in urine after the administration of caffeine and theophylline. The excretion of 7-methylxanthine, 1-methylxanthine, and 1,7-dimethylxanthine after the ingestion of caffeine has recently been reported by Weissmann et al. (4). The present investigation concerns the identification and quantitative determination of the methyluric acids and methylxanthines excreted in the urine of man after the ingestion of theobromine, theophylline, and caffeine. 65 to 75 per cent of 1 gm. oral doses of these compounds were accounted for in the urine as methyluric acids or methylxanthines.

Caffeine and related purine alkaloids: biosynthesis, catabolism, function and genetic engineering.

Abstract: Details of the recently elucidated biosynthetic pathways of caffeine and related purine alkaloids are reviewed. The main caffeine biosynthetic pathway is a sequence consisting of xanthosine-->7-methylxanthosine-->7-methylxanthine-->theobromine-->caffeine. Genes encoding N-methyltransferases involved in three of these four reactions have been isolated and the molecular structure of N-methyltransferases investigated. Pathways for the catabolism of caffeine have also been studied, although there are currently no reports of enzymatic and genetic studies having been successfully carried out. Metabolism of purine alkaloids in species including Camellia, Coffea, Theobroma and Ilex plants is summarised, and evidence for the involvement of caffeine in chemical defense and allelopathy is discussed. Finally, information is presented on metabolic engineering that has produced coffee seedlings with reduced caffeine content, and transgenic caffeine-producing tobacco plants with enhanced disease resistance.