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.

Interactions among chemical components of Cocoa tea (Camellia ptilophylla Chang), a naturally low caffeine-containing tea species.

Abstract: In the 1980s, a novel tea species, Cocoa tea (Camellia ptilophylla Chang), was discovered in Southern China with surprisingly low caffeine content (0.2% by dry weight). Although its health promoting characteristics have been known for a while, a very limited amount of scientific research has been focused on Cocoa tea. Herein, a systematic study on Cocoa tea and its chemical components, interactions and bioactivities was performed. YD tea (Yunnan Daye tea, Camellia sinensis), a tea species with a high caffeine content (5.8% by dry weight), was used as a control. By UV-Vis spectrometry, High Performance Liquid Chromatography (HPLC), and Flame Atomic Absorption Spectrometry (FAAS) for chemical composition analysis, C-2 epimeric isomers of tea catechins and theobromine were found to be the major catechins and methylxanthine in Cocoa tea, respectively. More gallated catechins, methylxanthines, and proteins were detected in Cocoa tea compared with YD tea. Moreover, the tendency of major components in Cocoa tea for precipitation was significantly higher than that in YD tea. Catechins, methylxanthines, proteins, iron, calcium, and copper were presumed to be the origins of molecular interactions in Cocoa tea and YD tea. The interactions between catechins and methylxanthines were highly related to the galloyl moiety in catechins and methyl groups in methylxanthines. In vitro anti-inflammatory activity assays revealed that Cocoa tea was a more potent inhibitor of nitric oxide (NO) in lipopolysaccharide (LPS)-stimulated macrophage cells (RAW 264.7) than YD tea. This study constructs a solid phytochemical foundation for further research on the mechanisms of molecular interactions and the integrated functions of Cocoa tea.

Differential effects of bitter compounds on the taste transduction channels TRPM5 and IP3 receptor type 3.

Abstract: Transient receptor potential cation channel subfamily M member 5 (TRPM5) is a Ca(2+)-activated nonselective cation channel involved in the transduction of sweet, bitter, and umami tastes. We previously showed that TRPM5 is a locus for the modulation of taste perception by temperature changes, and by quinine and quinidine, 2 bitter compounds that suppress gustatory responses. Here, we determined whether other bitter compounds known to modulate taste perception also affect TRPM5. We found that nicotine inhibits TRPM5 currents with an effective inhibitory concentration of ~1.3mM at -50 mV. This effect may contribute to the inhibitory effect of nicotine on gustatory responses in therapeutic and experimental settings, where nicotine is often employed at millimolar concentrations. In addition, it implies the existence of a TRPM5-independent pathway for the detection of nicotine bitterness. Nicotine seems to act from the extracellular side of the channel, reducing the maximal whole-cell conductance and inducing an acceleration of channel closure that leads to a negative shift of the activation curve. TRPM5 currents were unaffected by nicotine's metabolite cotinine, the intensive sweetener saccharin or by the bitter xanthines caffeine, theobromine, and theophylline. We also tested the effects of bitter compounds on another essential element of the sweet taste transduction pathway, the type 3 IP3 receptor (IP3R3). We found that IP3R3-mediated Ca(2+) flux is slightly enhanced by nicotine, not affected by saccharin, modestly inhibited by caffeine, theobromine, and theophylline, and strongly inhibited by quinine. Our results demonstrate that bitter compounds have differential effects on key elements of the sweet taste transduction pathway, suggesting for heterogeneous mechanisms of bitter-sweet taste interactions.

Analytical Techniques Used for Determination of Methylxanthines and their Analogues—Recent Advances

Abstract: Methylxanthines (caffeine, theophylline, theobromine) are a popular group of natural purine alkaloids, which are components of many commonly used drugs, parapharmaceuticals and a wide range of food products (e.g. coffee, tea, energy drinks, etc.). Caffeine metabolites (theophylline, paraxanthine, theobromine and other 1-, 3-, 7-methyl tri-, di- and mono-derivatives of xanthine) and hypoxanthine metabolites (xanthine, uric acid) play an important role in the biochemical processes of mammalian organisms. That is why they are the markers of many diseases and are in the focus of the clinicians, pharmaceutical industry and ecologists. In addition to the natural methylxanthines there are structurally related synthetic derivatives: pentoxifylline, dyphylline, xantinol nicotinate and 8-chlorotheophylline that are still valuable pharmaceuticals needing to be monitored. A review of the modern techniques used for determination of methylxanthines for the last 10 years (2000 – March 2010) is presented.

Molecular recognition of xanthine alkaloids: First synthetic receptors for theobromine and a series of new receptors for caffeine

Abstract: Synthetic receptors (H3, H4, H5 and H6) are designed and synthesised for the first time for theobromine, a xanthine alkaloid used as a diuretic. The synthesis of the receptor H6 is achieved by Co(PPh3)3Cl-mediated homocoupling of 3-(ethoxycarbonyl)benzyl bromide 12 under mild conditions. New caffeine receptors (H7, H8 and H9) are designed and synthesised. The binding results of theobromine and caffeine (both by NMR and UV studies) are reported.

Effect of methylxanthine derivatives on doxorubicin transport and antitumor activity.

Abstract: Biochemical modulation, which is more effective with the use of antitumor agents, has recently played very important role in cancer chemotherapy. In this review, it was reported that some of the methylxanthine derivatives, e.g. caffeine, were useful for modulator and attempted to defined the relation between the effect of methylxanthine derivatives on the doxorubicin transport and antitumor activity. Caffeine and theobromine inhibited the doxorubicin efflux from tumor cells, increased the doxorubicin concentration in a tumor, and enhanced the antitumor effect of doxorubicin. However, the caffeine metabolites, which had no effect on the doxorubicin efflux, did not increase antitumor activity. Moreover, caffeine and theobromine did not enhance the side toxicity of doxorubicin on the lipid peroxide level, DNA biosynthesis and the doxorubicin concentrations in normal tissues. Moreover, we investigated the effect of the combination of doxorubicin with caffeine or theobromine on the change in cyclic adenosine 3',5'-monophosphate (cyclic AMP) in tissues in vivo, and the effect of cyclic AMP on doxorubicin efflux in vitro, and measured the distribution of caffeine and theobromine in normal and tumor tissues. In Ehrlich ascites carcinoma bearing mice, the level of cyclic AMP in a tumor was decreased by doxorubicin. With the combination of caffeine or theobromine and doxorubicin, the cyclic AMP level recovered to the control level. This tendency was not seen in normal tissues (heart and liver). Moreover, the doxorubicin efflux from the Ehrlich cells was inhibited on the addition of cyclic AMP in vitro. And the caffeine concentration in the tumors was the same as that in the heart, and was increased in combination with doxorubicin compared with that in the caffeine-only group during the 4 hr after caffeine treatment. Furthermore, the doxorubicin efflux was promoted by the supply of energy (addition of glucose), influx was decreased relatively, doxorubicin efflux needs the existence of glucose and the inhibition of energy related drug export pump by caffeine induced inhibition of doxorubicin efflux. The treatment of doxorubicin nor caffeine, and any treatment schedule did not change the amount and appearance of GLUT 1 as glucose transporter on Ehrlich ascites carcinoma cell. For the mentioned above, we thought as concerns the increase of antitumor activity of doxorubicin by caffeine which is xanthine derivatives as follows. Caffeine distributes, high level in tumor, keeps the cyclic AMP level, and effects glucose transport or doxorubicin transport depend on energy and inhibits doxorubicin efflux. And then DNA synthesis was increased with the maintenance the concentration of doxorubicin in tumor. These action did not show in normal tissues, caffeine did not influence the side toxicity of doxorubicin. These results suggested that caffeine which is one of xanthine derivatives will be useful for biochemical modulator.