Paraxanthine

Paraxanthine

Paraxanthine
Skeletal formula of paraxanthine
Ball-and-stick model of the paraxanthine model
Names
IUPAC name
1,7-dimethyl-3H-purine-2,6-dione
Other names
paraxanthine,
1 ,7-Dimethylxanthine
Identifiers
 N
ChEBI  Y
ChEMBL  Y
ChemSpider  Y
Jmol-3D images Image
PubChem
UNII  Y
Properties
C7H8N4O2
Molar mass 180.17 g·mol−1
Melting point 351 to 352 °C (664 to 666 °F; 624 to 625 K)
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
 N  (: Y/N?)

Paraxanthine, or 1,7-dimethylxanthine, is a dimethyl derivative of xanthine, structurally related to caffeine. Like caffeine, paraxanthine is a psychoactive central nervous system (CNS) stimulant. It possesses a potency roughly equal to that of caffeine and is likely involved in the mediation of the effects of caffeine itself.

Contents

  • Production and metabolism 1
  • Physiological effects 2
  • Toxicity 3
  • References 4

Production and metabolism

Paraxanthine is not produced by plants and is only observed in nature as a metabolite of caffeine and theobromine in animals. After intake, roughly 84% of caffeine is demethylated at the 3-position to yield paraxanthine, making it the chief metabolite of caffeine in the body.[1]

Certain proposed synthetic pathways of caffeine make use of paraxanthine as a bypass intermediate. However, its absence in plant alkaloid assays implies that these are infrequently, if ever, directly produced by plants.

Physiological effects

Paraxanthine has a number of physiological effects on animals:

Toxicity

Paraxanthine is believed to exhibit a lower toxicity than caffeine.[7] While blood levels commensurate with average intake appear to be fairly innocuous, high blood concentrations of paraxanthine have been linked to miscarriage in pregnant mothers.[8]

References

  1. ^ Guerreiro S, Toulorge D, Hirsch E, Marien M, Sokoloff P, Michel PP (October 2008). "Paraxanthine, the primary metabolite of caffeine, provides protection against dopaminergic cell death via stimulation of ryanodine receptor channels". Mol. Pharmacol. 74 (4): 980–9.  
  2. ^ Essayan DM. (2001). "Cyclic nucleotide phosphodiesterases.". J Allergy Clin Immunol. 108 (5): 671–80.  
  3. ^ Deree J, Martins JO, Melbostad H, Loomis WH, Coimbra R. (2008). "Insights into the Regulation of TNF-α Production in Human Mononuclear Cells: The Effects of Non-Specific Phosphodiesterase Inhibition". Clinics (Sao Paulo). 63 (3): 321–8.  
  4. ^ Marques LJ, Zheng L, Poulakis N, Guzman J, Costabel U (February 1999). "Pentoxifylline inhibits TNF-alpha production from human alveolar macrophages". Am. J. Respir. Crit. Care Med. 159 (2): 508–11.  
  5. ^ a b Peters-Golden M, Canetti C, Mancuso P, Coffey MJ. (2005). "Leukotrienes: underappreciated mediators of innate immune responses". J Immunol. 174 (2): 589–94.  
  6. ^ Daly JW, Jacobson KA, Ukena D. (1987). "Adenosine receptors: development of selective agonists and antagonists". Prog Clin Biol Res. 230 (1): 41–63.  
  7. ^ Neal L. Benowitz, Peyton Jacob, Haim Mayan and Charles Denaro (1995). "Sympathomimetic effects of paraxanthine and caffeine in humans". Clinical Pharmacology & Therapeutics 58 (58): 684–691.  
  8. ^ Mark A. Klebanoff, M.D., M.P.H., Richard J. Levine, M.D., M.P.H., Rebecca DerSimonian, Sc.D., John D. Clemens, M.D., and Diana G. Wilkins, Ph.D. (1999). "Maternal Serum Paraxanthine, a Caffeine Metabolite, and the Risk of Spontaneous Abortion". New England Journal of Medicine 341 (22): 1639–1644.