A purine nucleoside that has hypoxanthine linked by the N9 nitrogen to the C1 carbon of ribose. It is an intermediate in the degradation of purines and purine nucleosides to uric acid and in pathways of purine salvage. It also occurs in the anticodon of certain transfer RNA molecules. (Dorland, 28th ed)
The primary popular claim made for inosine, that it enhances exercise and athletic performance, is refuted by the available research data. There is some preliminary evidence that inosine may have some neurorestorative, anti-inflammatory, immunomodulatory and cardioprotective effects.
Inosine may have neuroprotective, cardioprotective, anti-inflammatory and immunomodulatory activities.
Mechanism of action
Inosine has been found to have potent axon-promoting effects in vivo following unilateral transection of the corticospinal tract of rats. The mechanism of this action is unclear. Possibilities include serving as an agonist of a nerve growth factor-activated protein kinase (N-Kinase), conversion to cyclic nucleotides that enable advancing nerve endings to overcome the inhibitory effects of myelin, stimulation of differentiation in rat sympathetic neurons, augmentation of nerve growth factor-induced neuritogenesis and promotion of the survival of astrocytes, among others. The mechanism of inosine's possible cardioprotective effect is similarly unclear. Inosine has been reported to have a positive inotropic effect and also to have mild coronary vasodilation activity. Exogenous inosine may contribute to the high-energy phosphate pool of cardiac muscle cells and favorably affect bioenergetics generally. Inosine has also been reported to enhance the myocardial uptake of carbohydrates relative to free fatty acids as well as glycolysis. In cell culture studies, inosine has been found to inhibit the production, in immunostimulated macrophages and spleen cells, of the proinflammatory cytokines, tumor necrosis factor (TNF)-alpha, interleukin (IL)-1, interleukin (IL)-12, macrophage-inflammatory protein-1 alpha and interferon (IFN)-gamma. It also suppressed proinflammatory cytokine production and mortality in a mouse endotoxemic model. These actions might account for the possible immunomodulatory, anti-inflammatory and anti-ischemic actions of inosine.
Ingested inosine is absorbed from the small intestine.
Volume of distribution
In the liver, inosine may be catabolized by a series of reactions culminating in the production of uric acid and also may be metabolized to adenine- and guanine-containing nucleotides. Inosine not metabolized in the liver is transported via the systemic circulation and distributed to various tissues of the body, where it is metabolized in similar fashion as in the liver. Uric acid, the purine end-product of inosine catabolism, is excreted in the urine.
The purine nucleoside phosphorylases catalyze the phosphorolytic breakdown of the N-glycosidic bond in the beta-(deoxy)ribonucleoside molecules, with the formation of the corresponding free purine bases and pentose-1-phosphate.
Key enzyme in purine degradation. Catalyzes the oxidation of hypoxanthine to xanthine. Catalyzes the oxidation of xanthine to uric acid. Contributes to the generation of reactive oxygen species. Has also low oxidase activity towards aldehydes (in vitro).
STIRPE F, DELLACORTE E: REGULATION OF XANTHINE DEHYDROGENASE IN CHICK LIVER. EFFECT OF STARVATION AND OF ADMINISTRATION OF PURINES AND PURINE NUCLEOSIDES. Biochem J. 1965 Feb;94:309-13. [PubMed:14348191 ]
Pyrimidine- and adenine-specific:sodium symporter activity
Sodium-dependent, pyrimidine- and purine-selective. Involved in the homeostasis of endogenous nucleosides. Exhibits the transport characteristics of the nucleoside transport system cib or N3 subtype (N3/cib) (with marked transport of both thymidine and inosine). Employs a 2:1 sodium/nucleoside ratio. Also able to transport gemcitabine, 3'-azido-3'-deoxythymidine (AZT), ribavirin and 3-deazaurid...