Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P47989 (xanthine oxidase)
 8,633 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gout and pain are synonymous, and a study in this issue of the BJP reports a novel anti-nociceptive effect of allopurinol, the drug most commonly used to treat gout. Allopurinol works by inhibiting xanthine oxidase (XO), the enzyme responsible for converting hypoxanthine to uric acid which is deposited as crystals in the joints of gout sufferers. Hypoxanthine is a metabolite of, and a possible precursor to, adenosine. Schmidt et al., find that acute inhibition of XO with allopurinol produces a modest adenosine A(1) receptor-mediated anti-nociceptive effect in common tests of chemical and thermal nociception in mice. A concomitant increase in cerebrospinal fluid levels of adenosine supports their hypothesis that inhibiting XO increases adenosine levels via salvage from hypoxanthine. Elevating endogenous adenosine levels by inhibiting metabolism is a well-established strategy for producing anti-nociception in many preclinical models, but inhibiting XO is likely to be particularly beneficial in some chronic pain states because of the pro-nociceptive reactive oxygen species that are produced by XO activity. Thus, allopurinol may have unexpected benefits in pain associated with chronic inflammation, diabetes and vascular dysfunction.
 ...
PMID:Allopurinol for pain relief: more than just crystal clearance? 1913 97

Superoxide dismutase (SOD) is used to manage chronic pain, including neuropathic and inflammatory pain. However, data regarding the clinical effectiveness are conflicting and the neurophysiological mechanism of SOD has yet to be elucidated. The aim of the present study was to investigate whether SOD relieved chronic central pain (CCP) following spinal cord injury (SCI) and the possible underlying mechanisms. A CCP model was established using the Allen method and the CCP of the rats was measured using the paw withdrawal threshold. SOD was administered intraperitoneally following the establishment of CCP as a result of SCI. The results demonstrated that SOD relieved CCP in rats following SCI. In addition, the expression of spinal phosphorylated N-methyl-D-aspartate(NMDA) receptor subunit 1 (pNR-1) was inhibited in the CCP rats that had been treated with SOD. These observations indicated that SOD reduced mechanical allodynia and attenuated the enhancement of spinal pNR1 expression in rats with CCP. In addition, the results indicated that superoxide, produced via xanthine oxidase, and the participation of superoxide and nitric oxide (NO) as a precursor of peroxynitrite in NMDA, were involved in the mediation of central sensitization. Therefore, the observations support the hypothesis that SOD may have a potential therapeutic role for the treatment of CCP following SCI via the manipulation of superoxide and NO.
 ...
PMID:Supression of chronic central pain by superoxide dismutase in rats with spinal cord injury: Inhibition of the NMDA receptor implicated. 2518 11