I was confused by the discussion, in another article, of this article:
http://www.pnas.org/content/94/21/11601.full
That article shows that these people had reductions in uric acid excretion, probably as a result of their elevations in 5'-nucleotidase activity, and reductions in PRPP levels. Uridine decreased 5'-nucleotidase activity. This is an interesting article and suggests that uridine would help to oppose the increase 5'-nucleotidase activity, by some mechanism, that, as the authors of this article suggested (http://www.ncbi.nlm.nih.gov/pubmed/10871303?dopt=Abstract), may have occurred in response to the oral ATP. Another article, though, showed that thymidine or folinic acid, but not uridine, decreased the methotrexate-induced augmentation of 5'-ectonucleotidase activity:
http://www.jimmunol.org/cgi/content/full/167/5/2911
(pubmed: http://www.ncbi.nlm.nih.gov/pubmed/11509639?dopt=Abstract)
I can't really interpret that finding, in the case of the lack of effect of uridine , without more information (I'm talking about the above article). The authors of the first article, showing the uridine-induced decrease in 5'-nucleotidase activity, suggested that the "high-Km," cytosolic 5'-nucleotidase enzyme was the one whose activity had been suppressed in response to exogenous uridine. They also noted that some of the people had gotten benefit from ribose, but the benefits from uridine had been much more significant. That's one thing I've been trying to understand, why that's the case. I understand that uridine elevates the pools of many pyrimidines in cells, and I understand that exogenous uridine, as the authors mentioned, can increase intracellular PRPP levels by sparing PRPP that would otherwise be used in orotate phosphoribosyltransferase activity. But I think there are some other mechanisms at work.
I know one could say that uridine's effect would only occur in these people in the study, and that may be true. But I think the article has broader relevance. It's a great article.
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