This is an interesting article (by Hao Zeng et al.) showing that methotrexate and leucovorin/reduced folates can be transported by multidrug-resistance proteins (ATP-dependent, cellular efflux transporters). This could be relevant to an understanding of folate/purine interactions. It's possible that higher intracellular folate levels could limit purine efflux (purines can sometimes be substrates for MDR/MRP-mediated efflux).
http://cancerres.aacrjournals.org/cgi/content/full/61/19/7225
(pubmed: http://www.ncbi.nlm.nih.gov/pubmed/11585759?dopt=Abstract)
Here's an article (by Jan Wijnholds et al.) showing that MRP5/mdr5 can transport purines out of cells and may cause glutathione (GSH) efflux (such as in response to an excess of intracellular purines?), given the potential for GSH cotransport with purines:
http://www.pnas.org/content/97/13/7476.full
(pubmed: http://www.ncbi.nlm.nih.gov/pubmed/10840050?dopt=Abstract)
That could be a concern with the use of higher doses of purines/dietary nucleotides in the treatment of liver diseases or traumatic brain injury. They also mentioned the similarity with the organic anion transporters, and urate (uric acid) is transported by organic anion transporters (and some urate is excreted into the bile). Purines could compete with bile acids for efflux into the bile and thereby, conceivably, cause liver issues at high doses.
A lot of drugs and physiological mediators could conceivably influence folate metabolism by influencing MDR/MRP expression, etc.
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