The Nonoxidative Pentose Cycle: Not Just for Tumor Cells

This is a really good article that discusses the large contribution of the nonoxidative pentose cycle to the production of ribose-5-phosphate and thereby to nucleotide synthesis in tumor cells:

http://www.ncbi.nlm.nih.gov/pubmed/6445904

This has been studied quite a bit since then, and it's well-known that tumor cells or immortalized cell lines, derived from tumors, do rely on transketolase activity and the nonoxidative pentose cycle, as a whole, to make nucleotides and support their wild cell division. This type of phenomena has also been found to operate, albeit to a lesser extent, in red blood cell precursors (as in the case of thiamine-responsive megaloblastic anemia, discussed in a previous posting on this site, in which the decrease in transketolase activity, produced by thiamine starvation, prevents the cells from making enough ribose-5-phosphate for nucleotide salvage and for de novo purine and pyrimidine formation). The net effect is similar in the megaloblastic anemia of folic acid or B12 deficiencies, in which the cells cannot make enough thymidine, a pyrimidine nucleotide, or inosine monophosphate (IMP) to support DNA replication or prevent DNA damage. As a result, the cells enlarge and die off before they become mature red blood cells. A key point is that proliferating, nonimmortalized cells, like erythroblasts in the bone marrow, may be substantially dependent on ribose derived from the nonoxidative arm of the pentose cycle.

This is somewhat new information, but even newer research has shown that the nonoxidative arm of the pentose cycle in cells that are not strongly or actively dividing, such as in cells in the liver, may be much more active than researchers had previously thought. Here's one article on that topic:

http://www.jbc.org/cgi/content/full/275/47/36787