Nucleotide Metabolism Antibodies

Purine and pyrimidine nucleotides are the subunits of nucleic acids, DNA and RNA, and are the precursors of nucleotide cofactors, such as NAD. Nucleotide metabolism involves the synthesis and degradation of nucleotides, which are formed from a phosphate, pentose sugar (ribose or 2-deoxyribose), and a nitrogenous base (a purine or pyrimidine). Two major pathways are involved in the synthesis of nucleotides, the de novo pathway and the salvage pathway. Nucleotides are synthesized by the de novo pathway using amino acids, CO2, and tetrahydrofolate. The salvage pathway interconverts nucleosides and nucleotides and recycles purine and pyrimidine bases released as by-products from the breakdown of nucleotides and cofactors during cellular metabolism. The salvage pathway uses a smaller amount of energy than the de novo synthesis pathway.

The purine bases are adenine and guanine, while the pyrimidine bases are thymine, cytosine, and uracil. They form the adenosine and guanosine nucleosides, and the thymidine, cytidine and uridine nucleosides, respectively. RNA is a polymer that can contain all the nucleotides, while DNA does not contain uridine. Adding one or more phosphates to the nucleoside forms a nucleotide. The nitrogenous base constitutes the main difference between the purine and pyrimidine nucleotides, and therefore their synthesis is catalyzed by different routes. However, purine and pyrimidine synthesis, both require the use of phosphoribosyl pyrophosphate (PRPP) which donates the ribose sugar and phosphate needed to form the nucleotide. The breakdown or catabolism of pyrimidine leads to several products, that can be used for fatty acid synthesis or enter the urea cycle; while the breakdown of purine nucleotides leads to one final product, uric acid, which is insoluble and excreted in urine. High levels of uric acid can lead to gout, which involves the accumulation of uric acid crystals in joints. Deficiency or genetic defects in the enzymes involved in nucleotide metabolism often results in several diseases, such as deficiency of adenine deaminase, which leads to severe combined immunodeficiency (SCID).

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