Purine metabolism
(Redirected from Purine synthesis inhibitor)
Overview[edit | edit source]
Purine metabolism refers to the biochemical pathways responsible for the synthesis and degradation of purines, which are essential components of nucleotides and nucleic acids. Purines, such as adenine and guanine, are vital for various biological processes, including DNA and RNA synthesis, energy transfer, and cell signaling.
Synthesis of Purines[edit | edit source]
The synthesis of purines occurs through two main pathways: the de novo synthesis pathway and the salvage pathway.
De Novo Synthesis[edit | edit source]
In the de novo synthesis pathway, purines are synthesized from simple molecules such as amino acids, ribose-5-phosphate, carbon dioxide, and ammonia. The process begins with the formation of 5-phosphoribosyl-1-pyrophosphate (PRPP) and involves several enzymatic steps to produce inosine monophosphate (IMP), the precursor to both adenine and guanine nucleotides.
Salvage Pathway[edit | edit source]
The salvage pathway recycles free purine bases and nucleosides from the breakdown of nucleic acids. Enzymes such as hypoxanthine-guanine phosphoribosyltransferase (HGPRT) and adenine phosphoribosyltransferase (APRT) play crucial roles in converting free bases back into nucleotides.
Degradation of Purines[edit | edit source]
Purine degradation involves the breakdown of nucleotides into uric acid, which is excreted in the urine. The process begins with the dephosphorylation of nucleotides to nucleosides, followed by the removal of the ribose sugar to yield free bases. These bases are then oxidized to uric acid by enzymes such as xanthine oxidase.
Clinical Significance[edit | edit source]
Disorders of purine metabolism can lead to various medical conditions. For example, gout is caused by the accumulation of uric acid crystals in joints, leading to inflammation and pain. Lesch-Nyhan syndrome, a genetic disorder, results from a deficiency of HGPRT, leading to excessive uric acid production and neurological symptoms.
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