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Biosynthesis Of Pyrimidine Nucleotides


  1. CO2 reacts with N of glutamine to form carbamoyl phosphate, which fuses with aspartate to form carbamoyl aspartate.
  2. Carbamoyl aspartate on ring closure forms the first pyrimidine ring named OROTATE.
  3. Orotate combines with PRPP to form OMP which is the first pyrimidine nucleotide.
  4. OMP forms UMP which can be converted to CMP or dTMP
  1. Regulation of Pyrimidine nucleotide biosynthesis
    1. The first two enzymes of pyrimidine nucleotide biosynthesis are sensitive to allosteric regulation.
    2. The first three & last two enzymes of pathway are regulated at genetic level by co-ordinate repression and derepression.
  2. Catabolism of Purine nucleosides. Humans convert purine nucleosides adenosine and guanosine to uric acid.


Extra Edge
  1. DNA consists of four bases-A, G, C, and T-that are held in linear array by phosphodiester bond through the 3’ and 5’ positions of adjacent deoxyribose moieties.
  2. DNA is organized into two strands by the pairing of bases A to T and G to C on complementary strand. These strands form a double helix around a central axis


  1. Metabolic disorders of Purine catabolism
    1. Gout
    2. Lesch Nyhan Syndrome
      1. X-linked recessive disorder
      2. Complete deficiency of enzyme HGPRTase an enzyme of Purine salvage, results in Purine overproduction

C/F — Hyperuricemia, uric acid Lithiasis & a syndrome of Self mutilation.

  1. Von Gierke’s disease. Purine overproduction & Hyperuricemia in Von Gierke’s disease occurs secondarily to enhanced generation of PRPP Precursor Ribose -5- Phosphate.
  2. Hypouricemia. Hypouricemia and increased excretion of hypoxanthine & xanthine are associated with xanthine oxidase deficiency.
  3. Adenosine deaminase deficiency is associated with severe combined Immunodeficiency disease in which both T & B cells are sparse dysfunctional.
  4. Purine nucleoside phosphorylase deficiency is associated with a severe thymus derived Lymphocyte deficiency with apparently normal β-cell function.
  1. Recent Advances: Lysosomal Enzymes & Gout
    1. Catabolism of purines, nitrogen containing heterocyclic compounds found in nucleic acids, leads to formation of uric acid, which is excreted in urin.
    2. Clinical manifestations include inflammation, pain, swelling, and increased warmth of some joints, particularly the big toe.
    3. Crystals are phagocytized by cells in the joint, and they accumulate in intracellular digestive vacuoles that contain lysosomal enzymes. Crystals cause physical damage to the vacuoles, releasing lysosomal hydrolases into the cytosol. Even though the pH optimum of lysosomal enzymes is lower than the pH of the cytosol, they have some hydrolytic activity at the higher pH, which causes digestion of cellular components and cellular autolysis.
  2. Catabolism of Pyrimidines.
    1. The end products of Pyrimidine catabolism are CO2, NH3, β-alanine and β-aminoisobutyrate
    2. Disorder of pyrimidine nucleotides and deficient enzyme is as:
    3. Orotic aciduria type 1- orotate phosphoribosyl transferase and orotidylate decarboxylase
    4. Orotic aciduria type 2- orotidylate decarboxylase


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