Nucleoprotein Metabolism PDF

Metabolism of Nucleotides Pyrimidines and Purines  Pyrimidine and purine are the names of the parent compounds of two types of nitrogen- containing heterocyclic aromatic compounds. Important Pyrimidines  Pyrimidines that occur in DNA are cytosine and thymine.Cytosine and uracil ar...

Metabolism of Nucleotides Pyrimidines and Purines  Pyrimidine and purine are the names of the parent compounds of two types of nitrogen- containing heterocyclic aromatic compounds. Important Pyrimidines  Pyrimidines that occur in DNA are cytosine and thymine.Cytosine and uracil are the pyrimidines in RNA Important Purines  Adenine and guanine are the principal purines of both DNA and RNA Nucleosides Is a structure formed by the combination of nitrogen base and sugar. N2 base Sugars Nucleoside Adenine Deoxyribose/Ribose Adenosine Guanine Deoxiribose/Ribose Guanosine Thymine Deoxyribose Thymidine Cytosine Deoxyribose/Ribose Cytidine Uracil Ribose Uridine Nucleotides Nucleotides are phosphoric acid esters of nucleosides. Nucleoside Phosphoric acid Nucleotides Adenosine Phosphoric acid Adenylate (AMP) Guanosine Phosphoric acid Guanylate ( GMP) Thymidine Phosphoric acid Thymidylate ( TMP) Cytidine Phosphoric acid Cytidylate (CMP) Uridine Phosphoric acid Uridylate (UMP) 1 Degradation of purine nucleotides Disorders of purine metabolism  Gout  Lesch nyhan syndrome Gout  Metabolic disorders associated with overproduction of uric acid.  At physiological form, uric acid is found in more soluble form as sodium urate.  Normal serum uric acid range is 3-7 mg/dl  In severe hyperuricemia, crystal of sodium urate get deposited in the soft tissues, particularly in joints. Such deposits are commonly known as tophi.  This causes inflammation of joints resulting in gouty arthritis. 2   Historically, gout was found to be associated with high living, over eating and alcohol consumption. Primary metabolic gout It is an inborn error of purine metabolism due to overproduction of uric acid. Causes: Increasedactivityof PRPP (phosphoribosyl pyrophosphate) synthetase  Overactivityof PRPP amidotransferase  HGPRT (Hypoxanthine-guaninephosphoribosyltransferase) deficiency  Glucose6-phosphatase deficiency  Primary renal gout It is due to failure of uric acid excretion from the body so that uric acid level in the body gets increased. Secondary metabolic gout Secondary gout is due to secondary to certain diseases like leukemia, polycythemia, lymphoma, psoriasis and increased tissue breakdown like in trauma, starvation etc. Secondary renal gout It is due to secondary to defective glomerular filtration of urate due to generalized renal failure. 3  KIDNEY STONES When uric acid is present in high concentrations in the blood, it may precipitate as a salt in the kidneys. The salt can form stones, which can in turn cause pain, infection, and kidney damage Tratment of gout Is by. Use of colchicine & uricosuric drug:. To remove urates from the joint, colchine is the drug of choice To remove the urates from the body, urocosuric drugs such as probenecid, sulfinpyrazole, salicylates etc are used Use of Allopurinol : inhibits the activity of enzyme xanthine oxidase as a result of which uric acid-. is not produced (competitive enzyme inhibitor Lesch Nyhan syndrome It is X linked metabolic disorder since the structural genes for HGPRT is . located on the X chromosome It affects only males and is characterized by excessive uric acid  production and neurological abnormalities such as mental retardation,. aggressive behaviour, learning disability etc Treatment Allopurinol is used to treat hyperuricemia but it has no effect on the. neurological manifestation in theses patients Treatment for the neuro-behavioural features are limited to behavioural. therapy and providing protective physical device to prevent self-mutilation 4