核酸代谢(英).ppt

The Elevated Amount of Uric Acid Deposited : Gout In human, normally uric acid is excreted from body at a rate of 0.6 g in 24 hr, which resulted, in part, from ingested purine and the turnover of purine nucleotide of nucleic acid. The elevated concentration of uric acid causes the abnormal deposition of sodium urate crystals, called Gout, commonly depositing to joint and kidney and damaging these tissues. Gout occurs predominantly in male. The suspected mechanism for Gout : genetic deficiency or damage in enzymes of purine metabolism. The major alleviation of Gout has been achieved to apply to drug Allopurinol, which acts as competitive inhibitor against Xanthine Oxidase to stop conversion of xanthine to Uric Acid. * Allopurinol : Competitive Inhibitor against Xanthine Oxidase * Xanthine oxidase Allopurinol acts as competitive inhibitor against xanthine oxidase to interfere with uric acid genesis. Oxypurinol resulted from Allopurinol is more soluble to excrete from body. Diseases Caused by Purine Metabolism Abnormal Lesch-Nyhan Syndrome : X-linked inherited HGPRT deficiency in Purine Salvage Pathway, manifested by 2-years male children with hyperuricemia, gout and uric acid nephrolithiasis, mental retardation and self-mutilation. Gout : The elevated level of uric acid in blood crystallizes and is deposited in kidney, joint, tendon, and surrounding tissues, which suspected mechanism is deficient in one or more enzymes involving in purine metabolism. Adenosine Deaminase Deficiency (AD, or called severe combination immune deficiency) involved in adenylate catabolism. Lack of Adenosine Deaminase caused to 100-fold accumulation of ATP and to loss of proper development of T B lymphocytes, leading to deficiency in immune system. The patients with AD cant survive unless living in sterile bubble environment. * * The Pyrimidine catabolite is NH4+ , leading to urea product. Thymine is degraded into methyl-malonyl-semialdehyde, which is further degraded into succiny