One treatment for hyperuricemia is administration of xanthine oxidase inhibitors like allopurinol. What is the biochemical rationale for this treatment? Discuss the mechanism and show an illustration how this drug able to alleviate symptoms of hyperuricemia?
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One treatment for hyperuricemia is administration of xanthine oxidase inhibitors like
allopurinol. What is the biochemical rationale for this treatment? Discuss the
mechanism and show an illustration how this drug able to alleviate symptoms of
hyperuricemia?
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- What is the biochemical rationale for the use of low dose aspirin in patients withcoronary artery disease? Why is Ibuprofen not a good substitute for aspirin in thiscase?What are the measures to inhibit the Maillard reaction in undesirable situations. please explain detailedMost individuals with genetic defects in oxidative phosphorylation are found to have relatively high concentrations of alanine in their blood. how this in biochemical terms? please help :)
- One treatment for hyperuricemia is administration of xanthine oxidase inhibitors like allopurinol. Discuss the mechanism and show an illustration how this drug able to alleviate symptoms of hyperuricemia.An inhibitor that specifically labels chymotrypsin at histidine 57 is N-tosylamido-l-phenylethyl chloromethylketone. How would you modify the structure of this inhibitor tolabel the active site of trypsin?Using the principles described in the text regarding pyridoxal phosphate mechanisms, propose a mechanism for the reaction catalyzed by serine hydroxymethyltransferase.
- Draw a schematic illustration of the hydrolysis of N-acetylphenylalaninamide catalyzed byalpha-chymotrypsin in which you indicate the important catalytic residues in the active site and how thesubstrate undergoes transformation to products through two different tetrahedral intermediates.Is trimethoprim a mechanism-based inhibitor of bacterial dihydrofolate reductase?Insulin-dependent diabetes is often accompanied by hypertriglyceridemia, which is an excess blood level of triacylglycerols in the form of very low density lipoproteins. Suggest a biochemical explanation.
- What is the biochemical basis of allopurinol treatment for gout?UDP-glucuronosyltransferase enzymes bind the organic compound UDP-glucuronic acid (UDP-GA) in order to catalyse the transfer of a glucuronic acid group from UDP-GA to a drug molecule, releasing UDP from the active site as a product. UDP is then regenerated by the activity of another enzyme. What terms could be used to describe UDP-GA?An inhibitor that specifically labels chymotrypsin at histidine 57 is Ntosylamido-l-phenylethyl chloromethyl ketone. How would you modify the structure of this inhibitor to label the active site of trypsin?