Question

Prostaglandins are a class of eicosanoids, fatty acid derivatives with a variety of extremely potent actions on vertebrate tissues. They are responsible for producing fever and inflammation and its associated pain. Prostaglandins are derived from the 20-carbon fatty acid arachidonic acid in a reaction catalyzed by the enzyme prostaglandin endoperoxide synthase. This enzyme, a cyclooxygenase, uses oxygen to convert arachidonic acid to PGG2, the immediate precursor of many different prostaglandins. Arachidonic Rate of formation Rate of formation of PGG2 with 10 mg/ml acid (mm) of PGG2 (ml/min) ibuprofen (mM/min) 0.295 21.0 13.1 0.354 23.6 15.1 0.531 29.8 20.3 0.885 37.8 27.8 2.07 49.0 40.8 The kinetic data given in the table are for the reaction catalyzed by a mutant of prostaglandin endoperoxide synthase. Focusing here on the first two columns, determine the Vimax and Km of the enzyme. mM/min V K. Ibuprofen is an inhibitor of prostaglandin endoperoxide synthase. By inhibiting the synthesis of prostaglandins, ibuprofen reduces inflammation and pain. Using the data in the first and third columns of the table, determine the type of inhibition that ibuprofen exerts on prostaglandin endoperoxide synthase. O uncompetitive inhibition competitive inhibition O mixed inhibition

Answer 1

By considering the first two columns we need to plot the reciprocals of the first two columns (i.e., concentration and velocity) to get Lineweaver-Burk equation

1/V0 = Km/Vmax (1/[S]) + 1/Vmax

From the plot, we will get an equation y=mx+c

1/Vmax = 0.0163 $\Rightarrow$ Vmax = 1/0.0163 $\Rightarrow$ Vmax = 61.3496 mM/min

Similarly, Km/Vmax = 0.0088 $\Rightarrow$ Km = Vmax * 0.0088 = 61.349 * 0.0088 = 0.5398 mM

Vmax = 61.3496 mM/min; Km = 0.5398 mM

As per Lineweaver-Burk equation Km increased and Vmax unaffected with the above data. Therefore, it is competitive inhibition