Problem

Sarin is a gaseous organophosphate compound that is commonly used in chemical warfare, as it is a powerful nerve agent that can cause death to those who inhale the gas within minutes. Sarin is an irreversible inhibitor to the enzyme acetylcholinesterase, an enzyme that catalyzes the breakdown of the acetylcholine neurotransmitter into acetate and choline.
Acetylcholine is a neurotransmitter that is released from pre-synaptic neurons to bind to acetylcholine receptors on post-synaptic neurons to trigger a downstream signal. When exposed to sarin, a cell’s normal metabolism of acetylcholine via acetylcholinesterase is disrupted, leading to excessive activation of the post-synaptic acetylcholine receptors.
There are two rescue medications that can be used to treat sarin exposure. The first, Pralidoxime, functions by breaking the bond between the sarin molecule and the acetylcholinesterase enzyme, thereby ending the inhibition. The second, Atropine, is an acetylcholine receptor antagonist, which prevents the excess acetylcholine from continually activating the acetylcholine receptor. If these medications are not provided soon after being exposed, those affected by the toxin may die within hours.
It should be noted that not all acetylcholinesterase inhibitors are exclusively harmful. Myasthenia Gravis is a muscular disease that is caused by the production of auto-antibodies that inhibit the acetylcholine receptor. In individuals affected by Myasthenia Gravis, drugs like Pyridostigmine, a competitive inhibitor of acetylcholinesterase, may relieve the symptoms of the disease. By increasing the synaptic concentration of acetylcholine, pyridostigmine could counteract the effects of the acetylcholine receptor-inhibiting antibody.
How would you expect Pyridostigmine to affect to the apparent Km and Vmax values of the acetylcholinesterase enzyme?
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