In general, AChE is an enzyme that acts by hydrolyzing ACh in precursor molecules by rapidly closing the signaling of this molecule in the post-synaptic neuron or target tissue. AChE preferentially hydrolyzes ACh, whereas BuChE is less selective and acts by hydrolyzing both ACh and butyrylcholine (BuCh) in comparable amounts. The other 50% heterogeneity among amino acids is responsible for the selectivity differences of both the substrates and the inhibitors of these enzymes. Īcetylcholinesterase and BuChE exhibit structural similarities, with their amino acids having approximately 50% homology. AChE is found most abundantly in the central nervous system (CNS), in the skeletal muscles, and in the erythrocyte membrane, while BuChE is mostly found in blood plasma and is therefore also known as plasma cholinesterase. Īlthough they are evolutionarily similar, these enzymes differ in their distribution in tissues, their kinetic properties, and the specificity of their substrates. The most common cholinesterases present in the synaptic cleft are butyrylcholinesterase (BuChE) and AChE. In cholinergic synapses, cholinesterases are present, which consist of a class of enzymes that catalyze the hydrolysis of ACh in acetic acid and choline in the synaptic cleft, and thus allow the cholinergic neuron to return to its resting state after activation. It was the researcher Otto Loewi who discovered this molecule when he observed in his study the release of a biochemical substance by the parasympathetic nerve endings, which he called ACh. ACh is considered to be one of the major chemical neurotransmitters of the peripheral nervous system being released by all preganglionic, parasympathetic, and some sympathetic postganglionic fibers, as well as by motor neurons that project to the skeletal muscles. Within the neurotransmitters acting on the body’s nervous system is the so-called cholinergic system associated with the release of the acetylcholine (ACh) molecule in the synaptic cleft. Actions of the cholinergic system in the nervous system Studies indicate that the interaction between pyridostigmine bromide and stressors could trigger genotoxicity, the mechanism associated with the induction of oxidative stress that leads to this side effect of this drug however, this discussion needs to be better elucidated and may be more discussed as there is interaction between the pyridostigmine bromide and an endogenous oxidative imbalance caused by it or even by the possible interaction of this with genetic variations present in the antioxidant metabolism.Ģ. In this chapter the following topics will be addressed: (1) actions of the cholinergic system in the nervous system, commenting on acetylcholine metabolism and acetylcholinesterase metabolism (2) acetylcholinesterase inhibitors as subtitle in this topic: pharmacological characterization of pyridostigmine bromide, mechanism of action, and therapeutic effect of the drug (3) use of pyridostigmine bromide in Persian Gulf War and (4) potential effect of pyridostigmine bromide in oxidative stress, addressing as subtitle the influence of pyridostigmine bromide on the superoxide-hydrogen peroxide imbalance model.
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