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Direct-Acting Cholinergic Agonists: Therapeutic Uses

Direct-Acting Cholinergic Agonists: Therapeutic Uses

Direct-acting cholinergic agonists have many therapeutic uses in various medical fields. Choline esters, including acetylcholine, have limited clinical utility due to their non-selectivity and short duration of action. Still, acetylcholine and carbachol are applied topically during ophthalmologic surgery to induce miosis. Pilocarpine, a muscarinic and ganglionic stimulator, effectively treats open-angle glaucoma and alleviates xerostomia and dry mouth caused by radiotherapy or Sjögren syndrome.

Indirect-Acting Cholinergic Agonists: Pharmacological Actions

Indirect-Acting Cholinergic Agonists: Pharmacological Actions

Indirect-acting cholinergic agonists, also known as anticholinesterases, exert their pharmacological effects by enhancing cholinergic transmission in various body parts, including the neuromuscular junction, autonomic cholinergic synapses, and the brain.
At the neuromuscular junction, these agents work by inhibiting the breakdown of acetylcholine, allowing it to remain bound to the receptor and bind to nearby receptors. This process leads to repetitive firing of the endplate, causing muscle...

Indirect-Acting Cholinergic Agonists: Mechanism of Action

Indirect-Acting Cholinergic Agonists: Mechanism of Action

Indirect-acting cholinergic agonists work by interacting with an enzyme called acetylcholinesterase (AChE) in the synaptic cleft. They can be reversible or irreversible inhibitors and have different effects on the enzyme.
Reversible inhibitors like edrophonium bind to a specific part of the enzyme called the anionic catalytic site. They form noncovalent bonds, which means they are not strongly attached to the enzyme. This creates a temporary and less stable enzyme–inhibitor complex, leading to...

Indirect-Acting Cholinergic Agonists: Chemistry and Structure-Activity Relationship

Indirect-Acting Cholinergic Agonists: Chemistry and Structure-Activity Relationship

Indirect-acting cholinergic agonists are agents that interact with the acetylcholinesterase enzyme in the synaptic cleft, preventing the breakdown of acetylcholine into choline and acetate. Consequently, the concentration of acetylcholine in the synaptic cleft increases. These agonists can be classified into reversible and irreversible inhibitors based on their duration of action.
Reversible inhibitors display short to medium durations of action. Short-acting agents include simple alcohols with...

Phase II Reactions: Acetylation Reactions

Phase II Reactions: Acetylation Reactions

Acetylation, a phase II biotransformation reaction, introduces an acetyl group to drugs or their metabolites. Acetyltransferase enzymes facilitate this reaction, which resembles α-amino acid conjugation due to the addition of a functional group to the drug molecule.
The substrates for acetylation are typically drugs or their metabolites with an amino, sulfonamide, or hydrazine functional group. Acetylation can occur at several points in the drug molecule, including primary, secondary, and...

α-Hydroxy Ketones via Reductive Coupling of Esters: Acyloin Condensation Overview

α-Hydroxy Ketones via Reductive Coupling of Esters: Acyloin Condensation Overview

The pinacol and McMurry reactions involve the reductive coupling of ketones or aldehydes. Similarly, the bimolecular reductive coupling of two ester molecules in the presence of sodium metal in an aprotic solvent yields an α-hydroxy ketone product. The α-hydroxy ketone is also called acyloin, so the reaction is referred to as ‘acyloin condensation.’

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Correction: Kurhaluk et al. Role of Antioxidants in Modulating the Microbiota-Gut-Brain Axis and Their Impact on Neurodegenerative Diseases. <i>Int. J. Mol. Sci.</i> 2025, <i>26</i>, 3658.

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Related Experiment Video

Updated: Jul 16, 2026

A Facile Protocol to Generate Site-Specifically Acetylated Proteins in Escherichia Coli

A Facile Protocol to Generate Site-Specifically Acetylated Proteins in Escherichia Coli

Published on: December 9, 2017

N-Acetyl-L-Cysteine as a Potential Adjunctive Strategy in STEC-HUS: Mechanistic Rationale and Current Evidence.

Joanna Wróblewska¹, Marcin Wróblewski¹, Alina Woźniak¹

¹Department of Medical Biology and Biochemistry, Faculty of Medicine, Ludwik Rydygier Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University in Toruń, 24 Karłowicza St., 85-092 Bydgoszcz, Poland.

Molecules (Basel, Switzerland)

|July 15, 2026

Summary

N-acetyl-L-cysteine (NAC) may help treat Shiga toxin-producing E. coli (STEC) infections causing hemolytic uremic syndrome (HUS). NAC

Keywords:

Escherichia coli N-acetyl-L-cysteine Shiga toxin hemolytic anemia oxidative stress

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Quantification of Site-specific Protein Lysine Acetylation and Succinylation Stoichiometry Using Data-independent Acquisition Mass Spectrometry

Quantification of Site-specific Protein Lysine Acetylation and Succinylation Stoichiometry Using Data-independent Acquisition Mass Spectrometry

Published on: April 4, 2018

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Last Updated: Jul 16, 2026

A Facile Protocol to Generate Site-Specifically Acetylated Proteins in Escherichia Coli

A Facile Protocol to Generate Site-Specifically Acetylated Proteins in Escherichia Coli

Published on: December 9, 2017

Quantification of Site-specific Protein Lysine Acetylation and Succinylation Stoichiometry Using Data-independent Acquisition Mass Spectrometry

Quantification of Site-specific Protein Lysine Acetylation and Succinylation Stoichiometry Using Data-independent Acquisition Mass Spectrometry

Published on: April 4, 2018

Area of Science:

Nephrology
Hematology
Toxicology

Background:

Shiga toxin-producing Escherichia coli (STEC) infections cause hemolytic uremic syndrome (HUS), a severe condition involving kidney injury.
Shiga toxins (Stx) drive HUS pathogenesis via endothelial damage, inflammation, and thrombosis.
Free heme released during hemolysis exacerbates oxidative stress and tissue injury in STEC-HUS.

Purpose of the Study:

To review the roles of oxidative stress and free heme in STEC-HUS.
To examine the potential of N-acetyl-L-cysteine (NAC) as an adjunctive therapy for STEC-HUS.

Main Methods:

Literature review summarizing current knowledge on STEC-HUS pathogenesis.
Analysis of preclinical and indirect evidence for NAC's therapeutic mechanisms.

Main Results:

Oxidative stress and free heme are key contributors to STEC-HUS.
NAC exhibits antioxidant, anti-inflammatory, and cytoprotective properties.
NAC may mitigate heme-mediated damage and improve red blood cell resilience.

Conclusions:

NAC shows promise as a potential adjunctive therapy for STEC-HUS.
Current evidence is preclinical; further clinical investigation is required.