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Related Concept Videos

Urea Cycle01:23

Urea Cycle

45.1K
The urea cycle describes how liver cells convert ammonia to urea. Ammonia is a toxic waste product of protein catabolism. Land animals must convert ammonia into the less toxic urea which can be safely eliminated by the kidneys through urine. Marine animals excrete ammonia directly, and the surrounding water dilutes the ammonia to safe levels.
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Physical Properties of Amines01:26

Physical Properties of Amines

3.3K
Amines with low molecular weight are usually gaseous at room temperature, while those with high molecular weight are liquid or solids in nature. Usually, low molecular weight amines have a rotten fish-like smell. Diamines typically have a pungent smell. For instance, cadaverine and putrescine, depicted in Figure 1, are two molecules responsible for decaying tissue.
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Preparation of Amines: Alkylation of Ammonia and Amines01:30

Preparation of Amines: Alkylation of Ammonia and Amines

3.5K
Alkylation is one of the methods used to prepare amines. Direct alkylation of ammonia or a primary amine with an alkyl halide gives polyalkylated amines along with a quaternary ammonium salt through successive SN2 reactions. This process of making the quaternary salt through the direct alkylation method is called exhaustive alkylation.
Each alkylation step makes the nitrogen center more nucleophilic, which triggers successive alkylations until a quaternary ammonium salt is formed. Considering...
3.5K
Basicity of Aliphatic Amines01:21

Basicity of Aliphatic Amines

6.0K
Amines can behave as Brønsted–Lowry bases by accepting a proton from the acid to form corresponding conjugate acids. Due to a lone pair of nonbonding electrons, aliphatic amines can also act as Lewis bases by forming a covalent bond with an electrophile.
To measure the basicity of amines, two conventions are generally used. The first defines Kb as the basicity constant for the deprotonation reaction of water by the amine, as presented in Figure 1. Conventionally, lower Kb indicates...
6.0K
Anticholinesterase Agents: Poisoning and Treatment01:26

Anticholinesterase Agents: Poisoning and Treatment

939
Anticholinesterases, also known as cholinesterase inhibitors, work by blocking the breakdown of acetylcholine, leading to its accumulation in the synaptic cleft. This accumulation indirectly enhances both muscarinic and nicotinic actions. These agents are classified as reversible or irreversible based on their mechanism of action.     
Irreversible agents form a strong bond with the cholinesterase enzyme, making it inactive. The breakdown of the phosphorylated enzyme is...
939
Preparation of Amines: Reductive Amination of Aldehydes and Ketones01:38

Preparation of Amines: Reductive Amination of Aldehydes and Ketones

2.9K
Carbonyl compounds and primary amines undergo reductive amination first to produce imines, followed by secondary amines in the same reaction mixture, using selective reducing agents like sodium cyanoborohydride or sodium triacetoxyborohydride. Reductive amination produces different degrees of substitution of amines depending on the starting amine substrate.
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Updated: Jul 31, 2025

Microdialysis of Excitatory Amino Acids During EEG Recordings in Freely Moving Rats
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Microdialysis of Excitatory Amino Acids During EEG Recordings in Freely Moving Rats

Published on: November 8, 2018

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Drug-induced hyperammonaemia.

Loai Shakerdi1, Aidan Ryan2,3

  • 1National Centre for Inherited Metabolic Disorders, Mater Misericordiae University Hospital, Dublin, Ireland.

Journal of Clinical Pathology
|May 10, 2023
PubMed
Summary
This summary is machine-generated.

Drug-induced hyperammonaemia (HA), often linked to valproate, poses a neurological risk. Prompt consultation with a metabolic physician is crucial due to time-dependent neurotoxic effects.

Keywords:
chemistry, clinicaldiagnosiseducationgenetics

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Area of Science:

  • Neurology
  • Toxicology
  • Pharmacology

Background:

  • Hyperammonaemia (HA) results from various causes, leading to neurotoxicity, particularly in pediatric patients.
  • Drug-induced HA can stem from impaired ammonia elimination or increased production, frequently associated with valproate use.
  • Managing valproate-induced HA involves balancing therapeutic necessity against potential toxicity.

Conclusions:

  • Drug-induced hyperammonaemia requires prompt medical evaluation due to its time-dependent neurotoxicity.
  • Management strategies are often extrapolated from urea cycle disorder guidelines.
  • Further research and specific guidelines are needed for managing drug-induced HA.