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Urea Cycle

Urea Cycle

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.

Physical Properties of Amines

Physical Properties of Amines

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.

2° Amines to N-Nitrosamines: Reaction with NaNO2

2° Amines to N-Nitrosamines: Reaction with NaNO₂

Secondary amines react with nitrous acid to form N-nitrosamines, as depicted in Figure 1. Nitrous acid, a weak and unstable acid, is formed in situ from an aqueous solution of sodium nitrite and strong acids, such as hydrochloric acid or sulfuric acid, in cold conditions. In the presence of an acid, the nitrous acid gets protonated. The subsequent loss of water results in the formation of the electrophile known as nitrosonium ion.

Preparation of Amines: Alkylation of Ammonia and Amines

Preparation of Amines: Alkylation of Ammonia and Amines

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...

Amines: Introduction

Amines: Introduction

Amines are organic derivatives of ammonia. They are formed by replacing one or more ammonia protons with alkyl or aryl groups. Depending upon the number of organyl groups bonded to nitrogen, amines are classified as primary, secondary, or tertiary. Primary amines have one organyl group attached to the nitrogen atom, while secondary and tertiary amines have two and three organyl groups attached to the nitrogen atom, respectively.

Drug Toxicity: Dose-Dependent Reactions

Drug Toxicity: Dose-Dependent Reactions

Drug toxicities can be stratified into pharmacological, pathological, or genotoxic based on their mechanisms. The incidence and severity of these toxicities generally increase with the drug's concentration in the body and exposure time.Pharmacological toxicity is evident when the therapeutic effects of drugs overshoot into adverse reactions in a predictable, dose-dependent manner. Central nervous system (CNS) depression from barbiturates is a classic example, with effects escalating from...

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Updated: Mar 9, 2026

Ammonia Fiber Expansion AFEX Pretreatment of Lignocellulosic Biomass

Ammonia Fiber Expansion AFEX Pretreatment of Lignocellulosic Biomass

Published on: April 18, 2020

Ammonia toxicity: from head to toe?

Srinivasan Dasarathy¹, Rajeshwar P Mookerjee², Veronika Rackayova³

¹Department of Gastroenterology, Hepatology and Pathobiology, Cleveland Clinic, Cleveland, OH, USA.

Metabolic Brain Disease

|December 25, 2016

Summary

This summary is machine-generated.

Hyperammonemia, an increase in blood ammonia, affects all organs, not just the brain. Elevated ammonia levels can directly impair cellular function and contribute to multi-organ dysfunction, particularly in chronic liver disease.

Keywords:

Ammonia Brain Hepatic encephalopathy Liver Muscle Toxicity

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Published on: March 21, 2016

Area of Science:

Biochemistry
Cell Biology
Toxicology

Background:

Ammonia (NH3) freely crosses plasma membranes, leading to elevated levels in all body tissues during hyperammonemia.
While ammonia's neurotoxic effects are well-established, its impact extends beyond the central nervous system.
Chronic liver disease often involves multi-organ dysfunction, prompting a re-evaluation of ammonia's role.

Purpose of the Study:

To challenge the notion of ammonia solely as a neurotoxin.
To provide evidence for ammonia's detrimental effects on various organ and cell types.
To highlight ammonia's contribution to multi-organ dysfunction in conditions like chronic liver disease.

Main Methods:

Review of existing scientific literature and evidence.
Analysis of cellular mechanisms affected by ammonia.
Examination of ammonia's role in systemic physiological disturbances.

Main Results:

Hyperammonemia results in increased ammonia concentrations across all organs and tissues.
Ammonia exerts direct cellular effects, including alterations in pH, membrane potential, and metabolism, independent of neurological impact.
The toxic effects of ammonia are not confined to the brain but can impact any cell type.

Conclusions:

The role of ammonia in chronic liver disease and multi-organ dysfunction needs to be considered beyond its neurotoxic capacity.
Increased ammonia levels can directly induce cellular dysfunction in various organs.
Ammonia's widespread cellular impact supports its contribution to systemic disease pathology.