Registration Dossier
Registration Dossier
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EC number: 235-185-9 | CAS number: 12125-01-8
Basic toxicokinetics
Administrative data
- Endpoint:
- basic toxicokinetics
- Type of information:
- migrated information: read-across from supporting substance (structural analogue or surrogate)
- Adequacy of study:
- key study
- Study period:
- No data
- Reliability:
- 2 (reliable with restrictions)
- Rationale for reliability incl. deficiencies:
- other: Collection of data. Sources: data from toxicological databases and experimental data of unpublished toxicological tests.
Cross-reference
- Reason / purpose for cross-reference:
- reference to same study
Data source
Reference
- Reference Type:
- review article or handbook
- Title:
- Unnamed
- Year:
- 2 010
- Report date:
- 2010
Materials and methods
- Objective of study:
- absorption
- distribution
- excretion
- metabolism
- toxicokinetics
Test guideline
- Qualifier:
- no guideline available
- Principles of method if other than guideline:
- No data
- GLP compliance:
- not specified
Test material
- Reference substance name:
- Ammonium chloride
- EC Number:
- 235-186-4
- EC Name:
- Ammonium chloride
- Cas Number:
- 12125-02-9
- IUPAC Name:
- ammonium chloride
- Test material form:
- not specified
- Details on test material:
- No data
Constituent 1
- Radiolabelling:
- not specified
Test animals
- Species:
- other: No data
- Strain:
- not specified
- Sex:
- not specified
Administration / exposure
- Route of administration:
- oral: unspecified
- Vehicle:
- not specified
- Duration and frequency of treatment / exposure:
- No data
Doses / concentrations
- Remarks:
- Doses / Concentrations:
No data
- No. of animals per sex per dose / concentration:
- No data
- Control animals:
- not specified
Results and discussion
- Preliminary studies:
- No data
Main ADME resultsopen allclose all
- Type:
- absorption
- Results:
- After repeated oral application ammonium chloride enters readily the body as a result of absorption by the gastrointestinal tract and the main target for toxicity are the kidneys.
- Type:
- distribution
- Results:
- Repeated toxicity study on rats by oral exposure caused significant changes with metabolic effect.
- Type:
- metabolism
- Results:
- After absorption by the gastrointestinal tract, the test substance is utlized in the liver to form amino acids and proteins.
- Type:
- excretion
- Results:
- Increased excretion of electrolytes and water causes loss of extracellular fluid and promotes the mobilisation of edema fluid.
Toxicokinetic / pharmacokinetic studies
- Details on absorption:
- No more data
- Details on distribution in tissues:
- Test substance induces metabolic acidosis (shown by decreased plasma- and urinary-pH)
Feeding of high level of the test substance caused decreased appetite, growth retardation, increased water consumption and increased urinary volume.
Several studies with rats recorded increased kidney weight, renal hypertrophy with new cell formation (increase in total DNA and total RNA) and enlargement of existing cells.
Increase in urinary ammonium, urea, sodium, chloride and calcium were also recorded.
Chronic stimulation of adrenal cortex by NH4+ induced acidosis caused hypertrophy of adrenal zona glomerulosa.
Biochemistry showed:
- increased plasma chloride, BUN and plasma proteins
- increased urinary calcium and phosphate excretion
Haematology revealed:
- increase in total erythrocytes, haemoglobin and haematocrit concentration
- Details on excretion:
- No more data
Metabolite characterisation studies
- Metabolites identified:
- not specified
Bioaccessibility (or Bioavailability)
- Bioaccessibility (or Bioavailability) testing results:
- No data
Any other information on results incl. tables
Metabolism
When ammonium ions are converted to urea, liberated hydrogen ion reacts with bicarbonate ion to form water and carbon dioxide. The chloride ion displaces the bicarbonate ion. Chloride is loaded into the kidneys. The increased chloride concentration in the extracellular fluid produces an increased load to the renal tubules.
Human data
Human incidental exposure following oral administration showed that ammonium chloride is rapidly absorbed from the gastrointestinal tract and complete absorption occurs within 3 to 6 hours. In healthy persons absorption of ammonium chloride given by mouth was practically complete. Only 1 to 3% of the dose was recovered in the faeces. Substantial first pass metabolism occurs in the liver.
Applicant's summary and conclusion
- Conclusions:
- Interpretation of results (migrated information): no data
The test substance ammonium chloride enters readily the body after oral application as a result of absorption by the gastrointestinal (GI) tract. After absorption by the GI tract, the test substance is utlized in the liver to form amino acids and proteins.
The main target for toxicity are the kidneys. - Executive summary:
After oral application ammonium chloride enters readily the body as a result of absorption by the gastrointestinal (GI) tract. After absorption by the GI tract, the test substance is utlized in the liver to form amino acids and proteins. The main target for toxicity are the kidneys.
When ammonium ions are converted to urea, liberated hydrogen ion reacts with bicarbonate ion to form water and carbon dioxide. The chloride ion displaces the bicarbonate ion. Chloride is loaded into the kidneys. The increased chloride concentration in the extracellular fluid produces an increased load to the renal tubules.
Increased excretion of electrolytes and water causes loss of extracellular fluid and promotes the mobilisation of edema fluid.
Furthermore, the test substance induces metabolic acidosis (shown by decreased plasma- and urinary-pH) and feeding of high level of the test substance causes decreased appetite, growth retardation, increased water consumption and increased urinary volume. Several studies with rats recorded increased kidney weight, renal hypertrophy with new cell formation (increase in total DNA and total RNA) and enlargement of existing cells.
For the following parameters an increase was also recorded: urinary ammonium, urea, sodium, plasma chloride, BUN, plasma proteins, urinary calcium, phosphate excretion, total erythrocytes and haemoglobin and haematocrit concentration.
Chronic stimulation of adrenal cortex by NH4+ induced acidosis caused hypertrophy of adrenal zona glomerulosa.
Human incidental exposure following oral administration showed that ammonium chloride is rapidly absorbed from the gastrointestinal tract and complete absorption occurs within 3 to 6 hours. In healthy persons absorption of ammonium chloride given by mouth was practically complete. Only 1 to 3% of the dose was recovered in the faeces. Substantial first pass metabolism occurs in the liver.
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