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EC number: 211-162-9 | CAS number: 631-61-8
- Life Cycle description
- Uses advised against
- Endpoint summary
- Appearance / physical state / colour
- Melting point / freezing point
- Boiling point
- Density
- Particle size distribution (Granulometry)
- Vapour pressure
- Partition coefficient
- Water solubility
- Solubility in organic solvents / fat solubility
- Surface tension
- Flash point
- Auto flammability
- Flammability
- Explosiveness
- Oxidising properties
- Oxidation reduction potential
- Stability in organic solvents and identity of relevant degradation products
- Storage stability and reactivity towards container material
- Stability: thermal, sunlight, metals
- pH
- Dissociation constant
- Viscosity
- Additional physico-chemical information
- Additional physico-chemical properties of nanomaterials
- Nanomaterial agglomeration / aggregation
- Nanomaterial crystalline phase
- Nanomaterial crystallite and grain size
- Nanomaterial aspect ratio / shape
- Nanomaterial specific surface area
- Nanomaterial Zeta potential
- Nanomaterial surface chemistry
- Nanomaterial dustiness
- Nanomaterial porosity
- Nanomaterial pour density
- Nanomaterial photocatalytic activity
- Nanomaterial radical formation potential
- Nanomaterial catalytic activity
- Endpoint summary
- Stability
- Biodegradation
- Bioaccumulation
- Transport and distribution
- Environmental data
- Additional information on environmental fate and behaviour
- Ecotoxicological Summary
- Aquatic toxicity
- Endpoint summary
- Short-term toxicity to fish
- Long-term toxicity to fish
- Short-term toxicity to aquatic invertebrates
- Long-term toxicity to aquatic invertebrates
- Toxicity to aquatic algae and cyanobacteria
- Toxicity to aquatic plants other than algae
- Toxicity to microorganisms
- Endocrine disrupter testing in aquatic vertebrates – in vivo
- Toxicity to other aquatic organisms
- Sediment toxicity
- Terrestrial toxicity
- Biological effects monitoring
- Biotransformation and kinetics
- Additional ecotoxological information
- Toxicological Summary
- Toxicokinetics, metabolism and distribution
- Acute Toxicity
- Irritation / corrosion
- Sensitisation
- Repeated dose toxicity
- Genetic toxicity
- Carcinogenicity
- Toxicity to reproduction
- Specific investigations
- Exposure related observations in humans
- Toxic effects on livestock and pets
- Additional toxicological data
Basic toxicokinetics
Administrative data
- Endpoint:
- basic toxicokinetics in vivo
- Type of information:
- experimental study
- Adequacy of study:
- weight of evidence
- Reliability:
- 3 (not reliable)
- Rationale for reliability incl. deficiencies:
- other: Test method was not according to any guideline. No GLP.
Data source
Reference
- Reference Type:
- publication
- Title:
- Unnamed
- Year:
- 1 969
- Report date:
- 1968
Materials and methods
- Objective of study:
- absorption
- distribution
- excretion
- metabolism
- Principles of method if other than guideline:
- The uptake and urea formation of ammonia in the liver were studied in healthy volunteers by means of hepatic vein catheterization after an oral administration of Ammonium acetate.
- GLP compliance:
- no
Test material
- Reference substance name:
- Ammonium acetate
- EC Number:
- 211-162-9
- EC Name:
- Ammonium acetate
- Cas Number:
- 631-61-8
- Molecular formula:
- C2H4O2.H3N
- IUPAC Name:
- ammonium acetate
- Details on test material:
- - Name of test material (as cited in study report): Ammonium acetate
Constituent 1
- Radiolabelling:
- yes
Test animals
- Species:
- human
- Strain:
- other: not applicable
- Sex:
- not specified
- Details on test animals or test system and environmental conditions:
- Test subjects had been on the nitrogen-poor diet (2.7 g of N) for 4 days prior to the experiment. They were in the post absorptive state.
Administration / exposure
- Route of administration:
- oral: feed
- Vehicle:
- not specified
- Duration and frequency of treatment / exposure:
- One single administration
Doses / concentrations
- Remarks:
- Doses / Concentrations:
10.5-11.1 mg of ammonia nitrogen (0.80 meq) per minute.
- No. of animals per sex per dose / concentration:
- Two subjects (no data on sex distribution).
- Control animals:
- no
- Details on dosing and sampling:
- - Two or three basal periods were studied before starting the infusion.
- The estimated splanchnic blood flow (ESBF) was calculated by means of Cardio-Green throughout the experiments.
- Blood samples for determination of urea and ammonia were taken from a peripheral artery and from the hepatic vein at the beginning and at the end of periods of about 5-20 min, for about 2 hr.
- The production (output) and the consumption (uptake), respectively, of the liver were calculated by multiplying concentration differences between hepatic vein blood and peripheral arterial blood by ESBF.
- Heparinized blood samples for ammonia determinations were always examined immediately after withdrawing and rapid centrifuging.
- Ammonia, alfa-amino nitrogen, total protein, and urea nitrogen concentrations were determined in the plasma, as were the 24-hr excretion of ammonia, alfa-amino nitrogen, urea nitrogen, creatinine, and total nitrogen in the urine.
Results and discussion
Toxicokinetic / pharmacokinetic studies
- Details on absorption:
- N absorption after oral loading of NH4+ is complete.
- Details on distribution in tissues:
- Human oral exposure data for NH4+ clearly indicate that it readily enters the portal circulation and is delivered to the liver.
- Details on excretion:
- Urea, the main metabolite, was excreted in the urine. Output of urea from the liver corresponded to the amount of NH4+ ingested. Excretion data for humans orally exposed to ammonia have been quantified with respect to excretion of isotope from 15N-labeled ammonium salts, thus providing an indication of the turnover rate of the compound within the body and excretion route of its metabolites.
Metabolite characterisation studies
- Metabolites identified:
- yes
- Details on metabolites:
- In nitrogen-deficient persons, NH4+ (as ammonium acetate) administered orally was absorbed and carried directly to the liver where most of it was converted to urea.
Any other information on results incl. tables
Ammonium salt administered orally to humans led to a corresponding increase in blood urea concentration transported out of the liver, leading the authors to conclude that orally ingested ammonium salt is quickly and almost completely converted in the liver and eliminated from the body as urinary urea.
Applicant's summary and conclusion
- Conclusions:
- Interpretation of results: other: orally ingested ammonium salt is quickly and almost completely converted in the liver and eliminated from the body as urinary urea.
Ammonium salt administered orally to humans led to a corresponding increase in blood urea concentration transported out of the liver, leading the authors to conclude that orally ingested ammonium salt is quickly and almost completely converted in the liver and eliminated from the body as urinary urea. - Executive summary:
The uptake and urea formation of ammonia in the liver were studied in healthy volunteers by means of hepatic vein catheterization after an oral administration of Ammonium acetate.
N absorption after oral loading of NH4+ is complete.
Human oral exposure data for NH4+ clearly indicate that it readily enters the portal circulation and is delivered to the liver.
Urea, the main metabolite, was excreted in the urine. Output of urea from the liver corresponded to the amount of NH4+ ingested. Excretion data for humans orally exposed to ammonia have been quantified with respect to excretion of isotope from 15N-labeled ammonium salts, thus providing an indication of the turnover rate of the compound within the body and excretion route of its metabolites.
Ammonium salt administered orally to humans led to a corresponding increase in blood urea concentration transported out of the liver, leading the authors to conclude that orally ingested ammonium salt is quickly and almost completely converted in the liver and eliminated from the body as urinary urea.
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