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EC number: 271-231-4 | CAS number: 68526-83-0
- 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
Endpoint summary
Administrative data
Link to relevant study record(s)
Description of key information
Key value for chemical safety assessment
Additional information
Following a single oral dose in rats, Isooctanol (68526 -83 -0) is nearly completely absorbed following
oral administration and excreted primarily in the urine. Accordingly, tissue concentrations are highest
in the tissues associated with oral administration and urinary excretion, but [14C]-isooctanol and/or
its metabolites were detected in all tissues, usually at low or equivalent concentrations relative to the
plasma. There appeared to be little affinity for whole blood cells or any tissues types, and the majority
of the [14C]-isooctanol derived radioactivity was excreted in the first 24 hours postdose. There was
no notable difference in the absorption, distribution, or excretion of [14C]-isooctanol equivalents with
respect to the sex of the rats. In a repeat dose study, oral administration of Isooctanol (68526 -83 -0)
for 13 consecutive days and a single dose of [14C]-isooctanol equivalents to rats at dosage levels of
50 and 400 mg/kg/day was well tolerated. Isooctanol was nearly completely absorbed following oral
administration and excreted primarily in the urine. Accordingly, tissue concentrations were highest in the
tissues associated with oral administration and urinary excretion, but [14C]-isooctanol equivalents and/
or its metabolites were detected in all tissues, usually at low or equivalent concentrations relative to the
plasma. There appeared to be little affinity for whole blood cells or any tissues types, and the majority of
the Isooctanol was excreted in the first 24 hours postdosing. In an in vitro comparative metabolism study
in rat and rabbit hepatocytes, metabolism of [14C]-isooctanol was rapid and extensive in both species
tested with complete depletion of parent compound observed at 120 min. The metabolic profiles showed
21 areas of radioactivity being detected and quantified. Metabolism of [14C]-isooctanol was found to
occur via oxidation and Phase II conjugation (glucuronidation and sulphation). The following structures
were identified as metabolites in rat and rabbit: direct glucuronide conjugate(s) of [14C]-isooctanol,
hydroxy glucuronide conjugate(s), sulphate conjugates of hydroxy [14C]-isooctanol, isomers of hydroxy
[14C]-isooctanol, with the exception of carboxylic acid conjugate of [14C]-isooctanol (rabbit only).
Isotridecanol is nearly completely absorbed following a single oral administration in rats and excreted in
the urine, feces, and expired air. Plasma concentrations show proportionality relative to the administered
dose. Isotridecanol and/or its metabolites were detected in all tissues; for the tissues with the highest
concentration, AUClast values were often ≥ 3-fold higher relative to the plasma. There appeared
to be little affinity for whole blood cells. The majority of the [14C]-isotridecanol equivalents–derived
radioactivity was excreted in the first 24 hours postdose. There was no notable difference in the
absorption, distribution, or excretion of [14C]-isotridecanol equivalents with respect to the sex of
the rats. Based on the concentration of Isotridecanol equivalents remaining in tissue at 168 hours,
approximately 4% to 6% of the dose was present in the in the animals at the end of the study.
In addition, oral administration of Isotridecanol for 13 consecutive days and a single dose of [14C]-
isotridecanol equivalents to Crl:CD(SD) rats at dosage levels of 50 and 400 mg/kg/day was well
tolerated. Isotridecanol was nearly completely absorbed following oral administration and excreted
primarily in the urine. The majority of the [14C]-isotridecanol equivalents were excreted in the first 24
hours postdose. There appeared to be little affinity for whole blood cells or any tissues types. Tissue
concentrations were highest in the tissues associated with oral administration and urinary excretion,
but [14C]-isotridecanol equivalents and/or its metabolites were also detected in notable concentrations
in other tissues. [14C]-isotridecanol equivalents were still present in almost all tissues after 168 hours
postdose. Overall, the exposure to tissues was generally usually low or equivalent relative to the plasma.
Linear and branched chain alcohols exhibit similar patterns of absorption, metabolism, and excretion. Both linear and branched aliphatic alcohols are absorbed through the gastrointestinal tract and are rapidly eliminated from the blood (DeBruin, 1976; Lington and Bevan, 1994). Plasma half-lives are difficult to measure since many of the low molecular weight metabolites (e.g. aldehydes, carboxylic acids) are endogenous in humans (Lington and Bevan, 1994).
Linear and branched chain alcohols are initially oxidized to corresponding aldehydes and further to corresponding carboxylic acids by high capacity NAD+/NADH-dependent enzymes, which are then metabolized to carbon dioxide via the fatty acid pathways and the tricarboxylic acid cycle (Feron et al., 1991; Parkinson, 1996a).
Alcohol dehydrogenase (ADH) enzymes are the cytosolic enzymes that are primarily responsible for the oxidation of alcohols to their corresponding aldehydes. Alcohols also can be oxidized to aldehydes by non-ADH enzymes present in the microsomes and peroxisomes, but these are generally quantitatively less important than ADH. Aldehyde dehydrogenases (ALDH) oxidize aldehydes to their corresponding carboxylic acids. Branched-chain aliphatic alcohols and aldehydes have been shown to be excellent substrates for ADH and ALDH (Albro, 1975; Blair & Bodley, 1969; Hedlund & Kiessling, 1969). As carbon chain length increases, the rates of ALD-mediated oxidation also increase (Nakayasu et al., 1978).
The metabolism of branched-chain alcohols, aldehydes, and carboxylic acids containing one or more methyl substituents is determined primarily by the position of the methyl group on the branched-chain. Alcohols and aldehydes are rapidly oxidized to their corresponding carboxylic acids. The branched-chain acids are metabolized via beta-oxidation followed by cleavage to yield linear acid fragments which are then completely metabolized in the fatty acid pathway or the tricarboxylic acid cycle. Higher molecular weight homologues (>C10), may also undergo a combination of ω-, ω-1 and β-oxidation, and selective dehydrogenation and hydration to yield polar metabolites which are excreted as the glucuronic acid or sulfate conjugates in the urine and, to a lesser extent, in the feces (Diliberto et al., 1990). Thus, the principal metabolic pathways utilized for detoxification of these branched-chain substances are determined primarily by four structural characteristics: carbon chain length, and the position, number, and size of alkyl substituents.
Discussion on bioaccumulation potential result:
Alkyl Alcohols C6 to C13 are broken down by mitochondrial beta-oxidation or by cytochrome P450-mediated ω- and ω-1-oxidation (may be followed by β-oxidation). The alcohol undergoes various oxidative steps to yield other alcohols, ketones, aldehydes, carboxylic acids and carbon dioxide (Mann, 1987). Data for monohydric, saturated alcohols show a systematic variation according to molecular weight in a manner similar to many other homologous series (Monick, 1968). The analogs 1-hexanol and 1-dodecanol follow similar metabolic pathways by undergoing oxidative steps to yield aldehydes, carboxylic acid and eventually undergoing intermediary metabolism (van Beilen et al., 1992). Undegraded alcohols are conjugated either directly or as a metabolite with glucuronic acid, sulfuric acid, or glycine and are rapidly excreted (Lington and Bevan, 1994). Glucuronidation and glutathione conjugation are means of rapid elimination (Mann, 1987).
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