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EC number: 905-898-6
CAS number: -
experimental animals indicated that TEA is absorbed through the skin. No
data on oral and inhalation exposure is available. Besides data
regarding the dermal route, data on the i.v. route is also available.
Differences in the rate of absorption between rats and mice have been
described regarding dermal exposure. In mice, most of the topically
applied14C-TEA is absorbed, and only 2% to 11% is detected at
the site of application after 48 hours (Dow 1988,1989; Stott, 2000).The
dermal absorption of TEA in rats was less extensive and much slower than
in mice (Dow, 1988,1989).An
absorption, distribution, metabolism, and excretion study by the NTP
(2004) found that after 72 hours of exposure, only 20% to 30% of the
applied dermal dose of TEA (68 or 276 mg/kg) was absorbed in rats and
60% to 80% was absorbed in mice (79 or 1120 mg/kg). These differences in
absorption have been attributed either to the different doses used in
comparative studies or to species-specific factors. No differences in
tissue distribution were noted after i.v. or dermal exposure (NTP, 2004).
elimination of14C-TEA-derived radioactivity from the blood of
mice after a 1 mg/kg intravenous injection displays two-phase
elimination kinetics with an initial rapid distribution phase (0.3-0.6
hour half-life) followed by a slower elimination phase (10-hour
half-life) (Dow, 1988,1989; Stott, 2000).Radioactivity
in blood after dermal application of 2000 mg/kg neat TEA declined in a
bi-exponential manner through 3-hour post-dosing with a rapid initial
phase (half-life of 1.9 hr) followed by a slower terminal phase
(half-life of 31 hr)(Stott,
and mice rapidly excreted the absorbed dose, primarily in urine
(followed by faeces) after i.v. and dermal exposure. Regarding dermal
exposure, in rats, less than 1% of the dose was
present in the tissue samples (except the dose site) 72 hours after
treatment; the heart, kidney, liver, lung, and spleen contained elevated
concentrations of radiolabel relative to blood (NTP, 2004).
addition to animal studies, human skin penetration of TEA was tested in
vitro using diffusion cell techniques (Kraeling, 2003). Oil-in-water
emulsions containing 1% or 5%14C-TEA were added to the
stratum corneum side of 200-300 µm thick human skin sections and
penetration of radioactivity into and through the skin (into a receptor
fluid, sampled up to 24 hours after application) was determined. At pH
8.0, 1.1 and 1.2% of the dose was absorbed into the receptor fluid with
a total penetration of 22.0 and 16.5% for 1 and 5% TEA, respectively. At
pH 7.0, 0.43 and 0.28% was absorbed into the receptor fluid with a total
penetration of 9.8 and 5.8% after 24 hours for 1 and 5% TEA,
respectively. After 48 hours at pH 7.0, 0.68 and 0.60% was absorbed into
the receptor fluid with a total penetration of 9.6 and 6.9%, for 1 and
5% TEA respectively. This pH-related difference reflects the higher
percentage of unionised test material pH 8.0.
administration (in vivo) resulted in the following absorption figures:
3-16% in rats; 25-60% in mice. When applied dermally, DEA appears to
facilitate its own absorption, as higher doses were more completely
absorbed than lower doses.
mg/cm²) applied to skin preparations in vitro showed penetration rates
of 6.7% (mouse), > 2.8 % (rabbit), >0.56% (rat) and > 0.23% (human).
DEA is well
absorbed following oral administration in rats (57%).Distribution
to the tissues was similar via all routes examined. DEA is cleared from
the tissues with a half-life of approximately 6 days. The highest
concentrations are observed in liver and kidney.
after oral administration revealed non-metabolized DEA and smaller
proportions of N-methyl-DEA (N-MDEA), N,N-dimethyl-DEA (N’N-DMDEA) and
DEA-phosphates co-eluting with phosphatidyl ethanolamine and
phosphatidyl choline. After digestion 30% of the phospholipids were
identified as ceramides and the remaining 70% as phosphoglycerides.
excreted primarily in urine as the parent molecule (25-36%), with lesser
amounts of O-phosphorylated and N-methylated metabolites.
of DEA at high levels in liver and kidney is assumed
by a mechanism that normally conserves ethanolamine, a normal
constituent of phospholipids. DEA is incorporated as the head group to
form aberrant phospholipids, presumably via the same enzymatic pathways
that normally utilize ethanolamine.
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