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EC number: 931-335-9
CAS number: 90622-74-5
studies: Human liver microsome results: LDEA was also metabolised to
11- and 12-hydroxy derivatives by human liver microsomes at specific
activities of 0.22±0.06 and 0.84±0.26 nmol/min/mg protein, respectively.
A study was conducted to evaluate the in
vitro metabolism of N,N-bis(2-hydroxyethyl)dodecanamide (LDEA) in liver
or kidney microsomes from rat to: 1) determine the extent of its
hydroxylation, 2) identify the products formed and 3) examine whether
treatment with the cytochrome P4504A inducer and peroxisome proliferator
diethylhexyl phthalate(DEHP) would
affect hydroxylation rates. Liver and kidney microsomes from
DEHP-treated and control rats were incubated with 100 µM LDEA for 30 min
at 37°C in a shaking water bath. The metabolites were then separated and
analysed by GC-MS. 97% of the hydroxylated products were identified as
two major substances: 11- hydroxyl and 12-hydroxy derivatives of LDEA.
The specific activities for LDEA 11- and 12-hydroxylation in microsomes
prepared from control rats were 2.23±0.40 and 0.71±0.17 nmol/min/mg
protein, respectively. Treatment of rats with DEHP increased the LDEA
12-hydroxylation specific activity 5-fold to 3.50 ± 0.48 nmol/mm/mg
protein, whereas the LDEA 11-hydroxylase activity remained unchanged.
Incubating liver microsomes from DEHP-treated rats with a polyclonal
anti-rat 4A inhibited the formation of 12-OH-LDEA by 80% (3.98±0.10 vs.
0.80±0.08 nmol/min/mg protein), compared with the pre-immune serum, but
had no inhibitory effect on the rate of 1 1-OH-LDEA formation (1.93±0.09
vs. 2.20± 0.11 nmol/min/mg protein). Rat kidney microsomes also resulted
in hydroxylation of LDEA at its 11- and 12-carbon atoms, with specific
activities of 0.05±0.01 and 0.28±0.02 nmol/min/mg protein,
respectively. In conclusion, under the study conditions, the test
substance was rapidly converted into 11- and 12-hydroxy derivatives in
rat liver and kidney microsomes (Merdink, 1996).
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