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EC number: 205-480-7
CAS number: 141-32-2
Butyl acrylate is rapidly absorbed, distributed and excreted after oral
application or intravenous injection. In vitro and in vivo, BA is
rapidly and completely metabolized.
Butyl acrylate was tested for relative
rates of hydrolysis by a representative mammalian esterase (Porcine
hepatic esterase). At concentrations of 0.2, 0.5 and 2.0 mM, conversion
rates ranged between 54 - 69 μmol/min/mg protein (4 - 33 %) after 2
minutes, and 43 - 72 μmol/min/mg protein (10 - 68 %) after 5 minutes of
incubation at 37°C (BASF AG, 2001). Thus, BA was rapidly hydrolysed by
hepatic esterase activity under in-vitro conditions.
Recent investigations on the in vitro
metabolism of butyl acrylate after incubation with S9 fraction of rat
liver as well as with blood and plasma of rats have demonstrated that
the elimination is very rapidly (BASF SE, 2015). The cleavage of the
ester and formation of acrylic acid is the predominant metabolic step
after incubation with S9, while after incubation with blood and plasma
butyl acrylate reacts mainly with GSH. Acrylic acid occurred to a lesser
extent under these test conditions. These results are in line with
findings published in the literature (Miller et al., 1981; deBethizy et
al., 1987, Linhart et al., 1994).
In a study by Dow Chemical (1979), the
disappearance of butyl acrylate in rat blood in vitro and the conversion
of butyl acrylate to acrylic acid in rat liver homogenate and blood was
determined. Butyl acrylate disappeared rapidly when added to rat blood
in vitro with a half time of 7.7 min. Butyl acrylate was hydrolyzed to
acrylic acid in the liver in vitro at a rate of 26 nmoles/min and in
blood at a rate of 4.6 nmoles/min.
In a study by Stott (1985), the in vitro
activity of carboxylesterase was determined in mouse nasal mucosa,
liver, kidney, lung, and blood and in nasal mucosa of rat, rabbit, and
dog. The specific activity of nasal carboxylesterase in mice was found
to be equivalent to that of the liver and greater than that of the
kidney, lung or blood. Mice and dogs were found to have similar nasal
carboxylesterase activities which were slightly higher than that found
in rats and about six-fold higher than that found in rabbits. These data
suggest that extensive hydrolysis of acrylate esters occurs in the nasal
mucosa of animals exposed to these materials.
After oral administration (gavage),
Butyl [2,3-14C]-acrylate was rapidly absorbed and metabolized in male
Fischer 344 rats (75 % was eliminated as CO2, approximately 10 % via
urine and 2 % via faeces). The major portion of butyl acrylate was
hydrolysed by carboxyesterase to acrylic acid and butanol and eliminated
as CO2. A smaller portion was conjugated with endogenous GSH to be
subsequently excreted as mercapturic acids in the urine (Sanders, 1988).
After i.v. administration, the
labelled butyl acrylate was rapidly absorbed and metabolized. The
acrylate moiety was metabolized primarily to CO2, accounting for
elimination of up to 45 % of the administered radiolabel. The second
major route of elimination was in urine, with only trace amounts in
faeces and as volatiles (Sanders, 1988). No parent compound was detected
in any urine, bile, or tissue extract samples by HPLC analysis. The two
major metabolites in urine after both oral and intravenous routes of
exposure were identified as N-acetyl-S-(2-carboxyethyl)cysteine and
N-acetyl-S-(2-carboxyethyl)cysteine-S-oxide (Sanders, 1988).
Thus, after oral and i.v.
administration, butyl acrylate (BA) is rapidly absorbed and metabolized
in male rats. The major portion of BA was hydrolysed by carboxyesterase
to acrylic acid and butanol. The subsequent metabolism follows that for
acrylic acid, and involves metabolism to carbon dioxide via the
propionate degradation pathway (acrylic acid --> 3-hydroxypropionic acid
--> malonyl semialdehyde --> acetyl S CoA --> tricarboxylic acid cycle
--> CO2). Metabolism of butanol proceeds via the alcohol and aldehyd
dehydrogenase pathway. A smaller portion of the administered BA was
conjugated with endogenous GSH to be subsequently excreted as
mercapturic acids in the urine.
In a study by Sapota (1991), 36 male Wistar
rats were administered 100 mg/kg bw of BA-14C (about 435 kBq/rat)
intraperitoneally or by oral gavage. Urine, faeces, blood and expired
air was collected. Animals were killed 0.5, 4, 8, 12, 24 and 48 h after
administration of the test compound. Liver, kidneys, lungs, brain,
spleen, heart, stomach, a fragment of sciatic nerve and a section of fat
from the abdomen were collected for determination of radioactivity. Most
of 14C found in tissues was associated with the liver and kidneys. The
level of 14-C associated with most of the examined tissues remained
unchanged, at least for the first 8 - 12 hours, followed by its fairly
rapid loss. The expired air was found to be the main route of excretion
of 14C. More than 70 - 80% of the given dose of 14C was eliminated in
this way during 24 hours following the administration of butyl acrylate.
14C was also excreted in considerable amount (17 - 21 %) in urine,
mainly during the first 24 hours, and partly during the following day
and night. After 48 hours the total amount of the excreted 14C reached
- BASF SE (2015). Bachelor thesis Kertsin
Roos, unpublished data, Testing laboratory: BASF SE, Experimental
Toxicology and Ecology,67056 Ludwigshafen, Germany. Report date: 2013.
- deBethizy JD, Udensky JR, Scribner
HE, Frederick CB (1987). The disposition and metabolism of acrylic acid
and ethyl acrylate in male Sprague Dawley rats, Fund. Appl. Toxicol., 8,
- Linhart I, Vosmanska M, Smejkal J
(1994). Biotransformation of acrylates. Excretion of mercapturic acids
and changes in urinary carboxylic acid profile in rat dosed with ethyl
and 1-butyl acrylate, Xenobiotika, 24, 1043-1052.
- Miller RR, Ayres JA, Rampy LW,
McKenna MJ (1981). Metabolism of acrylate esters in rat tissue
homogenates, Fund. Appl. Toxicol., 1, 410-414.
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