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EC number: 218-414-7
CAS number: 2146-71-6
Vinyl laurate is hydrolytically unstable and it reacts with
humidity and with water under formation of vinyl alcohol and lauric
acid. As the resulting vinyl alcohol as an enol is not stable under
normal conditions it will tautomerize to form the respective
acetaldehyde. It can be assumed that in aqueous environment of
biological systems similar reactions occur probably supported in parts
by hydrolytic enzymes. The presence of carboxylesterases assumed to be
capable of hydrolysing vinyl laurate has been demonstrated in the nose,
oral cavity, respiratory tissue, skin, blood, and liver of several
species including man (Bogdanffy, M.S., Taylor, M.L. (1993), Kinetics of
nasal carboxylesterase-mediated metabolism of vinyl acetate, Drug Metab.
Dispos., 21, 1107-1111; Bogdanffy, M.S., Sarangapani, R., Kimbell, J.S.,
Frame, S.R., Plowchalk, D.R. (1998), Analysis of vinyl acetate
metabolism in rat and human nasal tissues by an in vitro gas uptake
technique, Toxicol. Sci., 46, 235-246.; Morris, J.B. (1997), Uptake of
acetaldehyde vapour and aldehyde dehydrogenase levels in the upper
respiratory tracts of the mouse, rat, hamster, and guinea pig, Fundam.
Appl. Toxicol, 35, 91-100.; Simon, P., Filser, J.G., Bolt, H.M. (1985),
Metabolism and pharmacokinetics of vinyl acetate, Arch. Toxicol., 57,
191-195.; Strong, H.A., Cresswell, D.G., Hopkins, R. (1980),
Investigations into the metabolic fate of vinyl acetate in the rat and
mouse, Report No. 2511-51/11-14, Part 2, Hazleton Laboratories Europe).
These tissues include the sites of entry following inhalation, oral and
dermal exposure; pre-systemic hydrolysis of vinyl laurate at these sites
will reduce systemic exposure to intact vinyl laurate to a degree in
proportion with enzyme activity i.e. where enzyme activity is highest,
systemic exposure will be lowest and visa-versa. The hydrolysis
will also be catalyzed at lower pHs like in the stomach. Thus it can be
assumed that after oral uptake resorption of at least the resulting
metabolites will occur. Both metabolites are well known.
Fatty acids like lauric acid are an important part of the normal
daily diet of mammals, birds and invertebrates. Lauric Acid is one of
the three most widely distributed naturally occurring saturated fatty
acids. The fatty acid content of the seeds of Lauraceae is greater than
90% Lauric Acid. Sources of Lauric Acid include coconut and palm kernel
oils, babassu butter (approximately 40%) and other vegetable oils, and
milk fats (2-8%). Camphor seed oil has a high Lauric Acid content.
(Final Report on the Safety Assessment of Oleic Acid, Lauric Acid,
Palmitic Acid, Myristic Acid, and Stearic Acid, Int J Toxicol 1987; 6;
After hydrolysis of fat, beta oxidation is the process by which
free fatty acids, in the form of Acyl-CoA molecules, are broken down in
mitochondria and/or in peroxisomes to generate Acetyl-CoA, the entry
molecule for the Krebs cycle. The ultimate metabolite is Acetyl-Coenzyme
A (Acetyl-CoA) which it is present in different metabolic pathways and
enters the citric acid cyle (krebs cycle) of organisms where it is
degraded to form water and carbon dioxide.
Offering humans a lauric acid rich diet the subjects’ serum total
cholesterol concentration increased as well as the
high-density-lipoprotein (HDL)-cholesterol concentrations. No effects
were seen in serum triacylglycerol and lipoprotein(a) concentrations
(E.H.M. Temme, R.P. Men-sink, G. Hornst, Am J Clin Nutr 1996;63:
897-903, M.B. Katan, P.L. Zock, R.P. Mensink Am J Clin Nutr
1994;60(suppl): 1017S-22S, R.P. Mensink, P.L. Zock, A.D.M. Kester, M.B.
Ka-tan, Am J Clin Nutr 2003;77:1146–55.). Other authors state that
lauric acid raises total and LDL cholesterol concentrations compared
with oleic acid, but no differences were noted in plasma triglycerides
or HDL cholesterol (MA Denke and SM Grundy , Am J Clin Nutr 1992;56:
Acetaldehyde is metabolized to acetic acid by nicotinamide adenine
dinucleotide (NAD)-dependent aldehyde dehydrogenase (ALDH), which exists
in the liver and nasal mucosa, and finally degraded to carbon dioxide
and water (J.F.Brien and C.W.Loomis, J. Physiol. Pharmacol. 61, 1983,
pp. 1–22 1983). ALDH is present in the tissues of experimental animals
including mice, rats, hamsters and guinea pigs. In all species except
guinea pig, data supports the presence of two isozymes characterised by
high and low affinity forms (Morris, 1997). Similar enzyme activity has
been obtained for human nasal and oral cavity tissues; additionally,
ALDH activity has been demonstrated in tissue from the human oesophagus
and stomach and in saliva (Bogdanffy et al., 1998; Dong, Y., Peng, T.,
Yin, S, (1996), Expression and activities of class IV alcohol
dehydrogenase and class III aldehyde dehydrogenase in human mouth,
Alcohol, 13, 257-262.; Yin, S., Liaou, C., Wu, C. et al., (1997), Human
stomach alcohol and aldehyde dehydrogenases: comparison of expression
pattern and activities in alimentary tract, Gastroenterology, 112,
Regarding ALDH, there are two types of ALDH in mitochondrial and
cytosolic forms. Kinetic characteristics of enzymatic reaction of liver
mitochondrial ALDH are similar among human, rat and Syrian hamster,
while, the Km value of human cytosolic ALDH1 was approximately 180 M but
those of rat and Syrian hamster were 15 and 12 M, respectively (.
Klyosov et al. BIOCHEMISTRY, 35, 4445-4456, 1996). In human
liver, mitochondrial ALDH alone oxidizes acetaldehyde at physiological
concentrations, but in rodent liver, both mitochondrial and cytosolic
ALDHs have a role in acetaldehyde metabolism (IARC Monographs on the
Evaluation of Carcinogenic risks to Humans 71: 319- 335, 1999).
Approximately 40% of oriental population is inactive in mitochondrial
ALDH2, which is associated with alcohol intolerance (Yoshida Alcohol
Alcohol. 29: 693-696, 1984). In humans, inhaled acetaldehyde is retained
in the respiratory tract at a high rate, and, therefore, acetaldehyde
metabolism is mainly associated with thiol compounds (cysteine and
glutathione) and subsequently hemimercaptal and thia-zolidine
intermediates are produced. Thioether and disulfide are excreted in the
urine, however, most of them are metabolized to acetic acid by ALDH2,
and finally degraded to carbon dioxide and water (Brien and Loomis,
1983; Cederbaum and Rubin, 1976; Hemminki, 1982; Nicholls et al., 1992;
Sprince et al., 1974). In an oral administration of acetaldehyde at a
dose of 600 mg/kg in dogs, no excretion of unmetabolized acetaldehyde
was comfirmed in urine (Booze and Oehme, 1986).
As for carboxylesterases, ALDH activity is present at the major
sites of exposure to vinyl laurate. At exposure levels that do not
exceed the capacity of the enzyme to oxidise any acetaldehyde to acetic
acid, there will be low local exposure to acetaldehyde. Systemically
available acetate will be incorporated into the citric acid cycle
ultimately either being incorporated into endogenous substances or
eliminated as CO2. Input of acetate resulting from vinyl laurate
metabolism will be within the capacity of the cycle which in man is
approximately 640mg acetate/kg/day (Simoneau, C., Pouteau, E., Maugeais,
P., Marks, L., Ranganathan, S., Champ, M., Krempf, M. (1994),
Measurement of whole body acetate turnover in healthy subjects with
stable isotopes, Biol. Mass Spectrom., 23, 430-433.).
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