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EC number: 205-500-4 | CAS number: 141-78-6
Following both the high and low dose bolus iv injections, a rapid distribution and equilibration phase was followed by very rapid elimination of the parent compound. Elimination half-lives of 33.4 s and 36.9 s were estimated from the first order elimination rate constants of 0.0208/s and 0.0188/s for the 10 and 100 mg/kg doses, respectively. Evidence that the carboxyesterase capacity was not saturated at the high dose level is found from the similar elimination rates for these two dose levels. Since depression of central nervous system function is noted following inhalation of ethyl acetate, concentrations of ethyl acetate and metabolites in brain tissue homogenates were assayed following the 100 mg/kg intravenous dose. Total [14C] concentrations in brain homogenates were approximately 75% of those seen in the blood following the 100 mg/kg administrations, suggesting that ethyl acetate and metabolites are not preferentially sequestered in this tissue. In addition, ethyl acetate in the brain was rapidly hydrolyzed (kelim = 0.0285/s), and the ethanol formed was rapidly eliminated evidence that supports the use of ethanol data in ethyl acetate risk assessment. An in vitro ethyl acetate blood kinetic study, conducted at approximately the same concentration as measured in the initial 100 mg/kg in vivo study samples, yielded an estimated elimination rate constant of 0.0298/min, only a fraction of that estimated from the in vivo studies. This indicates that systemic organ carboxyesterase activity is predominant in the in vivo hydrolysis of ethyl acetate.
The rate of hydrolysis of ethyl acetate in male rats in vivo and in vitro was studied by Deisinger and English (unpublished). Ethyl acetate was rapidly hydrolyzed to ethanol following intravenous injection in rats, with an in vivo elimination half-life in blood of 33-37 seconds.
Carboxyesterase capacity was not saturated at 100 mg/kg. There was no evidence that ethyl acetate or metabolites were preferentially sequestered in brain, based on total [14C] levels. The rapid in vivo hydrolysis of ethyl acetate to ethanol supports the use of ethanol systemic toxicity data in evaluating the potential effects of ethyl acetate exposure.
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