Absorption, Distribution and Excretion
Benzyl acetate is absorbed from the gastrointestinal tract of rats and mice, with approximately 90% of the administered dose excreted in the urine as various metabolites within 24 hours. …This absorption, metabolism, and disposal capacity is unaffected by the dose or frequency of administration. This study investigated the effects of excipients and blocking on the in vitro percutaneous absorption of [methylene-14C]-benzyl acetate (1.7–16.6 mg/cm²) using full-thickness skin from male Fischer 344 rats in a diffusion cell. After 48 hours, the absorption rate of pure benzyl acetate through rat skin sealed with a sealing film was 49.3 ± 2.0% (mean ± standard deviation, n = 4). When a benzyl acetate ethanol solution was applied to the skin and then sealed with a sealing film, the absorption rate after 48 hours was not significantly different from direct application. However, after 6 hours, the absorption rate of benzyl acetate through the sealed skin increased accordingly with increasing ethanol content in the applied mixture. When phenethyl alcohol was used as an excipient, the absorption rate of benzyl acetate through the closed skin was significantly higher after 48 hours than with direct application (P<0.05); when the phenethyl alcohol concentration was 50% (v/v), the absorption rate after 48 hours was 56.3±4.9%. However, this increase in absorption rate was independent of the proportion of phenethyl alcohol in the application mixture. When dimethyl sulfoxide (DMSO) was used as an excipient, the extent of benzyl acetate absorption through the closed skin was significantly increased after 48 hours compared with direct application (P<0.05) (the absorption rate was 59.3±3.7% of the application dose when using 50% (v/v) DMSO). The absorption of benzyl acetate increased proportionally with the increase of DMSO content in the application mixture. Sealing the skin surface with a occlusive film generally significantly increases the absorption rate (P<0.05), but this effect varies with time and excipient. Generally, the enhancement of absorption caused by the use of a carrier or skin occlusion is small and, in most cases, unlikely to be toxicologically significant.
The absorption of benzyl acetate in rat and human skin was compared using full-thickness dorsal skin obtained from shaved male Fischer 344 rats and full-thickness human skin obtained from surgically excised patients. Pure [methylene-14C]benzyl acetate (33.1 mg/cm²) was topically applied to the epidermal surface and sealed with a Teflon cap (cap 2.9 cm from the skin surface). The penetration of this compound into rat and human skin was then assessed in vitro in a flow-through diffusion cell. Benzyl acetate was rapidly and extensively absorbed through rat skin, reaching 34.3 ± 3.9% (11.3 ± 1.3 mg/cm²) of the administered dose after 24 hours (mean ± standard deviation, n=12) and 55.8 ± 5.0% (18.5 ± 1.7 mg/cm²) after 72 hours. Benzyl acetate permeated the skin of humans at a significantly lower rate and extent than in rats (P<0.05), reaching 5.5 ± 0.1% (1.8 ± 0.0 mg/cm²) of the administered dose after 24 hours (mean ± standard deviation, n=12) and 17.8 ± 3.3% (5.9 ± 1.1 mg/cm²) after 72 hours. At all study time points up to 72 hours, the permeation rate of benzyl acetate through rat skin was higher than that through human tissue. The maximum permeation rates through rat and human skin were 0.6 ± 0.0 mg/cm²/hr and 0.1 ± 0.0 mg/cm²/hr, respectively. These data suggest that systemic exposure may occur after human skin contact with benzyl acetate. They also support the evidence in the literature that human skin permeability to xenobiotics is generally lower than that of rat skin. Metabolites…Benzyl acetate is rapidly hydrolyzed to acetic acid and benzyl alcohol, the latter of which is oxidized to benzoic acid and excreted as hippuric acid. In rats, benzyl acetate is hydrolyzed to benzyl alcohol, which is then oxidized to benzoic acid and excreted as hippuric acid and benzyl mercaptouric acid. A chemical disposal study conducted by the National Toxicology Program (NTP) in the United States showed that male Fischer 344 rats and male B6C3F1 mice effectively absorbed, rapidly metabolized, and excreted orally administered benzyl acetate. The dosages used in this study were: single oral gavage of corn oil to rats at doses of 5, 50, or 500 mg/kg; single oral gavage of corn oil to mice at doses of 10, 100, or 1000 mg/kg; and daily oral gavage of 500 mg/kg to rats and 1000 mg/kg to mice, five times a week for two weeks, also using corn oil. Most (90%) of the benzyl acetate-derived radioactive material was recovered in the urine and was not detected in the liver, blood, muscle, adipose tissue, skin, lungs, kidneys, or stomach of the tested rats or mice. The main metabolite isolated in urine was hippuric acid (accounting for 94%–99% of the dose). Other metabolites included mercaptouric acid and benzyl alcohol. Benzyl acetate was not detected in the urine of the test animals. Dosage and frequency of administration did not affect the absorption, metabolism, or excretion of this compound. Within the studied dose range, there was no evidence of metabolic saturation in either animal. This study investigated the effects of gavage administration versus feed administration on the toxicokinetics of benzyl acetate in male F344 rats and B6C3F1 mice. Benzyl acetate is rapidly hydrolyzed to benzyl alcohol, which is then oxidized to benzoic acid. Higher plasma benzoic acid concentrations were observed in rats after gavage administration of benzyl acetate dissolved in corn oil (at doses of 500 mg/kg and 1000 mg/kg, respectively). In contrast, plasma benzoic acid concentrations were significantly reduced in rats and mice after feed administration at doses of approximately 615 mg/kg/day and approximately 850 mg/kg/day, respectively. The results showed that, despite comparable daily doses of benzyl acetate, gavage administration effectively saturated the benzoic acid clearance pathway, while feed administration did not. In contrast, plasma hippuric acid concentrations were similar after gavage and feed administration due to depletion of the glycine supply pool. ...
Phospoxanase (PON1) is a key enzyme in organophosphate metabolism. PON1 can inactivate certain organophosphates through hydrolysis. PON1 hydrolyzes active metabolites in various organophosphate pesticides and nerve agents such as soman, sarin, and VX. The presence of PON1 polymorphism leads to differences in the enzyme activity level and catalytic efficiency of this esterase, which in turn suggests that different individuals may be more susceptible to the toxic effects of organophosphate exposure.

Toxicity Summary
Compound Identification: Benzyl acetate is a solvent used in fragrance and chemical synthesis. Human Exposure: Benzyl acetate can be absorbed through the gastrointestinal tract, lungs, and intact skin. In the human body, it is hydrolyzed to benzyl alcohol and acetate; the benzyl radical is oxidized to benzoic acid and excreted as hippuric acid. Animal/Bacterial Studies: This compound can be hydrolyzed in vitro by pancreatic enzyme preparations. Benzyl mercaptouric acid and hippuric acid were isolated from the urine of rats injected subcutaneously with benzyl acetate. Mice and rats were administered 14C-labeled benzyl acetate intravenously or orally, respectively. Benzyl acetate is excreted in very small amounts as carbon dioxide or volatile substances. The 14C-labeled form is primarily excreted in urine, with less than 1% excreted in feces. Over 90% of the 14C in urine is present as hippuric acid, with a small amount present as benzyl alcohol. Neither the route of administration nor the dosage significantly affected the elimination pattern. Five male and five female B6C3F1 mice were administered benzyl acetate dissolved in corn oil by gavage once daily for 14 days. All male mice in the highest dose group died on day 3 of the study. Weight change was not dose-dependent. Post-mortem examination revealed that the only observed adverse reaction was thickening of the gastric and cardia mucosa in two male mice and all female mice in the highest dose group, and one female mouse in the medium dose group. Fifty male and fifty female B6C3F1 mice were administered benzyl acetate dissolved in corn oil by gavage five days a week for 103 weeks. Another 50 male and female mice served as a solvent control group and were administered corn oil by gavage. The high mortality rate in female mice was associated with infection, leading to inflammation or abscesses in the ovaries, uterus, mesentery, peritoneum, or multiple organs. The incidence of hepatocellular carcinoma and forestomach tumors was not associated with benzyl acetate administration. Fifty male and fifty female F344/N rats (n=50 per group) were administered benzyl acetate dissolved in corn oil by gavage five days a week for 103 weeks. The control group (n=50 per group) was administered corn oil by gavage. The incidence of all malignant epithelial tumors of the prepuce glands was increased in male rats in the high-dose group. The incidence of retinopathy and cataracts was increased in both male rats in the high-dose group and female rats in the low-dose group. Mutagenicity tests using Salmonella Typhimurium TA100, TA1535, TA1537, and TA98 were negative regardless of the use of rat or hamster-9 activators. In in vitro mammalian cytogenetics, chromosomal aberration tests in Chinese hamster ovary cells were negative regardless of the presence of induced rat liver S-9 fractions. In mouse lymphoma cell assays, mutagenicity was positive upon induction by metabolic activation but negative without activation. Bacterial gene mutation tests using Bacillus subtilis and in vitro and in vivo unplanned DNA synthesis tests were all negative. Benzyl acetate is a cholinesterase, or acetylcholinesterase (AChE) inhibitor. Cholinesterase inhibitors (or "anticholinesterases") inhibit the activity of acetylcholinesterase. Because acetylcholinesterase plays a crucial role, chemicals that interfere with its activity are potent neurotoxins; even low doses can cause excessive salivation and lacrimation, followed by muscle spasms and ultimately death. Neurotoxins and substances in many pesticides have been shown to exert their effects by binding to serine residues at the active site of acetylcholinesterase, thus completely inhibiting the enzyme's activity. Acetylcholinesterase breaks down the neurotransmitter acetylcholine, which is released at the neuromuscular junction, causing muscle or organ relaxation. Inhibition of acetylcholinesterase results in the accumulation and sustained action of acetylcholine, leading to continuous nerve impulse transmission and an inability to stop muscle contractions. The most common acetylcholinesterase inhibitors are phosphorus-containing compounds designed to bind to the enzyme's active site. The structural requirements are: one phosphorus atom bonded to two lipophilic groups, one leaving group (e.g., a halide or thiocyanate), and one terminal oxygen atom.

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Toxicity Data
LC50 (cat) = 245 ppm/8 hours
LD50: 2490 mg/kg (oral, rat) (L1223)
LD50: 830 mg/kg (oral, mouse) (L1223)
LC50: 245 ppm/8 hours (inhalation, cat) (L1223)

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Non-human Toxicity Values
Rat (Osborne-Mendel) oral 2.49 g/kg

[1]. Odor compound detection in male euglossine bees. J Chem Ecol. 2003 Jan;29(1):253-7.

Benzyl acetate is a colorless liquid with a pear-like odor. (USCG, 1999)
Benzyl acetate is an acetate ester of benzyl alcohol. It is a metabolite. It is both an acetate and a benzyl ester.
Benzyl acetate has been reported to be found in Streptomyces, Streptomyces, and other organisms with relevant data.
Benzyl acetate is found in alcoholic beverages. It is also found in jasmine, apples, cherries, guava fruit and peel, wine grapes, white wine, tea, plums, cooked rice, bourbon vanilla, Solanum quitoense, Chinese cabbage, and quince. Benzyl acetate is a flavoring agent. Benzyl acetate is an organic compound with the molecular formula C9H10O2. It is an ester formed by the condensation of benzyl alcohol and acetic acid. It is one of many compounds that attract male orchid bees, who apparently collect this chemical to synthesize pheromones; it is often used as bait to attract and collect these bees for research purposes.
Benzyl acetate belongs to the benzyloxycarbonyl compound family. These are organic compounds containing carbonyl groups substituted with benzyloxy groups. Benzyl acetate is described as a common odor component in orchids pollinated by orchid bees. In gas chromatography-antennae potential detection (GC-EAD) experiments using the antennae of male orchid bees (Euglossa cybelia), the antennae responded to benzyl acetate. In an antennal electrogram (EAG) experiment using male polychromatic orchid bees (Eulaema polychroma), each application of 10 µg of benzyl acetate elicited a strong relative EAG response of 600% (±14.29%) compared to the control group. When benzyl acetate was mixed with 1,8-cineole or methyl salicylate, the resulting EAG response was even stronger (871.43% and 864.29%, respectively), indicating a synergistic effect in olfaction. This study cites previous behavioral field studies that have shown that benzyl acetate can attract certain species of male serpentine wasps. [1]

C9H10O2

150.1745

150.068

140-11-4

Benzyl acetate-d5;1398065-57-0

8785

Colorless to light yellow liquid

1.1±0.1 g/cm3

213.5±0.0 °C at 760 mmHg

−51 °C(lit.)

102.2±0.0 °C

0.2±0.4 mmHg at 25°C

1.505

1.93

0

2

3

11

126

0

O(C(C([H])([H])[H])=O)C([H])([H])C1C([H])=C([H])C([H])=C([H])C=1[H]

QUKGYYKBILRGFE-UHFFFAOYSA-N

InChI=1S/C9H10O2/c1-8(10)11-7-9-5-3-2-4-6-9/h2-6H,7H2,1H3

benzyl acetate

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~125 mg/mL (~832.33 mM)

Solubility in Formulation 1: ≥ 2.08 mg/mL (13.85 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.08 mg/mL (13.85 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.08 mg/mL (13.85 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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 (Please use freshly prepared in vivo formulations for optimal results.)