Absorption, Distribution and Excretion
Benzyl acetate was absorbed from the gastrointestinal tract of rats and mice, with approximately 90% of the administered dose recovered as various metabolites in the urine within 24 hr. ... This capacity for absorption, metabolism, and disposition was unaffected by the amount or number of doses administered.
The effect of vehicle and occlusion on the in vitro percutaneous absorption of [methylene-14C]-benzyl acetate (1.7-16.6 mg/sq cm) has been studied in diffusion cells using full thickness skin from male Fischer 344 rats. Absorption of neat benzyl acetate through rat skin occluded with parafilm was 49.3 +/- 2.0% (mean +/- SD, n=4) after 48 hr. When benzyl acetate in ethanol was applied to the skin and the skin was occluded with parafilm, the extent of absorption at 48 hr was not significantly different from that after neat application. However at 6 hr, as the ethanol content of the application mixture was increased, the absorption of benzyl acetate through occluded skin was enhanced proportionally. When phenylethanol was used as a vehicle, the extent of the benzyl acetate absorption through occluded skin at 48 hr was enhanced (P less than 0.05) compared with that after application neat; with 50% (v/v) phenyl-ethanol, absorption at 48 hr was 56.3 +/- 4.9%. However, this enhanced absorption did not correlate with the proportion of phenylethanol in the application mixture. When dimethylsulphoxide was used as a vehicle, the extent of absorption of benzyl acetate through occluded skin at 48 hr was enhanced (P less than 0.05) compared with that after application neat (absorption was 59.3 +/- 3.7% of the applied dose when 50% (v/v) dimethylsulphoxide was used). As the dimethylsulphoxide content of the application mixture was increased, the absorption of benzyl acetate was enhanced proportionally. Occlusion of the skin surface with parafilm often significantly enhanced absorption (P less than 0.05), although the effect varied with time and vehicle. In general, the degree of any enhanced absorption caused by the use of a vehicle or occlusion of the skin was small, and, in most cases, would be unlikely to be toxicologically significant.
The comparative absorption of ... benzyl acetate has been studied in rat and human skin, using shaved, full-thickness dorsal skin of male Fischer 344 rats and full-thickness human skin obtained from patients undergoing surgical resection. Penetration of the compound through rat and human skin was evaluated in vitro in flow-through diffusion cells following topical application of neat [methylene-14C] benzyl acetate (33.1 mg/sq cm) to the epidermal surface and occlusion with a teflon cap, 2.9 cm above the skin surface. The absorption of benzyl acetate across rat skin was rapid and extensive, reaching 34.3 +/- 3.9% of the applied dose (11.3 +/- 1.3 mg/sq cm) (mean +/-SD, n=12) at 24 hr and 55.8 +/- 5.0% of the applied dose (18.5 +/- 1.7 mg/sq cm)at 72 hr. The penetration of benzyl acetate was significantly (P<0.05) less rapid and extensive through human skin, reaching 5.5 +/- 0.1% of the applied dose (1.8 +/- 0.0 mg/sq cm) (mean +/- SD, n=12) at 24 hr and 17.8 +/- 3.3% of the applied dose (5.9 +/-1.1 mg sq cm) at 72 hr. The rate of penetration of benzyl acetate was greater through rat skin than through human tissue at all time points studied up to 72 hr. The maximum rate of skin penetration was 0.6 +/- mg/sq cm/hr and 0.1 +/_- 0.0 mg/sq cm/hr through rat and human skin, respectively. These data indicate that systemic exposure to benzyl acetate may occur after skin contact in humans. They also support the evidence from the literature that human skin is generally less permeable to xenobiotics than rat skin.

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Metabolism / Metabolites
... BENZYL ACETATE IS RAPIDLY HYDROLYZED TO ACETIC ACID AND BENZYL ALCOHOL, AND THE LATTER OXIDIZED TO BENZOIC ACID & ... EXCRETED AS HIPPURIC ACID.
In rats, benzyl acetate is hydrolyzed to benzyl alcohol, which is oxidized to benzoic acid and excreted as hippuric acid and benzyl mercapturic acid.
In a chemical disposition study conducted by the NTP, male Fischer 344 rats and male B6C3F1 mice were shown to efficiently absorb and rapidly metabolize and excrete orally administered benzyl acetate. The doses used in this study were 5, 50, or 500 mg/kg for rats and 10, 100, or 1000 mg/kg for mice in single dose corn oil gavage administrations and 500 mg/kg for rats and 1000 mg/kg for mice daily five times per week for two weeks, also administered by gavage in corn oil. Most (90%) of the benzyl acetate-derived radioactivity was recovered in the urine and none was detected in the liver, blood, muscle, adipose tissue skin, lung, kidney, or stomach of treated rats or mice. The major metabolite isolated in the urine was hippuric acid (94%-99% of the dose). Other metabolites found were mercapturic acid and benzyl alcohol. Benzyl acetate was not detected in the urine of treated animals. Neither the size of the dose nor the frequency of dosing had any effect on the absorption, metabolism, or excretion of this compound. There was no evidence to indicate any saturation of this metabolizing capacity in either species over the range of doses studied.
Effects of gavage versus dosed feed administration on the toxicokinetics of benzyl acetate were studied in male F344 rats and B6C3F1 mice. Benzyl acetate was rapidly hydrolyzed to benzyl alcohol and then oxidized to benzoic acid. After gavage administration of benzyl acetate in corn oil at 500 mg/kg (rats) and 1000 mg/kg(mice), high benzoic acid plasma concentrations were observed. In contrast, much lower benzoic acid plasma concentrations were found after dosed feed administration at about 615 mg/kg/day for rats and about 850 mg/kg/day for mice. Results show that although the daily doses of benzyl acetate are comparable, bolus gavage administration effectively saturated the benzoic acid elimination pathway whereas dosed feed administration did not. In contrast, hippuric acid plasma concentrations were similar after both gavage and dosed feed administration due to the depletion of the glycine supply pool. ...
Paraoxonase (PON1) is a key enzyme in the metabolism of organophosphates. PON1 can inactivate some organophosphates through hydrolysis. PON1 hydrolyzes the active metabolites in several organophosphates insecticides as well as, nerve agents such as soman, sarin, and VX. The presence of PON1 polymorphisms causes there to be different enzyme levels and catalytic efficiency of this esterase, which in turn suggests that different individuals may be more susceptible to the toxic effect of OP exposure.

Toxicity Summary
IDENTIFICATION: Benzyl acetate is a solvent used in perfumery and in chemical synthesis. HUMAN EXPOSURE: Benzyl acetate is absorbed from the gastrointestinal tract, through the lungs and through intact skin. It is hydrolyzed in man to benzyl alcohol and acetate; the benzyl radical is oxidized to benzoic acid and excreted as hippuric acid. ANIMAL/BACTERIAL STUDIES: This compound is hydrolyzed in vitro with a pancreatin preparation. Benzylmercapturic acid and hippuric acid were isolated from the urine of rats that had been injected sc with benzyl acetate. Mice and rats were dosed either iv or po with (14)C labeled benzyl acetate. Elimination of benzyl acetate as carbon dioxide or volatiles was minimal. The elimination of the (14)C label occurred mainly in urine with less than 1% excreted in the feces. More than 90% of the (14)C in urine was present as hippuric acid with minor amounts present as benzyl alcohol. Neither route of administration or dose had any significant effect on the pattern of elimination. Groups of 5 B6C3F1 mice of each sex were dosed with benzyl acetate in corn oil by gavage daily for 14 days. All male mice at the highest dose level had died by day 3 of the study. Weight changes were not dose related. At autopsy the only effect reported was a thickening of the mucosa of the stomach and in the cardiac region in two males and all females in the highest dose group and one female in the medium dose group. Groups of 50 male and female B6C3F1 mice were administered benzyl acetate in corn oil by gavage for 5 days/wk for 103 weeks. Vehicle control groups of 50 animals per sex were administered corn oil by gavage. The high mortality rate in female mice was associated with infection, resulting in inflammation or abcesses of the ovaries, uterus, mesentery, peritoneum or multiple organs. There was no association of treatment with the reported incidences of hepatocellular and forestomach tumors after the administration of benz yl acetate. Groups of 50 male and female F344/N rats of each sex were administered benzyl acetate in corn oil 5 days/wk for 103 weeks. Vehicle control groups consisted of 50 animals per sex were administered corn oil by gavage. The incidence of all malignant epithelial tumors in the preputial gland of male rats was elevated in the high dose group. There was increased incidence of retinopathy and cataracts in the high dose males and low dose females. In mutagenicity tests using Salmonella typhimurium TA100, TA1535, TA1537, TA98 with or without rat or hamster-9 activation results were negative. In vitro mammalian cytogenicity chromosomal aberrations in Chinese hamster ovary cells produced a negative response, in presence or absence of induced rat liver S-9 fraction. In the mouse lymphoma cell assay, it was positive for mutagenicity when induced by metabolic activation and negative in the absence of activation. Bacterial gene mutation with Bacillus subtilus and unscheduled DNA synthesis in vitro and in vivo were both negative.[
Benzyl acetate is a cholinesterase or acetylcholinesterase (AChE) inhibitor. A cholinesterase inhibitor (or 'anticholinesterase') suppresses the action of acetylcholinesterase. Because of its essential function, chemicals that interfere with the action of acetylcholinesterase are potent neurotoxins, causing excessive salivation and eye-watering in low doses, followed by muscle spasms and ultimately death. Nerve gases and many substances used in insecticides have been shown to act by binding a serine in the active site of acetylcholine esterase, inhibiting the enzyme completely. Acetylcholine esterase breaks down the neurotransmitter acetylcholine, which is released at nerve and muscle junctions, in order to allow the muscle or organ to relax. The result of acetylcholine esterase inhibition is that acetylcholine builds up and continues to act so that any nerve impulses are continually transmitted and muscle contractions do not stop. Among the most common acetylcholinesterase inhibitors are phosphorus-based compounds, which are designed to bind to the active site of the enzyme. The structural requirements are a phosphorus atom bearing two lipophilic groups, a leaving group (such as a halide or thiocyanate), and a terminal oxygen.

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Toxicity Data
LC50 (cat) = 245 ppm/8hr
LD50: 2490 mg/kg (Oral, Rat) (L1223)
LD50: 830 mg/kg (Oral, Mouse) (L1223)
LC50: 245 ppm over 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 an odor of pears. (USCG, 1999)
Benzyl acetate is the acetate ester of benzyl alcohol. It has a role as a metabolite. It is an acetate ester and a benzyl ester.
Benzyl acetate has been reported in Mandragora autumnalis, Streptomyces, and other organisms with data available.
Benzyl acetate is found in alcoholic beverages. Benzyl acetate occurs in jasmine, apple, cherry, guava fruit and peel, wine grape, white wine, tea, plum, cooked rice, Bourbon vanilla, naranjila fruit (Solanum quitoense), Chinese cabbage and quince. Benzyl acetate is a flavouring agent Benzyl acetate is an organic compound with the molecular formula C9H10O2. It is the ester formed by condensation of benzyl alcohol and acetic acid. It is one of many compounds that is attractive to males of various species of orchid bees, who apparently gather the chemical to synthesize pheromones; it is commonly used as bait to attract and collect these bees for study.

Benzyl acetate belongs to the family of Benzyloxycarbonyls. These are organic compounds containing a carbonyl group substituted with a benzyloxyl group.

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.)