3,4-(Methylendioxy)phenol

Crystals from chloroform/petroleum ether

Beige crystals

64.9 °C

65.8 °C

Light brown crystalline powder; [Alfa Aesar MSDS]

Solid

MP: 65.8 °C. BP: 135-140 at 13 mm Hg

Enthalpy of sublimation: 82.1 kJ.mol at 301 K

When heated to decomposition it emits acrid smoke and irritating fumes.

This chemical does not meet GHS hazard criteria for 3.2% (2 of 62) of reports.

Warning

H315 (83.9%): Causes skin irritation [Warning Skin corrosion/irritation]

P261, P264, P264+P265, P271, P280, P302+P352, P304+P340, P305+P351+P338, P319, P321, P332+P317, P337+P317, P362+P364, P403+P233, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 62 reports by companies from 13 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Chemical: 1,3-Benzodioxol-5-ol

Commission Regulation (EC) No 1565/2000 (Repealed by Com. Implementing Reg. (EU) No 872/2012)

Status: Active Update: 20-02-2018 https://echa.europa.eu/registration-dossier/-/registered-dossier/19428

1,3-Benzodioxol-5-ol: Does not have an individual approval but may be used under an appropriate group standard

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Avoid dust formation. Avoid breathing vapors, mist or gas. Environmental precautions: No special environmental precautions required. Methods and materials for containment and cleaning up: Sweep up and shovel. Keep in suitable, closed containers for disposal.

SRP: Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in air, soil or water; effects on animal, aquatic and plant life; and conformance with environmental and public health regulations. If it is possible or reasonable use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination.

Product: Offer surplus and non-recyclable solutions to a licensed disposal company. Contaminated packaging: Dispose of as unused product.

Gloves must be inspected prior to use. Use proper glove removal technique (without touching glove's outer surface) to avoid skin contact with this product. Dispose of contaminated gloves after use in accordance with applicable laws and good laboratory practices. Wash and dry hands.

Further processing of solid materials may result in the formation of combustible dusts. The potential for combustible dust formation should be taken into consideration before additional processing occurs. Provide appropriate exhaust ventilation at places where dust is formed.

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Avoid dust formation. Avoid breathing vapors, mist or gas. Environmental precautions: No special environmental precautions required.

General industrial hygiene practice.

SRP: Local exhaust ventilation should be applied wherever there is an incidence of point source emissions or dispersion of regulated contaminants in the work area. Ventilation control of the contaminant as close to its point of generation is both the most economical and safest method to minimize personnel exposure to airborne contaminants. Ensure that the local ventilation moves the contaminant away from the worker.

Eye/face protection: Use equipment for eye protection tested and approved under appropriate government standards such as NIOSH (US) or EN 166 (EU).

Skin protection: Handle with gloves.

Body Protection: Choose body protection in relation to its type, to the concentration and amount of dangerous substances, and to the specific work-place.

Respiratory protection: Respiratory protection is not required. Where protection from nuisance levels of dusts are desired, use type N95 (US) or type P1 (EN 143) dust masks. Use respirators and components tested and approved under appropriate government standards such as NIOSH (US) or CEN (EU).

Sesamol, a nutritional component from sesame, possesses antioxidant, lipid lowering and antidepressant activities. Nonetheless, few studies report its effects on high-energy-dense diet-induced cognitive loss. The present research aimed to elucidate the action of sesamol on high-fat and high-fructose (HFFD) "western"-diet-induced central nervous system insulin resistance and learning and memory impairment, and further determined the possible underlying mechanism. 3 month-old C57BL/6J mice were divided into 3 groups with/without sesamol in the drinking water (0.05%, w/v) and standard diet, HFFD, and HFFD with sesamol supplementation. Morris water maze tests demonstrated that sesamol improved HFFD-elicited learning and memory loss. Sesamol was also found to attenuate neuron damage in HFFD-fed mice. Importantly, sesamol treatment up-regulated brain insulin signaling by stimulating IRS-1/AKT as well as ERK/CREB/BDNF pathways; meanwhile it down-regulated neuronal death signaling GSK3beta and JNK. Moreover, sesamol also normalized mRNA expressions of neurotrophins including BDNF and NT-3, as well as expressions of mitochondrial metabolic and biogenesis related genes Sirt1 and PGC1a. Consistently, sesamol also reversed high-glucose-induced oxidized cellular status, mitochondrial membrane potential loss, insulin signaling inhibition and cell death in SH-SY5Y neuronal cells. Taken together, the current study proved that sesamol reduced western-diet-induced cognitive defects in a mouse model by inhibiting insulin resistance, normalizing mitochondrial function and cell redox status, and improving IRS/AKT cell surviving and energy metabolism regulating signaling. This compelling evidence indicated that sesamol is a potential nutritional supplement to prevent unhealthy-diet-induced learning and memory loss.

Ionizing radiation exposure is harmful and at high doses can lead to acute hematopoietic radiation syndrome. Therefore, agents that can protect hematopoietic system are important for development of radioprotector. Sesamol is a potential molecule for development of radioprotector due to its strong free radical scavenging and antioxidant properties. In the present study, sesamol was evaluated for its role in DNA damage and repair in hematopoietic system of gamma-irradiated CB57BL/6 mice and compared with amifostine. C57BL/6 male mice were administered with sesamol 20 mg/kg (i.p.) followed by 2 Gy whole body irradiation (WBI) at 30 min. Mice were sacrificed at 0.5, 3, 24 hr postirradiation; bone marrow, splenocytes, and peripheral blood lymphocytes were isolated to measure DNA damages and repair using alkaline comet, gamma-H2AX and micronucleus assays. An increase in % of tail DNA was observed in all organs of WBI mice. Whereas in pre-administered sesamol reduced %DNA in tail (P=0.05). Sesamol has also reduced formation of radiation induced gamma-H2AX foci after 0.5 hr in these organs and further lowered to respective control values at 24 hr of WBI. Similar reduction of % DNA in tail and gamma-H2AX foci were observed with amifostine (P=0.05). Analysis of mnPCE frequency at 24 hr has revealed similar extent of protection by sesamol and amifostine. Interestingly, both sesamol and amifostine, alone and with radiation, also increased the granulocytes count significantly compared to the control (P=0.05). These findings suggest that sesamol has strong potential to protect hematopoietic system by lowering radiation induced DNA damages and can prevent acute hematopoietic syndrome in mice.

BACKGROUND: Sesamol, a component of sesame seed oil, exhibited significant antioxidant activity in a battery of in vitro and ex vivo tests including lipid peroxidation induced in rat liver homogenates. Latter established its potential for hepatoprotection. However, limited oral bioavailability, fast elimination (as conjugates) and tendency towards gastric irritation/toxicity (especially forestomach of rodents) may limit its usefulness. Presently, we packaged sesamol into solid lipid nanoparticles (S-SLNs) to enhance its biopharmaceutical performance and compared the efficacy with that of free sesamol and silymarin, a well established hepatoprotectant, against carbon tetrachloride induced hepatic injury in rats, post induction. A self recovery group in which no treatment was given was used to observe the self-healing capacity of liver. METHODS: S-SLNs prepared by microemulsification method were administered to rats post-treatment with CCl4 (1 mL/kg body weight (BW) twice weekly for 2 weeks, followed by 1.5 mL/kg BW twice weekly for the subsequent 2 weeks). Liver damage and recovery on treatment was assessed in terms of histopathology, serum injury markers (alanine aminotransferase, aspartate aminotransferase), oxidative stress markers (lipid peroxidation, superoxide dismutase, and reduced glutathione) and a pro-inflammatory response marker (tumor necrosis factor alpha). RESULT: S-SLNs (120.30 nm) at a dose of 8 mg/kg BW showed significantly better hepatoprotection than corresponding dose of free sesamol (FS; p < 0.001). Effects achieved with S-SLNs were comparable with silymarin (SILY), administered at a dose of 25 mg/kg BW. Self recovery group confirmed absence of regenerative capacity of hepatic tissue, post injury. CONCLUSION: Use of lipidic nanocarrier system for sesamol improved its efficiency to control hepatic injury. Enhanced effect is probably due to: a) improved oral bioavailability, b) controlled and prolonged effect of entrapped sesamol and iii) reduction in irritation and toxicity, if any, upon oral administration. S-SLNs may be considered as a therapeutic option for hepatic ailments as effectiveness post induction of liver injury, is demonstrated presently. /Sesamol-loaded solid lipid nanoparticles/

Ionizing radiation causes free radical-mediated damage in cellular DNA. This damage is manifested as chromosomal aberrations and micronuclei (MN) in proliferating cells. Sesamol, present in sesame seeds, has the potential to scavenge free radicals; therefore, it can reduce radiation-induced cytogenetic damage in cells. The aim of this study was to investigate the radioprotective potential of sesamol in bone marrow cells of mice and related haematopoietic system against radiation-induced genotoxicity. A comparative study with melatonin was designed for assessing the radioprotective potential of sesamol. C57BL/6 mice were administered intraperitoneally with either sesamol or melatonin (10 and 20 mg/kg body weight) 30 min prior to 2-Gy whole-body irradiation (WBI) and sacrificed after 24 hr. Total chromosomal aberrations (TCA), MN and cell cycle analyses were performed using bone marrow cells. The comet assay was performed on bone marrow cells, splenocytes and lymphocytes. Blood was drawn to study hematological parameters. Prophylactic doses of sesamol (10 and 20 mg/kg) in irradiated mice reduced TCA and micronucleated polychromatic erythrocyte frequency in bone marrow cells by 57% and 50%, respectively, in comparison with radiation-only groups. Sesamol-reduced radiation-induced apoptosis and facilitated cell proliferation. In the comet assay, sesamol (20 mg/kg) treatment reduced radiation-induced comets (% DNA in tail) compared with radiation only (P < 0.05). Sesamol also increased granulocyte populations in peripheral blood similar to melatonin. Overall, the radioprotective efficacy of sesamol was found to be similar to that of melatonin. Sesamol treatment also showed recovery of relative spleen weight at 24 hr of WBI. The results strongly suggest the radioprotective efficacy of sesamol in the hematopoietic system of mice.

For more Interactions (Complete) data for Sesamol (39 total), please visit the HSDB record page.

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 48(SRC), determined from a structure estimation method(2), indicates that sesamol is expected to have very high mobility in soil(SRC). The pKa of sesamol is 9.97(3), indicating that this compound exists as a weak anion and anions generally do not adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(4). Volatilization of sesamol from moist soil surfaces is expected to be an important fate process(SRC) given an estimated Henry's Law constant of 8.7X10-6 atm-cu m/mole(SRC), developed using a fragment constant estimation method(2). Sesamol is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 6.9X10-3 mm Hg at 25 °C(SRC), determined from a fragment constant method(2). Biodegradation data in soil were not available(SRC, 2018).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 48(SRC), determined from a structure estimation method(2), indicates that sesamol is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is expected(3) based upon an estimated Henry's Law constant of 8.7X10-6 atm-cu m/mole(SRC), developed using a fragment constant estimation method(2). Using this Henry's Law constant and an estimation method(3), volatilization half-lives for a model river and model lake are 5 and 41 days, respectively(SRC). According to a classification scheme(6), an estimated BCF of 5(SRC), from an estimated log Kow of 1.57(2) and a regression-derived equation(2), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Biodegradation data in water were not available(SRC, 2018).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), sesamol, which has an estimated vapor pressure of 6.9X10-3 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase sesamol is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be 2 hrs(SRC), calculated from its rate constant of 2.0X10-10 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(2). Sesamol contains chromophores that absorb at wavelengths >290 nm(3) and, therefore, may be susceptible to direct photolysis by sunlight(SRC).

IDENTIFICATION AND USE: Sesamol, generally regarded as the main antioxidative component in sesame oil, can be generated from sesamolin by roasting sesame seed or bleaching sesame oil. The content of sesamol is increased after heating oil at frying temperature for 1 to 2 hr. Sesamol possesses antioxidant, lipid lowering and antidepressant activities. It was tested as experimental therapy. HUMAN STUDIES: In patients with contact allergy to sesame oil, patch tests showed that 8 of the 13 patients were positive to sesamol. Sesamol demonstrated weak estrogenic/antiestrogenic activity when tested on human breast cancer cells. Sesamol could efficiently induce apoptosis of HepG2 cells. Oxidation product - tetramer of sesamol inhibited growth of human leukemia K562 cells. ANIMAL STUDIES: In mice, acute toxicological effects were observed at 2000 mg/kg, while no adverse effects observed at 300 mg/kg. The effects of 2000 mg/kg were manifested as severe histopathological changes in all organs (femur, spleen, gastrointestine, lungs, heart, kidney, liver, stomach and brain) and excessive DNA strand breaks occurred in femoral bone marrow cells and splenocytes. Sesamol at a dietary level of 2% induced squamous cell carcinomas in the forestomach of rats and mice, males being more susceptible than females. However, sesamol treatment led to 50% reduction in mouse skin papillomas at 20 weeks after promotion with 12-O-tetradecanoylphorbol 13-acetate. Sesamol also demonstrated protection against ionizing radiation and UV radiation in vivo and in vitro. Sesamol was shown to exhibit strong antimutagenic effects in the Ames tester strains TA100 and TA102. Mutagenicity was induced by the generation of oxygen radicals by tert-butylhydroperoxide or hydrogen peroxide. Sesamol was also protective against CCl4 toxicity and acute hepatic injury following acetaminophen overdose. It demonstrated protective effects in experimental animal models of streptozotocin-induced diabetes and isoproterenol-induced myocardial infraction.

The following link will take the user to the National Toxicology Program (NTP) Test Status of Agents Search page, which tabulates the results and current status of tests such as "Short-Term Toxicity Studies", "Long-term Carcinogenicity Studies", "Developmental Studies", "Genetic Toxicology Studies", etc., performed with this chemical. Testing status for sesamol is available.[Available from, as of February 1, 2019: https://ntpsearch.niehs.nih.gov/?e=True&ContentType=Testing+Status]

EPA has released the Interactive Chemical Safety for Sustainability (iCSS) Dashboard. The iCSS Dashboard provides an interactive tool to explore rapid, automated (or in vitro high-throughput) chemical screening data generated by the Toxicity Forecaster (ToxCast) project and the federal Toxicity Testing in the 21st century (Tox21) collaboration. /The title compound was tested by ToxCast and/or Tox21 assays/[USEPA; ICSS Dashboard Application; Available from, as of February 4, 2019: http://actor.epa.gov/dashboard/]

Using a structure estimation method based on molecular connectivity indices(1), the Koc of sesamol can be estimated to be 48(SRC). According to a classification scheme(2), this estimated Koc value suggests that sesamol is expected to have very high mobility in soil(SRC). The pKa of sesamol is 9.97(3), indicating that this compound exists as a weak anion and anions generally do not adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(4).

/HUMAN EXPOSURE STUDIES/ In 13 patients with contact allergy to sesame oil, studies were undertaken to elucidate the nature of the allergens. Sesamol, sesamin and sesamolin were identified in crude and purified (pharmaceutical) sesame oil. Patch tests showed 8 of the 13 patients to be positive to sesamol and 12 to sesamolin and sesamin. Patch tests with the pure substances on thin-layer sheets were inconclusive as to any difference between these substances. Group allergy to several substances related to sesamol could not be clearly demonstrated.

/HUMAN EXPOSURE STUDIES/ Sesame oil has been reported to contain sesamolin, sesamin and sesamol as contact allergens. A female patient had cheilitis due to sesame oil in a lipstick. She reacted to sesamolin and sesamin, but not to sesamol. We carried out analysis of the sesame oil by high performance liquid chromatography. We detected sesamolin and sesamin but not sesamol in sesame oil. /Sesame oil/

/ENDOCRINE MODULATION/ Sesame lignans (sesamin, sesamolin) and their metabolites (enterodiol, ED; enterolactone, EL; and sesamol) have been evaluated for their estrogenic activities. ED and EL have been indicated to have estrogenic/antiestrogenic properties on human breast cancer cells; however the estrogenic activities of sesamin, sesamolin and sesamol have not been reported. In the present study, estrogenic potencies of sesame lignans and their metabolites were determined by estrogen responsive element (ERE) luciferase reporter assay in T47D cells stably transfected with ERE-luc (T47D-KBluc cells) and quantifying pS2 and progesterone receptor gene expression in T47D cells. All tested compounds except ED possessed ability of ERE activation with a very low potency compared to estradiol (E2). These effects were abolished by coincubating tested compounds with 1 uM ICI 182 780, suggesting that estrogen receptors were directly involved in their ERE activations. Among tested compounds, sesamol showed the highest ability in ERE induction. The coincubation of increasing concentration of E2 (10(-12)-10(-6) M) with 10 uM of tested compounds resulted in a downward shift of E2-ERE dose-response curves. In contrast, at the low concentration of E2 (10(-12) M), sesamin and sesamol significantly exhibited additive effects on the E2 responses. The inhibitory effect in a dose-dependent manner was also observed when 1-100 uM sesamol was coincubated with 1 nM E2. Sesamin, sesamol and EL significantly induced pS2 gene expression whereas only sesamol could significantly induce progesterone receptor gene. The data obtained in this study suggested that sesame lignans and their metabolites possess weak estrogenic/antiestrogenic activity.

/ALTERNATIVE and IN VITRO TESTS/ Sesamol, a nutritional antioxidant phenolic compound present in sesame seed, has a potential therapeutic molecule effect against cancers. In this study, the interaction between sesamol and DNA was investigated by employing ultraviolet/visible (UV/Vis), fluorescence, circular dichroism (CD), Fourier transform infrared spectroscopy (FT-IR), and molecular modeling. The fluorescence analysis indicated that the fluorescence quenching mechanism of sesamol by calf thymus DNA (ctDNA) occurred through static quenching. The UV/Vis, CD, FT-IR spectra and molecular docking results implied that the primary binding mode was minor groove binding. Furthermore, the intracellular interaction of sesamol with DNA and its bioactivity effect were explored. The cell activity results demonstrated that sesamol induced hepatic cell line (HepG2) death. The acridine orange (AO)/ethidium bromide (EB) staining assay and DNA fragmentation confirmed that sesamol could efficiently induce the apoptosis of HepG2 cells. Moreover, addition of sesamol to HepG2 cells resulted in nuclear localization, as visualized by confocal microscopy.

For more Human Toxicity Excerpts (Complete) data for Sesamol (11 total), please visit the HSDB record page.

An estimated BCF of 5 was calculated in fish for sesamol(SRC), using an estimated log Kow of 1.57(1) and a regression-derived equation(1). According to a classification scheme(2), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC).

The Henry's Law constant for sesamol is estimated as 8.7X10-6 atm-cu m/mole(SRC) developed using a fragment constant estimation method(1). This Henry's Law constant indicates that sesamol is expected to volatilize from water surfaces(2). Based on this Henry's Law constant, the volatilization half-life from a model river (1 m deep, flowing 1 m/sec, wind velocity of 3 m/sec)(2) is estimated as 5 days(SRC). The volatilization half-life from a model lake (1 m deep, flowing 0.05 m/sec, wind velocity of 0.5 m/sec)(2) is estimated as 41 days(SRC). Sesamol is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 6.9X10-3 mm Hg(SRC), determined from a fragment constant method(1).

/LABORATORY ANIMALS: Acute Exposure/ The objective of this study was to evaluate organ-wise toxicological effects of sesamol and determine the LD50 cut-off value and GHS category following acute oral toxicity method OECD 423. An acute oral toxicity study was carried out in female C57BL/6 mice. Observations for physical behavior and measurements on hematology, biochemistry, histology of vital organs were performed. In addition, genotoxicity assessment using comet and micronuclei assays was also performed. Acute toxicological effects were observed at 2000 mg/kg, while no adverse effects observed at 300 mg/kg. The effects of 2000 mg/kg were manifested as severe histopathological changes in all organs (femur, spleen, gastrointestine, lungs, heart, kidney, liver, stomach and brain) and excessive DNA strands breaks occurred in femoral bone marrow cells and splenocytes. A single dose of sesamol (2000 mg/kg, body weight) caused the death of two mice (out of three) within 2 hr. Hence, sesamol is in GHS category 4 (>300-2000) with LD50 cut-off value of 500 mg/kg body weight. In contrast, this study is correlated with the obtained GHS category 4 and LD50 cut-off value 580 mg/kg body weight by ProTox. In conclusions, the present study has classified sesamol toxicity and assessed organ-wise acute oral toxicity of sesamol in female C57BL/6 mice. Therefore, these findings may be useful for the selection of dosages for further pre-clinical evaluation and potential drug developmental of sesamol.

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ Highly electronegative low-density lipoprotein (LDL) L5 induces endothelial cell (EC) apoptosis, which leads to the development of atherosclerosis. We examined the effects of sesamol (1), a natural organic component of sesame oil, on plasma L5 levels and atherosclerosis development in a rodent model and on the L5-induced apoptosis of ECs. Syrian hamsters, which have an LDL profile similar to that of humans, were fed a normal chow diet (control), a high-fat diet (HFD), or a HFD supplemented with the administration of 50 or 100 mg/kg of 1 via oral gavage (HFD+1) for 16 weeks (n = 8 per group). Hamsters in the HFD+1 groups had reduced plasma L5 levels when compared with the HFD group. Oil Red O staining showed that atherosclerotic lesion size was markedly reduced in the aortic arch of hamsters in the HFD+1 groups when compared with that in the HFD group. In human aortic ECs, 0.3-3 uM 1 blocked L5-induced apoptosis in a dose-dependent manner. Further mechanistic studies showed that 1 inhibited the L5-induced lectin-like oxidized LDL receptor-1 (LOX-1)-dependent phosphorylation of p38 MAPK and activation of caspase-3 and increased phosphorylation of eNOS and Akt. Our findings suggest that sesamol (1) protects against atherosclerosis by reducing L5-induced atherogenicity.

/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ The effects of naturally occurring antioxidants on rat forestomach epithelium were compared with those of synthetic antioxidants, butylated hydroxyanisole (BHA) and butylated hydroxytoluene (BHT), of which the former is a known forestomach carcinogen. Groups of five F344 male rats were given diet containing BHA, BHT, gallic acid, syringic acid, sesamol, caffeic acid, chlorogenic acid, ferulic acid, eugenol or esculin for 4 weeks at a level of 0.7% for BHT or 2% for other compounds. Histological examination of the forestomach showed that BHA induced hyperplasia mainly in the prefundic region near the esophageal orifice, caffeic acid induced pronounced hyperplasia throughout the forestomach epithelium, and sesamol induced large ulcers and hyperplasia in the central region. Thus, these naturally occurring antioxidants showed different toxicities and abilities to induce hyperplasia in the rat forestomach.

/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ The carcinogenic potential of caffeic acid, sesamol and catechol was examined in male and female F344 rats and B6C3F1 mice, groups of 30 animals being treated with diets containing 2% caffeic acid, 2% sesamol or 0.8% catechol for 104 weeks (rats) or 96 weeks (mice). Histological examination revealed that caffeic acid induced forestomach squamous cell carcinoma in 57% (P less than 0.001 vs. controls) and 50% (P less than 0.001) of male and female rats, respectively, whereas sesamol was associated with squamous cell carcinoma at incidences of 31% (P less than 0.001) in male rats, and 38% (P less than 0.001) and 17% (P less than 0.05) in male and female mice, respectively. Catechol induced glandular stomach adenocarcinomas in 54% (P less than 0.001) and 43% (P less than 0.001) of male and female rats, respectively. The results thus clearly demonstrated that all three antioxidants are carcinogenic in rodent stomach epithelia.

For more Non-Human Toxicity Excerpts (Complete) data for Sesamol (16 total), please visit the HSDB record page.

Sesamol (3,4-methylenedioxyphenol), a phenolic constituent in roasted sesame, was reported to exhibit various beneficial activities. To understand the metabolic transformation of sesamol in vivo, rats were given sesamol intravenously and orally. The blood samples were withdrawn via cardiopuncture at specific time points. The serum samples were assayed by high-performance liquid chromatography method before and after hydrolysis with sulfatase and beta-glucuronidase. Our results indicated that following either intravenous or oral administration, sesamol declined rapidly and the sulfate/glucuronide of sesamol emerged instantaneously. The peak serum concentration and systemic exposure of sesamol were markedly lower than sesamol sulfate/glucuronide. Ex vivo evaluation revealed that sesamol exerted profoundly higher capability against 2,2'-azo-bis(2-amidinopropane)dihydrochloride-induced hemolysis than the serum metabolites. In conclusion, sulfate and glucuronide of sesamol were the principle metabolites of sesamol in the bloodstream of rats. The conjugated metabolites of sesamol warrant more bioactivity investigations to understand the in vivo effect of sesamol.

This paper reports the bioavailability of sesamol in Sprague-Dawley (SD) rats... Sesamol conjugated metabolites were widely distributed in SD rat tissues, with the highest concentrations in the liver and kidneys and the lowest in the brain. It is postulated that sesamol is incorporated into the liver first and then transported to the other tissues (lung, kidneys, and brain). The major metabolites of sesamol distributed in the lung and kidney were glucuronide and sulfate.

Sesamol, generally regarded as the main antioxidative component in sesame oil, can be generated from sesamolin by roasting sesame seed or bleaching sesame oil. This paper reports the bioavailability of sesamol in Sprague-Dawley (SD) rats. Biological fluid was sampled following a dose of sesamol of 50 mg/kg by gastric gavage (p.o.) or by intravenous injection. The pharmacokinetic data of sesamol were calculated by noncompartmental model. The tissue distribution of sesamol (p.o., 100 mg/kg) in SD rats was also investigated. The concentration changes of sesamol were determined in various tissues and plasma within a 24 hr period after oral administration of sesamol. The results showed that the oral bioavailability of sesamol was 35.5 +/- 8.5%. Sesamol was found to be able to penetrate the blood-brain barrier and go through hepatobiliary excretion. Sesamol conjugated metabolites were widely distributed in SD rat tissues, with the highest concentrations in the liver and kidneys and the lowest in the brain. It is postulated that sesamol is incorporated into the liver first and then transported to the other tissues (lung, kidneys, and brain). The major metabolites of sesamol distributed in the lung and kidney were glucuronide and sulfate.

Component of sesame oil; [ChemIDplus]

MEDICATION

1,3-Benzodioxol-5-ol: ACTIVE

Antioxidative constituents in roasted sesame seed oil were studied mainly by an antioxidative assay and HPLC analysis, in comparison with unroasted sesame seed oil. The main active constituent in fresh roasted seed oil was gamma-tocopherol, but after heating at frying temperature for 1 to 2hr, this was identified as sesamol, which was produced by hydrolysis of sesamolin that is present to a large degree in roasted sesame seed oil. This conversion of sesamolin to sesamol is catalyzed by acids.