HuagongsheHuagongshe Chemistry Print Report · For research reference only
Ferulic Acid
Isooctyl Ferulate · 2-Ethylhexyl ferulate · Piperazine ferulate 99% · Piperazine ferulate USP/EP/BP · 4-hydroxy-3-octyl methoxycinnamate · Piperazine 3-methoxy-4-hydroxycinnamate · Piperazine 3-(4-hydroxy-3-methoxyphenyl)acrylate · 2-Ethylhexyl 3-(4-hydroxy-3-methoxyphenyl)acrylate
Identifiers & Physical Properties
| CAS No. | 1135-24-6 |
|---|---|
| Molecular formula | C10H10O4 |
| Average molar mass | 194.18 g/mol |
| Monoisotopic mass | 194.0579088 g/mol |
| SMILES | COc1cc(/C=C/C(=O)O)ccc1O |
| InChIKey | KSEBMYQBYZTDHS-HWKANZROSA-N |
| PubChem CID | 445858 |
| ChEBI | CHEBI:193350 |
| EC No. | 208-679-7 |
| DTXSID | DTXSID70892035 |
Chemical & Physical Properties
| XLogP | 1.5 |
|---|---|
| Topological polar surface area | 66.8 |
| Hydrogen bond donors | 2 |
| Hydrogen bond acceptors | 4 |
| Rotatable bonds | 3 |
| Heavy atoms | 14 |
| Formal charge | 0 |
| Complexity | 224 |
| LogP (partition coefficient) | log Kow = 1.51 |
| Melting point | 168 - 171 °C |
| Vapor pressure | 0.00000269 [mmHg] |
| Physical Description | cis-Form is a yellow liquidtrans-Form is a solid[Merck Index] trans-Isomer: Tan powder[Alfa Aesar MSDS] |
| Dissociation Constants | pKa = 4.58 |
| Kovats Retention Index | 1897.11881186719111875 |
| Collision Cross Section | 134.13 Ų [M+H]+ [CCS Type: TWMethod: calibrated with polyalanine and drug standards]130.77 Ų [M+H-H2O]+ [CCS Type: TW139.8 Ų [M-H]- [CCS Type: DTMethod: single field calibrated with ESI Low Concentration Tuning Mix (Agilent)]128.8 Ų [M+H]+ [CCS Type: TW140.1 Ų [M-H]- |
| Other Experimental Properties | Yellow oil. UV max (alcohol): 316 nm /cis-Form/Orthorhombic needles from water, mp 174 °C. UV max (alcohol): 236, 322 nm. Soluble in hot water, alcohol, ethyl acetate. Moderately soluble in ether. Sparingly soluble in petroleum ether, benzene. Forms a sodium salt. /trans-Form/ |
| Boiling point | 425.8±30.0 °C(Predicted) |
| Density | 1.061±0.06 g/cm3(Predicted) |
| Solubility | Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc. |
| Physical state | Powder |
| pKa (acidity coefficient) | 8+-.0.20(Predicted) |
| CAS DataBase Reference | 171876-65-6(CAS DataBase Reference) |
| GHS pictogram | GHS07 |
| Signal word | Warning |
| GHS hazard statements | H317 |
| GHS precautionary statements | P261-P272-P280-P302+P352-P333+P313-P321-P363-P501 |
Safety & Regulations
| GHS classification | This chemical does not meet GHS hazard criteria for 2.4% (8 of 329) of reports.WarningH315 (97.6%): Causes skin irritation [Warning Skin corrosion/irritation]H319 (97.6%): Causes serious eye irritation [Warning Serious eye damage/eye irritation]H335 (97.6%): May cause respiratory irritation [Warning Specific target organ toxicity, single exposureRespiratory tract 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 329 reports by companies from 8 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.Reported as not meeting GHS hazard criteria per 8 of 329 reports by companies.There are 7 notifications provided by 321 of 329 reports by companies with hazard statement code(s).Information may vary between notifications depending on impurities, additives, and other factors. The percentage value in parenthesis indicates the notified classification ratio from companies that provide hazard codes. Only hazard codes with percentage values above 10% are shown. For more detailed information, please visit ECHA C&L website. |
|---|---|
| Regulatory information | Chemical: 2-Propenoic acid, 3-(4-hydroxy-3-methoxyphenyl)-Commission Regulation (EC) No 1565/2000 (Repealed by Com. Implementing Reg. (EU) No 872/2012)PMN - indicates a commenced PMN (Pre-Manufacture Notices) substance.Status: Active Update: 05-10-2020 https://echa.europa.eu/registration-dossier/-/registered-dossier/213632-Propenoic acid, 3-(4-hydroxy-3-methoxyphenyl)-: Does not have an individual approval but may be used under an appropriate group standard |
| Hazards summary | Causes changes in motor activity, ataxia, and rigidity (including catalepsy) in intraperitoneal lethal-dose studies of mice (LD50 > 350 mg/kg)[RTECS] May cause irritation[Alfa Aesar MSDS] See Cinnamic acid. See See Sinapinic acid.A skin and strong eye irritant[Alfa Aesar MSDS] See Ferulic acid. |
| Hazard Classes and Categories | Skin Irrit. 2 (97.6%)Eye Irrit. 2 (97.6%)STOT SE 3 (97.6%)Skin Irrit. 2 (99%)Eye Irrit. 2A (99%)STOT SE 3 (98.1%)Skin Sens. 1 (100%) |
| Disposal methods | SRP: At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices. |
| Interactions | The effects of topically applied curcumin, chlorogenic acid, caffeic acid, and ferulic acid on 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced epidermal ornithine decarboxylase activity, epidermal DNA synthesis, and the promotion of skin tumors were evaluated in female CD-1 mice. Topical application of 0.5, 1, 3, or 10 umol of curcumin inhibited by 31, 46, 84, or 98%, respectively, the induction of epidermal ornithine decarboxylase activity by 5 nmol of TPA. In an additional study, the topical application of 10 umol of curcumin, chlorogenic acid, caffeic acid, or ferulic acid inhibited by 91, 25, 42, or 46%, respectively, the induction of ornithine decarboxylase activity by 5 nmol of TPA. The topical application of 10 umol of curcumin together with 2 or 5 nmol of TPA inhibited the TPA-dependent stimulation of the incorporation of [3H]-thymidine into epidermal DNA by 49 or 29%, respectively, whereas lower doses of curcumin had little or no effect. Chlorogenic acid, caffeic acid, and ferulic acid were less effective than curcumin as inhibitors of the TPA-dependent stimulation of DNA synthesis. Topical application of 1, 3, or 10 mumol of curcumin together with 5 nmol of TPA twice weekly for 20 weeks to mice previously initiated with 7,12-dimethylbenz[a]anthracene inhibited the number of TPA-induced tumors per mouse by 39, 77, or 98%, respectively. Similar treatment of mice with 10 mumol of chlorogenic acid, caffeic acid, or ferulic acid together with 5 nmol of TPA inhibited the number of TPA-induced tumors per mouse by 60, 28, or 35%, respectively, and higher doses of the phenolic acids caused a more pronounced inhibition of tumor promotion. The possibility that curcumin could inhibit the action of arachidonic acid was evaluated by studying the effect of curcumin on arachidonic acid-induced edema of mouse ears. The topical application of 3 or 10 umol of curcumin 30 min before the application of 1 umol of arachidonic acid inhibited arachidonic acid-induced edema by 3... A series of in vivo experiments/were/ carried out to evaluate the ability of caffeic and ferulic acids to reduce, in healthy human volunteers, UVB-induced skin erythema, monitored by means of reflectance spectrophotometry. Caffeic and ferulic acids, dissolved in saturated aqueous solution pH 7.2, proved to afford a significant protection to the skin against UVB-induced erythema...A variety of synthetic and dietary polyphenols protect mammalian and bacterial cells from cytotoxicity induced by hydroperoxides, especially hydrogen peroxide (H2O2). Cytotoxicity of H2O2 on Chinese hamster V79 cells was assessed with a colony formation assay. Cytotoxicity and mutagenicity of H2O2 on Salmonella TA104 were assessed with the Ames test. SOS response induced by H2O2 was investigated in the SOS chromotest with Escherichia coli PQ37. The polyphenol-bearing o-dihydroxy (catechol) structure, i.e., nordihydroguaiaretic acid, caffeic acid ester, gallic acid ester, quercetin, and catechin, were effective for suppression of H2O2-induced cytotoxicity in these assay systems. In contrast, neither ferulic acid ester-bearing o-methoxyphenol structure nor alpha-tocopherol were effective, indicating that o-dihydroxy or its equivalent structure in flavonoids is essential for the protection. There are many reports describing that polyphenols act as prooxidants in the presence of metal ions. /These/ results suggest, however, that they act as antioxidants in the cells, when no metal ions are added to the medium.This review describes the modes of mice radiation injuries induced by soft X-irradiation under various conditions and the protective effects of several kinds of substances on these injuries. The models of radiation injuries in this study were bone marrow death after lethal irradiation, skin damage induced by irradiation with long length soft X-ray and leukocytopenia in the peripheral blood after sublethal irradiation. Two bioassay methods were established for the survival effect on the lethal irradiation and protective potency on the skin damage induced by soft X-irradiation. The protective potencies of various sulfur compounds, related compounds of ferulic acid, nucleic acid constitutional compounds, crude drugs and Chinese traditional medicines were determined and then many effective drugs were recognized. Effective components in the methanol extracts of Cnidii Rhizoma and Aloe arborescens recognized as radioprotectable were fractionated. As a result of these studies, it was observed that the active principles in Cnidii Rhizoma were identified as ferulic acid and adenosine. The scavenger action of active oxygens, a protective effect on the damages of deoxyribonucleic acid and superoxide dismutase by in vitro soft X-irradiation were evaluated as radiation protective mechanisms.For more Interactions (Complete) data for FERULIC ACID (8 total), please visit the HSDB record page. |
| Environmental fate | TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 57(SRC), determined from a log Kow of 1.51(2) and a regression-derived equation(3), indicates that ferulic acid is expected to have high mobility in soil(SRC). The pKa of ferulic acid is 4.58(4), indicating that this compound will almost entirely exist in the anion form. In the environment, anions generally do not adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(5). Volatilization of ferulic acid from moist soil surfaces is not expected to be an important fate process(SRC) given the anionic nature of ferulic acid in the environment. Ferulic acid is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 2.7X10-6 mm Hg(SRC), determined from a fragment constant method(6). Under neutral and acidic conditions in soil, ferulic acid is expected to undergo rapid aerobic biodegradation(7)(8). Under alkaline conditions in soil, ferulic acid is not expected to undergo rapid aerobic biodegradation(8).AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 57(SRC), determined from a log Kow of 1.51(2) and a regression-derived equation(3), indicates that ferulic acid is not expected to adsorb to suspended solids and sediment(SRC). A pKa of 4.58(4) indicates ferulic acid will exist almost entirely in the anion form at pH values of 5 to 9, and therefore volatilization from water surfaces/moist soil is not expected to be an important fate process(5). According to a classification scheme(6), an estimated BCF of 3.2(SRC), from its log Kow of 1.51(2) and a regression-derived equation(7), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Ferulic acid is expected to biodegrade rapidly in water under anaerobic conditions(8).ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), ferulic acid, which has a an estimated vapor pressure of 2.7X10-6 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), will exist in both the vapor and particulate phases. Vapor-phase ferulic acid 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 8 hours(SRC), calculated from its rate constant of 4.8X10-11 cu cm/molecule-sec at 25 °C(SRC), derived using a structure estimation method(3). Particulate-phase ferulic acid may be removed from the air by wet or dry deposition(SRC). Ferulic acid contains a chromophore that absorbs light at wavelengths >290 nm(4) and therefore may be susceptible to direct photolysis by sunlight(SRC). |
| Adverse effects | Neurotoxin - Other CNS neurotoxin |
| Soil Adsorption/Mobility | The Koc of ferulic acid is estimated as 57(SRC), using a log Kow of 1.51(1)(SRC) and a regression-derived equation(2). According to a classification scheme(3), this estimated Koc value suggests that ferulic acid is expected to have high mobility in soil. The pKa of ferulic acid is 4.58(4), indicating that this compound will almost entirely exist in the anion form in the environment. Anions generally do not adsorb more strongly to soils containing organic carbon and clay, in comparison with their neutral counterparts(5). |
| Natural Pollution Sources | Ferulic acid is found in soil humus, and is derived from the breakdown of lignin from wood/plant materials(1). Ferulic acid has been found in atmospheric particulate matter, the source of which is wood combustion(2). |
| Atmospheric Concentrations | URBAN/SUBURBAN: Ferulic acid was detected in five out of eight atmospheric fallout samples collected in Tokyo (Japan) between February 1976 and January 1978 at concentrations ranging from 0.06 and 0.74 ug/sq m-day, with an average of 0.43 ug/sq m-day(1). Ferulic acid was detected in two out of two atmospheric particulate samples collected in Bakersfield (California) and Fresno (California) between December 5, 1995 and January 6, 1996 and at concentrations ranging from 0.3 ng/cu m, with an average of 0.45 ng/cu m(2).RURAL/REMOTE: Ferulic acid was not detected in one atmospheric particulate sample collected in the Kern Wildlife Refuge (Delano, California) between December 5, 1995 and January 6, 1996(1). |
| Human Toxicity Excerpts | /HUMAN EXPOSURE STUDIES/ The aim of this study is to investigate the effects of ferulic acid (FA) on human sperm motility, viability, lipid peroxidation, and cyclic nucleotides in fertile and asthenozoospermic infertile individuals in vitro. The sperm samples were obtained from 10 fertile volunteers and 10 asthenozoospermic infertile patients. Washed spermatozoa were incubated at 37 degrees C in Ham's F-10 medium with 0, 0.1, 0.2, 0.4, 0.8, or 1.6 mM of FA. Samples were analyzed for viability, determined by eosin-Y dye exclusion method at 0, 1, 2, 3, 5, and 6 hr of incubationmotility, determined by the trans-membrane migration method within 2 hr of incubationLPO, determined by thiobarbituric acid (TBA) method at 3 hr of incubation and the intracellular cAMP and cGMP, determined, respectively, by 3H-cAMP and 125I-cGMP radioimmunoassay at 3 hr of incubation. The results showed: in both fertile and infertile spermatozoa, the viability, trans-membrane migration ratio (TMMR) and the levels of intracellular cAMP and cGMP in FA-treated spermatozoa were significantly higher than those of spermatozoa in control groups, while TBA-reactive substances contents in treated spermatozoa were significantly lower than those in control spermatozoa. The effects of FA on these processes were concentration dependent. These data suggested that FA is beneficial to sperm viability and motility in both fertile and infertile individuals, and that reduction of lipid peroxidative damage to sperm membranes and increase of intracellular cAMP and cGMP may be involved in these benefits./GENOTOXICITY/ In the present study, the effects of extracts and polyphenol-rich fractions as well as monomer polyphenols identified in them, from both red and white grapes, on mitomycin C (MMC) induced sister chromatid exchanges (SCEs) in human peripheral blood lymphocytes were investigated. The grape extracts and two of the three polyphenol-rich fractions promoted MMC-induced SCEs at concentrations from 75 to 300 ug/mL. However, none of the extracts or fractions alone induced SCEs. Thus, these results suggest caution especially with regard to the use of grape extracts as dietary supplements. On the other hand, the fact that these extracts were not genotoxic alone may indicate a selective activity against genetically damaged cells. This is the first study regarding the clastogenic effects of grape extracts in human cells. Moreover, from the tested polyphenols, caffeic acid, gallic acid, and rutin hydrate enhanced MMC-induced clastogenicity, whereas ferulic acid, protocatechuic acid, (+)-catechin, (-)-epicatechin, and trans-resveratrol had no effect at concentrations between 5 and 100 uM. The differences in the chemical structures of the tested polyphenols may account for their differential effects on MMC clastogenicity./ALTERNATIVE and IN VITRO TESTS/ ... The effects of more physiological concentrations (0.1 um) of various individual polyphenols on gene expression were ... investigated in cultured human umbilical vein endothelial cells (HUVEC) using both microarray and quantitative RT-PCR methodologies. Treatment of HUVEC with ferulic acid, quercetin or resveratrol (0.1 um) resulted in changes to gene expression that for the three treatments amounted to significant (>2-fold) down-regulation of the expression of 363 genes and significant (>2-fold) up-regulation of 233 genes of the 10,000 genes present on the microarray. The majority of these genes were affected by resveratrol. Quantitative RT-PCR studies indicated that resveratrol (0.1 um) significantly increased the expression of the gene encoding endothelial NO synthase (eNOS), which synthesizes the vasodilator molecule NO, and both resveratrol and quercetin decreased expression of the potent vasoconstrictor, endothelin-1 (ET-1), while ferulic acid had no effect.../ALTERNATIVE and IN VITRO TESTS/ The possible effects of naturally occurring plant phenolics, caffeic acid (CA), chlorogenic acid (CGA) and ferulic acid (FA) on arylamine N-acetyltransferase (NAT) activities on human gastrointestinal microflora, Escherichia coli, Klebsiella pneumoniae, Enterobacter aerogenes, Citrobacter koseri and Pseudomonas aeruginosa, were examined. The bacterial NAT activities were determined by HPLC measuring the acetylation of 2-aminofluorene (2-AF). Among all examined bacteria, P. aeruginosa exerted the highest NAT activity while C. koseri possessed the lowest NAT activity. CA, CGA and FA could suppress the bacterial NAT activities dose-dependently both in the intact cell and cytosolic fraction analysis. According to the analysis of kinetic parameters in E. coli and P. aeruginosa, CA, CGA and FA were shown to be potent noncompetitive inhibitors of bacterial NAT activities. For the time course experiment, 4 mM of CA and FA could inhibit bacterial NAT activities for at least 4 hour but 4 mM of CGA could only significantly suppress NAT activity in E. coli for the same reaction time. These results strongly demonstrated that CA, CGA and FA inhibited NAT activities in human gastrointestinal bacteria. |
| Environmental Biodegradation | AEROBIC: Ferulic acid, present at 100 ppm in Greenfield (California) sandy loam with a pH of 7, underwent 60-72% decomposition via 14-CO2 evolution in 28 days(1). In a similar study, ferulic acid, present at 100 ppm in Chino (California) loam with a pH of 5.6, underwent 77% decomposition via 14-CO2 evolution after 28 days(2)in San Jacinto (California) sandy loam with a pH of 8, 100 ppm ferulic acid underwent 13% decomposition by 14-CO2 evolution over 28 days(2). This lower level of decomposition was thought to be due to polymerization of ferulic acid to humic acid type compounds(2). Therefore, under neutral and acidic conditions in soil, ferulic acid is expected to biodegrade rapidlyunder alkaline conditions in soil, biodegradation of ferulic acid is not expected to be rapid.ANAEROBIC: Ferulic acid, present at 300 ppm in water, reached 86% of its theoretical degradation by conversion to CO2 in 24 days, employing a mixed inoculum obtained from sludge(1). Ferulic acid, present at 300 ppm in water, reached 98% of its theoretical degradation by CO2 production in 9 days, employing a mixed inoculum obtained from sludge(2), in which the medium had been acclimated with ferulic acid for 540 days. Degradation products detected were p-hydroxycinnamic acid, cinnamic acid, and phenylpropionic acid(2). Therefore, ferulic acid is expected to biodegrade rapidly in water under anaerobic conditions. |
| Sediment/Soil Concentrations | SEDIMEMT: Ferulic acid was detected in four out of four sediment samples collected from the Tama River (Japan), Yatsuse River (Japan), Lake Haruma (Japan) and Komgari Reservoir (Japan) on unknown dates at concentrations ranging from 6.5-22 ug/g dry sediment, with an average of 13 ug/g dry sediment(1)the source was likely from the detritus of vascular plants(1).SOIL: Ferulic acid was detected in one soil sample collected in Tokyo (Japan) between February 1976 and January 1978 at the concentration of 11 ug/g dry soil(1). |
| Environmental Bioconcentration | An estimated BCF of 3.2 was calculated in fish for ferulic acid, using a measured log Kow of 1.51 (1) and a regression-derived equation (2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organism is low(SRC), provided the compound is not metabolized by the organism(SRC). |
| Volatilization from Water/Soil | Ferulic acid, with a pKa of 4.58(1), will almost entirely exist in the anion form in the environment at pH values of 5 to 9, and therefore ferulic acid is expected to be essentially nonvolatile from water surfaces and moist soil(2). Ferulic acid is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 2.7X10-6 mm Hg(SRC), determined from a fragment constant method(3). |
| Non-Human Toxicity Excerpts | /LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ The modifying effects of dietary administration of the plant phenolic antioxidants caffeic acid (CA), ellagic acid (EA), chlorogenic acid (CGA) and ferulic acid (FA) during the initiation phase on 4-nitroquinoline-1-oxide (4-NQO)-induced tongue carcinogenesis and on the number and area of silver-stained nucleolar organizer region proteins (AgNORs), a new cell proliferation marker, of the tongue squamous epithelium were investigated in male F344 rats. Rats were fed the diet containing 500 ppm CA, 400 ppm EA, 250 ppm CGA or 500 ppm FA for 7 weeks. One week after the commencement of the diets, 4-NQO (20 p.p.m.) was administered in the drinking water for 5 weeks. Feeding of four phenolic compounds significantly reduced the incidences of tongue neoplasms (squamous cell papilloma and carcinoma) and preneoplastic lesions (hyperplasia and dysplasia) by 32 weeks, and rats fed CA or EA had no tongue neoplasms. The number and area of AgNORs per nucleus were decreased significantly by dietary treatment with these four phenolics. Thus, CA, EA, CGA and FA inhibited the tongue carcinogenesis induced by 4-NQO when they were administered concurrently with the carcinogen. These results might suggest possible application of these natural substances for cancer chemoprevention in tongue in addition to other tissues (skin, lung, liver and esophagus)./LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ Effects of ... on -induced oral carcinogenesis were examined in 4 groups of male rats. The incidences of tongue carcinomas and preneoplastic lesions (severe dysplasia) in rats of the group given ferulic acid (FA) in the diet at a dose of 500 ppm after exposure to 4-nitroquinoline-1-oxide (4NQO) for 5 weeks in drinking water at a dose of 20 ppm, was significantly lower on termination of the experiment (32 weeks) in the group with the carcinogen alone (P less than 0.005 and P less than 0.001 respectively). The results suggest chemopreventive activity for this phenolic compound on oral cancer./ALTERNATIVE and IN VITRO TESTS/ The modifying effects of dietary administration of the plant phenolic antioxidants caffeic acid (CA), ellagic acid (EA), chlorogenic acid (CGA) and ferulic acid (FA) during the initiation phase on 4-nitroquinoline-1-oxide (4-NQO)-induced tongue carcinogenesis and on the number and area of silver-stained nucleolar organizer region proteins (AgNORs), a new cell proliferation marker, of the tongue squamous epithelium were investigated in male F344 rats. Rats were fed the diet containing 500 ppm CA, 400 ppm EA, 250 ppm CGA or 500 ppm FA for 7 weeks. One week after the commencement of the diets, 4-NQO (20 p.p.m.) was administered in the drinking water for 5 weeks. Feeding of four phenolic compounds significantly reduced the incidences of tongue neoplasms (squamous cell papilloma and carcinoma) and preneoplastic lesions (hyperplasia and dysplasia) by 32 weeks, and rats fed CA or EA had no tongue neoplasms. The number and area of AgNORs per nucleus were decreased significantly by dietary treatment with these four phenolics. Thus, CA, EA, CGA and FA inhibited the tongue carcinogenesis induced by 4-NQO when they were administered concurrently with the carcinogen. These results might suggest possible application of these natural substances for cancer chemoprevention in tongue in addition to other tissues (skin, lung, liver and esophagus)./ALTERNATIVE and IN VITRO TESTS/ The ... study describes the protective effect of ferulic acid (FA), a naturally occurring nutritional compound on nicotine-induced DNA damage and cellular changes in cultured rat peripheral blood lymphocytes in comparison with N-acetylcysteine (NAC), a well-known antioxidant. One-hour exposure of lymphocytes to nicotine at the doses of 0.125, 0.25, 0.5, 1, 2, 3 and 4 mM induced a statistically significant dose-dependent increase in the levels of thiobarbituric acid reactive substances (TBARS), a lipid peroxidative marker and decrease in the levels of reduced glutathione (GSH), an important endogenous antioxidant. The lowest concentration eliciting significant damage was 1 mM nicotine and maximum damage was observed with 3 mM concentration. Hence, the test concentration was fixed at 3 mM nicotine. ... 5 different doses of FA (10, 50, 100, 150 and 300 uM) and NAC (0.25, 0.5, 1, 2 and 4 mM) /were used/ to test their protective effects. In all the groups, FA and NAC showed a dose-dependent inhibitory effect. Maximum protection was observed at the dose of 150 microM FA and 1mM NAC. So, 150 microM FA and 1mM NAC were used for further studies. There was a significant increase in the levels of lipid peroxidative index (TBARS and hydroperoxides (HP)), severity of DNA damage (evaluated by comet assay) in nicotine-treated group, which were significantly decreased in FA and NAC-treated groups. Nicotine treatment significantly decreased the endogenous antioxidant status viz., superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), GSH, vitamin A, E and C. Co-administration of FA and NAC to nicotine-treated lymphocytes showed a significant increase in the antioxidant status. The protective effect of FA was merely equal to that of NAC effect. FA and NAC treatment alone did not produce any toxicity to the normal lymphocytes at their effective doses. On the whole, there is overwhelming evidence that FA has the ability to modulateFor more Non-Human Toxicity Excerpts (Complete) data for FERULIC ACID (7 total), please visit the HSDB record page. |
| Signal word | Warning |
| GHS pictogram | GHS07 |
| GHS hazard statements | H317 |
| GHS precautionary statements | P261-P272-P280-P302+P352-P333+P313-P321-P363-P501 |
Applications & Uses
Uses
Piperazine ferulate is mainly used for various glomerular diseases with microscopic hematuria and hypercoagulability, such as nephritis, chronic nephritis, early uremia of nephrotic syndrome, coronary heart disease, cerebral infarction, vasculitis etc. adjuvant therapy.
Preparation & Synthesis
Preparation
Piperazine ferulate was prepared by reacting ethyl ferulate and isooctyl alcohol in prestence of p-toluenesulfonic acid as catalyst.