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PubMedDate not supplied

Effects of eugenol on excitation-contraction coupling in skeletal muscle.

The effects of eugenol on the excitation-contraction coupling of the toad (Bufo paracnemis) sartorius were studied. Eugenol (0.1-2.5 mM) blocked the contracture induced by 80 mM K+. At 2.5 mM, it decreased the depolarization, induced by 80 mM K+, by 14 mV. This is not sufficient to explain the complete blockade of the potassium contracture. At higher concentrations (3-12 mM), eugenol induced contractures, without causing a depolarization of the membrane. Contractures were blocked by procaine and potentiated by caffeine and by cooling of the muscle. For concentrations of eugenol in the upper range of the dose-response curve (10 mM), the contracture was independent of the Ca++ concentration in the medium. At lower concentrations (5 mM), the contractures induced by eugenol were potentiated by divalent cations, in the order: Mg++ < Ba++ < Zn++ < Co++ < Ca++ < Mn++. We infer that the eugenol-induced contractures are caused, primarily, by a release of Ca++ from the sarcoplasmic reticulum and, secondarily, by a mechanism related to the presence of some divalent cations in the extracellular space.

Animals↗

PubMed1996

Clinical and radiological evaluation of zinc oxide-eugenol and Maisto's paste as obturating materials in infected primary teeth--nine months study.

The present study, performed in-vivo, included 30 infected primary teeth in 26 children in the age group of 3-8 years. The purpose of this study was to compare the efficacy of two obturating materials, zinc oxide-eugenol and Maisto's paste, in infected primary teeth. 30 teeth were divided into two groups of 15 teeth. Teeth in Group I were obturated using zinc oxide-eugenol and those in Group II were obturated using Maisto's paste. On clinical evaluation, teeth obturated with Maisto's paste showed 100% success. Five teeth that were overfilled with Maisto's paste showed complete resorption of excess material within 3 months while the two teeth overfilled with zinc oxide-eugenol showed incomplete resorption of the excess material even after 9 months. Zinc oxide-eugenol treated cases showed only 26.7% bone regeneration while in case of Maisto's paste, it was 93%. Complete healing of the inter-radicular pathology was seen with Maisto's paste. However, the pathology was present in 40% of the zinc oxide-eugenol treated teeth even after 9 months. Maisto's paste was thus seen to be superior to zinc oxide-eugenol both in clinical as well as radiological evaluation, done over a period of 9 months in relation to bone regeneration, healing of inter-radicular pathology and resorption of excess material.

Abscess↗

PubMed1996

In vitro evaluation of the cytotoxicity of pure eugenol.

The aim of this study was to assess the cytotoxicity of pure eugenol in an in vitro method by diluting it to various concentrations in alcohol and determining the maximum noncytotoxic concentration. We used solutions of eugenol and ethyl alcohol that are soluble in water in any given proportion. The cytotoxicity of the alcohol itself was determined by using a dose-response curve for concentrations of between 0.017 M and 1.7 M. Various strength concentrations (0.015 to 947 microM) of eugenol in alcohol were prepared; 20 microliters (0.34 M) of ethyl alcohol was added to 1 ml of cell medium. The experiment showed that pure eugenol is toxic for human gingival fibroblasts. Eugenol in an alcohol solution at concentrations of < 1.9 microM is noncytotoxic.

Cell Survival↗

PubMed1988

In vivo and in vitro effects of zinc oxide-eugenol (ZOE) on biosynthesis of cyclo-oxygenase products in rat dental pulp.

To determine the in vivo effects of a zinc oxide-eugenol mixture (ZOE) on the cyclo-oxygenase system in dental pulp, we used radioimmunoassay to measure the levels of prostaglandin E2 (PGE2), 13,14-dihydro-15-keto-PG (DHK-PG), thromboxane B2 (TXB2), and 6-keto-PGF1 alpha in the dental pulp of rats. When the dental pulp was irritated by a hole made in the dentin of the mandibular incisors without use of any coolants, the levels of these cyclo-oxygenase products in the pulp were increased to, respectively, 2.8, 1.7, 10.0, and 2.6 times those in the normal pulp at six hr after treatment. In contrast, these increases in cyclo-oxygenase products disappeared immediately when the artificial cavity in the dentin was filled with ZOE (P/L; 1 g/0.25 mL), but were not altered when the cavity was filled with zinc oxidewater (ZOW, 1 g/1.5 mL). Most of the eugenol portion of ZOE was released into the pulp within two hr after the cavity was filled with ZOE. The maximal eugenol content was 35 pmol per mg of pulp. Furthermore, when the cavity was filled either with ZOE or by the addition of 10 mumol/L eugenol to the pulp homogenate, biosynthesis of 14C-6-keto-PGF1 alpha, PGF2 alpha, and PGE2 from 14C-arachidonic acid in the homogenate was inhibited. These results suggest that eugenol released from ZOE in the cavity prepared in the dentin inhibited the biosynthesis of cyclo-oxygenase products during pulp irritation.

Animals↗

PubMed2000

In vitro and in vivo activity of eugenol on human herpesvirus.

Eugenol (4-allyl-1-hydroxy-2-methoxybenzene) was tested for antiviral activity against HSV-1 and HSV-2 viruses. In vitro, it was found that the replication of these viruses was inhibited in the presence of this compound. Inhibitory concentration 50% values for the anti-HSV effects of eugenol were 25.6 microg/mL and 16.2 microg/mL for HSV-1 and HSV-2 respectively, 250 microg/mL being the maximum dose at which cytotoxicity was tested. Eugenol was virucidal and showed no cytotoxicity at the concentrations tested. Eugenol-acyclovir combinations synergistically inhibited herpesvirus replication in vitro. Topical application of eugenol delayed the development of herpesvirus induced keratitis in the mouse model.

Acyclovir↗

PubMed1994

Studies on the inhibitory effects of curcumin and eugenol on the formation of reactive oxygen species and the oxidation of ferrous iron.

The spice principles curcumin (from turmeric) and eugenol (from cloves) are good inhibitors of lipid peroxidation. Lipid peroxidation is known to be initiated by reactive oxygen species. The effect of curcumin and eugenol on the generation of reactive oxygen species in model systems were investigated. Both curcumin and eugenol inhibited superoxide anion generation in xanthine-xanthine oxidase system to an extent of 40% and 50% at concentrations of 75 microM and 250 microM respectively. Curcumin and eugenol also inhibited the generation of hydroxyl radicals (.OH) to an extent of 76% and 70% as measured by deoxyribose degradation. The .OH-radical formation measured by the hydroxylation of salicylate to 2,3-dihydroxy benzoate was inhibited to an extent of 66% and 46%, respectively, by curcumin and eugenol at 50 microM and 250 microM. These spice principles also prevented the oxidation of Fe2+ in Fentons reaction which generates .OH radicals.

Curcumin↗

PubMed1995

Effect of eugenol on drug-metabolizing enzymes of carbon tetrachloride-intoxicated rat liver.

The chemoprotection extended by eugenol against carbon tetrachloride (CCl4) intoxication was established by studies on drug-metabolizing phase I and phase II enzymes. An overall decrease in drug-metabolizing enzymes, namely NADPH-cytochrome c reductase, NADH-cytochrome reductase, coumarin hydroxylase, 7-ethoxy coumarin-O-deethylase, UDP-glucuronyltransferase and glutathione-S-transferase, was observed with CCl4 intoxication, with a subsequent decrease in cytochrome P450 and cytochrome b5 content. CCl4 caused a significant decrease in microsomal phospholipids and the marker enzymes glucose-6-phosphatase and 5'-nucleotidase, and an increase in thiobarbituric acid reactive substances (TBARS). Simultaneous administration of eugenol with CCl4 inhibited the accumulation of TBARS and the decrease in the microsomal phospholipids and marker enzymes. Further, the chemical onslaught imposed by CCl4 on the drug-metabolizing system was removed successfully by eugenol. Eugenol appears to act as an in vivo antioxidant and as a better inducer of phase II enzymes than phase I enzymes. It is therefore suggested that eugenol could be an interesting basic structure for drug design.

5'-Nucleotidase↗

PubMed1987

Eugenol: antipyretic activity in rabbits.

The analgesic agent eugenol reduced fever when given intravenously in small doses to rabbits made febrile by interleukin 1. To test this observation further, the drug was given intragastrically and its antipyretic effect was compared with that of a molar equivalent dose of acetaminophen. Eugenol was more effective in reducing fever than acetaminophen. Tests with intracerebroventricular injections indicated that eugenol could act centrally to reduce fever in doses much smaller than those which were effective peripherally. Other tests with the presumed fever mediators sodium archidonate and prostaglandin E2 (PGE2), suggest that the central action of eugenol is similar to that of acetaminophen. Eugenol, a derivative of clove oil, has marked antipyretic activity when given intravenously, intragastrically and centrally and may reduce fever primarily through a central action that is similar to that of common antipyretic drugs such as acetaminophen.

Acetaminophen↗

PubMed1995

Eugenol--an inhibitor of lipoxygenase-dependent lipid peroxidation.

The effect of eugenol on enzymatic lipid peroxidation catalyzed by soybean lipoxygenase was studied in an in vitro system. Lipid peroxidation was inhibited by eugenol in a concentration-dependent manner. The half-maximal inhibition (IC50) was found to be 380 microM eugenol. Enzyme kinetic studies showed that eugenol non-competitively inhibited lipid peroxidation by altering the maximum velocity (Vmax) and without any change in Michaelis-Menten constant (Km) values. The inhibitory mechanism implies that eugenol does not inactivate the enzyme directly but may interfere with fatty acid radical intermediates due to its hydroxy radical scavenging ability and thus play a role in inhibiting the propagation of lipid peroxidation.

Eugenol↗

PubMed2006

Transport of methyl eugenol-derived sex pheromonal components in the male fruit fly, Bactrocera dorsalis.

Males of Bactrocera dorsalis (Diptera: Tephritidae) are attracted strongly to and feed compulsively on methyl eugenol (1,2-dimethoxy- 4 -(2-propenyl)benzene), a highly potent male attractant. Pharmacophagy of methyl eugenol results in the production of phenylpropanoids 2-allyl-4,5-dimethoxyphenol and (E)-coniferyl alcohol that are sequestered and stored in the rectal gland prior to release as sex pheromonal components during mating at dusk. While these pheromonal components have also been detected in the hemolymph and crop of methyl eugenol-fed males, there is currently little information on the transport of these compounds from the crop to rectal gland in male B. dorsalis. Therefore, using physiological techniques such as parabiosis, rectal gland transplantation and hemolymph transfusion coupled with gas chromatography-mass spectrometry (GC-MS) analyses, we were able to ascertain and confirm the role of the hemolymph in the transport of these sex pheromonal components from the crop to the rectal gland. Further, the temporal profile of these methyl eugenol-derived bioactive compounds in the hemolymph also shows an increase with time post-methyl eugenol-feeding, i.e., 2-allyl-4,5-dimethoxyphenol attaining maximum amounts 15 min after ME consumption and decreasing thereafter, while for (E)-coniferyl alcohol-the increase and decrease are more gradual. These results further demonstrate the ability of insect hemolymph to transport many diverse forms of bioactive molecules including attractant-derived sex pheromonal components.

Animals↗

PubMed2006

Protective effects of eugenol against oxidized LDL-induced cytotoxicity and adhesion molecule expression in endothelial cells.

Eugenol, a natural constituent of a number of aromatic plants and their essential oil fractions, has several biological effects. However, its protective effects against endothelial injury remain unclarified. This study investigates how eugenol affects human umbilical vein endothelial cells (HUVECs) dysfunction mediated by oxidized low density lipoprotein (oxLDL). Our results showed that the suppression of endothelial NO synthase (eNOS) expression, enhancement of adhesion molecules (ICAM, VCAM, and E-selectin) expression, and adherence of monocytic THP1 cells caused by a non-cytotoxic concentration (100 microg/ml) of oxLDL were ameliorated following a eugenol treatment (12.5-100 microM) in HUVECs. Eugneol also inhibited the reactive oxygen species (ROS) generation, intracellular calcium accumulation, and the subsequent mitochondrial membrane potential collapse, cytochrome c release and caspase-3 activation induced by oxLDL. The cytotoxicity and apoptotic features induced by a cytotoxic concentration (200 microg/ml) of oxLDL was also attenuated by eugenol. Our results suggest that eugenol may protect against the oxLDL-induced dysfunction in endothelial cells.

Antioxidants↗

PubMed2005

Genotoxic effects of eugenol, isoeugenol and safrole in the wing spot test of Drosophila melanogaster.

In the present study, the phenolic compounds eugenol, isoeugenol and safrole were investigated for genotoxicity in the wing spot test of Drosophila melanogaster. The Drosophila wing somatic mutation and recombination test (SMART) provides a rapid means to evaluate agents able to induce gene mutations and chromosome aberrations, as well as rearrangements related to mitotic recombination. We applied the SMART in its standard version with normal bioactivation and in its variant with increased cytochrome P450-dependent biotransformation capacity. Eugenol and safrole produced a positive recombinagenic response only in the improved assay, which was related to a high CYP450-dependent activation capacity. This suggests, as previously reported, the involvement of this family of enzymes in the activation of eugenol and safrole rather than in its detoxification. On the contrary, isoeugenol was clearly non-genotoxic at the same millimolar concentrations as used for eugenol in both the crosses. The responsiveness of SMART assays to recombinagenic compounds, as well as the reactive metabolites from eugenol and safrole were considered responsible for the genotoxicity observed.

Animals↗

PubMed2003

Eugenol suppresses cyclooxygenase-2 expression in lipopolysaccharide-stimulated mouse macrophage RAW264.7 cells.

Inducible cyclooxygenase (COX-2) has been implicated in the processes of inflammation and carcinogenesis. Thus, the potential COX-2 inhibitors have been considered as anti-inflammatory or cancer chemopreventive agents. In this study, the methanolic extract of the cortex of Eugenia caryophyllata Thunberg (Myrtaceae) was found to potently inhibit the prostaglandin E(2) production in lipopolysaccharide (LPS)-activated mouse macrophage RAW264.7 cells (98.3% inhibition at the test concentration of 10 microg/ml). Further, hexane-soluble layer was the most active partition compared to ethyl acetate, n-butanol, and water-soluble parts. By bioassay-guided fractionation of hexane-soluble partition, eugenol was isolated and exhibited a significant inhibition of PGE(2) production (IC(50) = 0.37 microM). In addition, eugenol suppressed the cyclooxygenase-2 (COX-2) gene expression in LPS-stimulated mouse macrophage cells. On the line of COX-2 playing an important role in colon carcinogenesis further study was designed to investigate the effect of eugenol on the growth and COX-2 expression in HT-29 human colon cancer cells. Eugenol inhibited the proliferation of HT-29 cells and the mRNA expression of COX-2, but not COX-1. This result suggests that eugenol might be a plausible lead candidate for further developing the COX-2 inhibitor as an anti-inflammatory or cancer chemopreventive agent.

Animals↗

PubMed1996

Saturated and monofluoro analogs of the oriental fruit fly attractant methyl eugenol show reduced genotoxic activities in yeast.

Methyl eugenol, is a commercially used fruit fly attractant and a suspected carcinogen. Several phenylpropenes, including methyl eugenol and the known carcinogen safrole, score negative in the Salmonella assay but score positive in the yeast DEL assay that selects for intrachromosomal recombination events in the yeast Saccharomyces cerevisiae. In an attempt to dissociate the beneficial properties of methyl eugenol from its genotoxic properties, saturated or fluorinated analogs were evaluated for their ability to induce intrachromosomal (DEL) recombination in yeast. Field tests have previously shown that all of the analogs used have appreciable properties as fruit fly attractants. The analogs 1,2-dimethoxy-4-ethylbenzene, 1,2-dimethoxy-4-(2-fluoro-2-propenyl)benzene, 1,2-dimethoxy-4-(2-fluoroethyl)benzene and 1,2-dimethoxy-4-(3-fluoro-2-propenyl)benzene all showed reduced toxicity and reduced recombinagenicity in yeast compared to methyl eugenol. These results confirm the validity of fluorination and/or removal of the 2-propenyl moiety in reducing the toxicity and recombinagenicity of methyl eugenol derivatives.

Animals↗

PubMed2001

Anti-genotoxicity of trans-anethole and eugenol in mice.

The naturally occurring flavouring agents trans-anethole and eugenol were evaluated for antigenotoxic effects in mice. The test doses of trans-anethole (40-400 mg/kg body weight) and eugenol (50-500 mg/kg weight) were administered by gavage 2 and 20 h before the genotoxins were injected intraperitoneally. Anti-genotoxic effects were assessed in the mouse bone marrow micronucleus test. Pretreatment with trans-anethole and eugenol led to significant antigenotoxic effects against cyclophosphamide (CPH), procarbazine (PCB), N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and urethane (URE). In addition, trans-anethole inhibited the genotoxicity of ethyl methane sulfonate (EMS). Both trans-anethole and eugenol exerted dose-related antigenotoxic effects against PCB and URE. There was no significant increase in genotoxicity when trans-anethole (40-400 mg/kg body weight) and eugenol (50-500 mg/kg body weight) were administered alone.

Allylbenzene Derivatives↗

PubMed2002

Safety assessment of allylalkoxybenzene derivatives used as flavouring substances - methyl eugenol and estragole.

This publication is the seventh in a series of safety evaluations performed by the Expert Panel of the Flavor and Extract Manufacturers' Association (FEMA). In 1993, the Panel initiated a comprehensive program to re-evaluate the safety of more than 1700 GRAS flavouring substances under conditions of intended use. In this review, scientific data relevant to the safety evaluation of the allylalkoxybenzene derivatives methyl eugenol and estragole is critically evaluated by the FEMA Expert Panel. The hazard determination uses a mechanism-based approach in which production of the hepatotoxic sulfate conjugate of the 1'-hydroxy metabolite is used to interpret the pathological changes observed in different species of laboratory rodents in chronic and subchronic studies. In the risk evaluation, the effect of dose and metabolic activation on the production of the 1'-hydroxy metabolite in humans and laboratory animals is compared to assess the risk to humans from use of methyl eugenol and estragole as naturally occurring components of a traditional diet and as added flavouring substances. Both the qualitative and quantitative aspects of the molecular disposition of methyl eugenol and estragole and their associated toxicological sequelae have been relatively well defined from mammalian studies. Several studies have clearly established that the profiles of metabolism, metabolic activation, and covalent binding are dose dependent and that the relative importance diminishes markedly at low levels of exposure (i.e. these events are not linear with respect to dose). In particular, rodent studies show that these events are minimal probably in the dose range of 1-10 mg/kg body weight, which is approximately 100-1000 times the anticipated human exposure to these substances. For these reasons it is concluded that present exposure to methyl eugenol and estragole resulting from consumption of food, mainly spices and added as such, does not pose a significant cancer risk. Nevertheless, further studies are needed to define both the nature and implications of the dose-response curve in rats at low levels of exposure to methyl eugenol and estragole.

Animals↗

PubMed1990

Sensitive high-performance liquid chromatographic assay for the determination of eugenol in body fluids.

The high-performance liquid chromatographic assay described permitted a simple, rapid, sensitive, selective and precise quantitative determination of eugenol in body fluids (serum, urine and bile) without derivatization. Amounts in the range 0.02-100 micrograms of eugenol per millilitre of body fluid were determined with intra-assay coefficients of variation below 4% (3.72-1.13%). The short analysis time for each sample and the selectivity even at low concentrations made this assay suitable for pharmacokinetic studies. Eugenol undergoes a pronounced first-pass effect; in serum, unconjugated eugenol was not detected after an oral dose of 150 mg. The kinetics of eugenol conjugates were measured. More than 80% of the dose was excreted within 6 h after oral administration.

Adult↗

PubMed1997

Skin sensitization to eugenol and isoeugenol in mice: possible metabolic pathways involving ortho-quinone and quinone methide intermediates.

With the aim of providing further mechanistic insights into the mode of action of eugenol (4-allyl-2-methoxyphenol) and isoeugenol (4-propenyl-2-methoxyphenol), we have synthesized two series of modified compounds which were tested in the mouse local lymph node assay for their skin sensitizing potential. The replacement of the methoxy group by an isopropoxy group led to a complete loss of sensitization for the eugenol derivative 6a, while no significant effect was observed for the isoeugenol derivative 6b. In the eugenol series, when methyl groups were present in the 3-, 5-, or 6-position a significant reduction in sensitization potential was observed while in the isoeugenol series only methyl substitution in the 3- and 5-position had a discernable effect. Introduction of three methyl groups on the aromatic ring of eugenol (3,5,6-trimethyl-4-allyl-2-methoxyphenol, 7) and of a tert-butyl substituent at the gamma-position of the alkyl chain of isoeugenol (4-[3',3',3'-trimethylpropenyl]-2-methoxyphenol, 8) led to a strong decrease of the sensitizing capacity. Our findings indicate that, at least in the mouse, eugenol could sensitize via a demethylation pathway followed by oxidation to the o-quinone which could act directly as a hapten even if we cannot exclude a reaction via its tautomeric p-quinone methide. Isoeugenol, on the other hand, could act via a mechanism not involving demethylation and for which the evidence is consistent with a direct oxidation to the p-quinone methide.

Animals↗