SEARCH · Search PubMed

Results for “Allyl Compounds”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 343 records · Page 19Linked to original sources

PubMed1993

Growth inhibition and modulation of cell markers of melanoma by S-allyl cysteine.

A sulfur-containing amino acid compound, S-allyl cysteine (SAC), derived from garlic extract inhibited proliferation of nine human and murine melanoma cell line in a dose-dependent manner (1.2-10 mM) assessed by a [3H]thymidine incorporation assay. Three control human lymphoblastoid cell lines were not inhibited by SAC concentrations < 5 mM. Four human melanoma cell lines in a soft-agar assay also showed dose-dependent inhibition of colony formation by SAC. Melanin content was increased up to 95% compared to the same untreated cell lines in these four human melanoma and two B16 murine melanoma sublines. Expression of cell surface gangliosides, cellular-differentiation and transformation markers, decreased after SAC treatment. Significant morphological changes including 'flattening and/or dendritic-like elongations' were also observed. Thus SAC inhibited cellular growth and proliferation and modulated major cell differentiation markers of melanoma.

Animals↗

PubMed2006

Down-regulation of P-glycoprotein expression in MDR breast cancer cell MCF-7/ADR by honokiol.

P-glycoprotein accounts for the most intrinsic and acquired cancer multidrug resistance. To inhibit the expression of P-glycoprotein is one of the effective ways to reverse cancer drug resistance. Honokiol, a naturally occurring compound, has been demonstrated to combat cancer through mechanisms including inhibition of angiogenesis and induction of apoptosis. Here, we show that honokiol down-regulated the expression of P-glycoprotein at mRNA and protein levels in MCF-7/ADR, a human breast MDR cancer cell line. The down-regulation of P-glycoprotein was accompanied with a partial recovery of the intracellular drug accumulation, and of the sensitivities toward adriamycin. This study reveals a novel function of honokiol as an anti-cancer agent.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

PubMed2005

Honokiol overcomes conventional drug resistance in human multiple myeloma by induction of caspase-dependent and -independent apoptosis.

Honokiol (HNK) is an active component purified from magnolia, a plant used in traditional Chinese and Japanese medicine. Here we show that HNK significantly induces cytotoxicity in human multiple myeloma (MM) cell lines and tumor cells from patients with relapsed refractory MM. Neither coculture with bone marrow stromal cells nor cytokines (interleukin-6 and insulin-like growth factor-1) protect against HNK-induced cytotoxicity. Although activation of caspases 3, 7, 8, and 9 is triggered by HNK, the pan-caspase inhibitor z-VAD-fmk does not abrogate HNK-induced apoptosis. Importantly, release of an executioner of caspase-independent apoptosis, apoptosis-inducing factor (AIF), from mitochondria is induced by HNK treatment. HNK induces apoptosis in the SU-DHL4 cell line, which has low levels of caspase 3 and 8 associated with resistance to both conventional and novel drugs. These results suggest that HNK induces apoptosis via both caspase-dependent and -independent pathways. Furthermore, HNK enhances MM cell cytotoxicity and apoptosis induced by bortezomib. In addition to its direct cytotoxicity to MM cells, HNK also represses tube formation by endothelial cells, suggesting that HNK inhibits neovascurization in the bone marrow microenvironment. Taken together, our results provide the preclinical rationale for clinical protocols of HNK to improve patient outcome in MM.

Antineoplastic Agents, Phytogenic↗

PubMed2005

Differential inhibitory effects of honokiol and magnolol on excitatory amino acid-evoked cation signals and NMDA-induced seizures.

The effects of honokiol and magnolol, two major bioactive constituents of the bark of Magnolia officinalis, on Ca(2+) and Na(+) influx induced by various stimulants were investigated in cultured rat cerebellar granule cells by single-cell fura-2 or SBFI microfluorimetry. Honokiol and magnolol blocked the glutamate- and KCl-evoked Ca(2+) influx with similar potency and efficacy, but did not affect KCl-evoked Na(+) influx. However, honokiol was more specific for blocking NMDA-induced Ca(2+) influx, whereas magnolol influenced with both NMDA- and non-NMDA activated Ca(2+) and Na(+) influx. Moreover, the anti-convulsant effects of these two compounds on NMDA-induced seizures were also evaluated. After honokiol or magnolol (1 and 5 mg/kg, i.p.) pretreatment, the seizure thresholds of NMRI mice were determined by tail-vein infusion of NMDA (10 mg/ml). Data showed that both honokiol and magnolol significantly increased the NMDA-induced seizure thresholds, and honokiol was more potent than magnolol. These results demonstrated that magnolol and honokiol have differential effects on NMDA and non-NMDA receptors, suggesting that the distinct therapeutic applications of these two compounds for neuroprotection should be considered.

Analysis of Variance↗

PubMed2005

The natural product honokiol induces caspase-dependent apoptosis in B-cell chronic lymphocytic leukemia (B-CLL) cells.

B-cell chronic lymphocytic leukemia (B-CLL) remains an incurable disease that requires innovative new approaches to improve therapeutic outcome. Honokiol is a natural product known to possess potent antineoplastic and antiangiogenic properties. We examined whether honokiol can overcome apoptotic resistance in primary tumor cells derived from B-CLL patients. Honokiol induced caspase-dependent cell death in all of the B-CLL cells examined and was more toxic toward B-CLL cells than to normal mononuclear cells, suggesting greater susceptibility of the malignant cells. Honokiol-induced apoptosis was characterized by the activation of caspase-3, -8, and -9 and cleavage of poly(adenosine diphosphate-ribose) polymerase (PARP). Exposure of B-CLL cells to honokiol resulted in up-regulation of Bcl2-associated protein (Bax) and down-regulation of the expression of the key survival protein myeloid-cell leukemia sequence 1 (Mcl-1), which is associated with response to treatment in B-CLL patients. In addition, B-CLL cells pretreated with interleukin-4 (IL-4), a cytokine known to support B-CLL survival, underwent apoptosis when subsequently incubated with honokiol, indicating that honokiol could also overcome the prosurvival effects of IL-4. Furthermore, honokiol enhanced cytotoxicity induced by fludarabine, cladribine, or chlorambucil. These data indicate that honokiol is a potent inducer of apoptosis in B-CLL cells and should be examined for further clinical application either as a single agent or in combination with other anticancer agents.

Antineoplastic Agents↗

PubMed1994

Enhancement by organosulfur compounds from garlic and onions of diethylnitrosamine-induced glutathione S-transferase positive foci in the rat liver.

Ten organosulfur compounds from garlic and onions were studied for their modifying effects on diethylnitrosamine-induced neoplasia of liver in male F344 rats using the medium-term bioassay system of Ito based on the two-step model of hepatocarcinogenesis. Carcinogenic potential was scored by comparing the number and area per cm2 of induced glutathione S-transferase placental form-positive foci in the liver with those of the corresponding control group given diethylnitrosamine alone. In experiments 1 and 2, high doses of diallyl sulfide, diallyl trisulfide, allyl methyl sulfide, allyl methyl trisulfide, and dipropyl sulfide had enhancing effects on focus formation. In contrast, high doses of methyl propyl disulfide and propylene sulfide significantly decreased the number of glutathione S-transferase placental form-positive foci. In the third experiment, combined treatment with the five chemicals that had enhancing activity were fed at low doses and increased the induction of glutathione S-transferase placental form-positive foci. To investigate the mechanism of the modifying effect on hepatocarcinogenesis, ornithine decarboxylase activity was measured in diallyl sulfide-, allyl methyl sulfide-, and dipropyl sulfide-treated liver tissue without prior initiation with diethylnitrosamine, and its activity was increased compared to controls. Spermidine/spermine N1-acetyltransferase activity was not significantly changed. Formation of 8-hydroxydeoxyguanosine, a DNA adduct generated by activated oxygen species, and lipid peroxidation (2-thiobarbituric acid-reacting substance production) were also not changed. These results suggest that the promoting effect could be caused by increased cell proliferation with increased polyamine biosynthesis. In evaluating relationships between diet and cancer, it is appropriate to consider not only the possible protective role of garlic and onions but also their enhancing effects.

Allium↗

PubMed1990

A double-blind, placebo-controlled study of the tolerability and effects on platelet MAO-B activity of single oral doses of MDL 72.974A in normal volunteers.

MDL 72.974A [(E) 4-fluoro-beta-fluorethylene benzene butanamine] has been shown in animal studies, both in vitro and in vivo, to be a potent, selective, enzyme-activated irreversible inhibitor of MAO-B (Zreika et al., 1989). This compound is under clinical development for the treatment of Parkinson's disease. In this double blind, randomized, placebo-controlled normal volunteer study the tolerability, effects on platelet MAO-B activity and associated pharmacokinetics of increasing single oral doses of MDL 72.974A (0.1-12 mg) were assessed. MDL 72.974A was extremely well tolerated and no treatment-related changes in vital signs or the adjectival check-list (EWL-N) occurred. The compound caused significant dose-dependent inhibition of platelet MAO-B activity at all dose levels with a return to baseline values by day 14. The mean (+/- S.D.) elimination half-life of parent compound was 51 +/- 26 min and mean (+/- S.D.) urinary excretion was 0.54 +/- 0.26% of the administered dose. These results, long action on platelet MAO-B and short elimination half-life, demonstrate MDL 72.974A to be a potent, irreversible inhibitor of MAO-B in man.

Adult↗

PubMed2004

Mononuclear, five-coordinate lanthanide amido and aryloxide complexes bearing tetradentate (N2O2) Schiff bases.

Two monomeric, five-coordinate lanthanide complexes, [bis-5,5'-(1,3-propanediyldiimino)-2,2-dimethyl-4-hexene-3-onato]samarium[2,6-bis(tert-butyl)-4-methylphenoxide] and [bis-5,5'-(1,3-propanediyldiimino)-2,2-dimethyl-4-hexene-3-onato]erbium[2,6-bis(tert-butyl)-4-methylphenoxide], were isolated from the reactions of 2,6-bis(tert-butyl)-4-methylphenol with [bis-5,5'-(1,3-propanediyldiimino)-2,2-dimethyl-4-hexene-3-onato]lanthanide[bis(trimethylsilyl)amido] (lanthanide = Er(3+) and Sm(3+)). The purified phenoxides were recovered in excellent yields and analytical purity, and the reactions proceeded cleanly without Schiff-base degradation or cluster formation. Analogously, [bis-3,3'-(1,3-propanediyldiimino)-1-phenyl-2-butene-1-onato]erbium[bis(trimethylsilyl)amido] was also directly converted to [bis-3,3'-(1,3-propanediyldiimino)-1-phenyl-2-butene-1-onato]erbium[2,6-bis(tert-butyl)-4-methylphenoxide]; however, a less sterically demanding alcohol (i.e., ethanol) yielded a neutral trinuclear oxo alkoxide species with each dianionic Schiff base asymmetrically bridging through micro-oxo interactions. In this polynuclear cluster, each symmetry-related, seven-coordinate erbium(III) ion exhibits monocapped trigonal prismatic geometry, which assembles by sharing triangular capped faces. Single-crystal X-ray diffraction revealed square-pyramidal metal coordination in each five-coordinate lanthanide ion with varied S(4) ruffling of the "square base" donor atoms and the six-membered propylene diamine chelate ring adopting the boat conformation. To contrast the effect of subtle ligand changes, we also report the synthesis and characterization of [bis-5,5'-(2,2-dimethyl-1,3-propanediyldiimino)-2,2-dimethyl-4-hexene-3-onato]samarium[bis(trimethylsilyl)amido], having gem-dimethyl substituents appended to the propylene bridge central carbon. The six-membered diamine chelate ring in this compound adopts the chair conformation without metal-hydrocarbon interaction. Also presented are qualitative activity observations and polymerization data for the polymerization of rac-lactide and epsilon-caprolactone using the five-coordinate lanthanide amidos and phenoxides.

Allyl Compounds↗

PubMed2003

Honokiol protects rat brain from focal cerebral ischemia-reperfusion injury by inhibiting neutrophil infiltration and reactive oxygen species production.

We have previously shown that honokiol, an active component of Magnolia officinalis, displayed protective effect against focal cerebral ischemia-reperfusion (FCI/R) injury in rats. Production of reactive oxygen species (ROS) and infiltration of neutrophils to injured tissue play deleterious roles during cerebral ischemia. To study the mechanism(s) in mediating neuroprotective effect of honokiol, FCI/R-induced neutrophil infiltration and lipid peroxidation in brain tissue, and activation of neutrophils in-vitro were examined. Intravenous administration of honokiol (0.01-1.0 microg/kg) 15 min before (pretreatment) or 60 min after (post-treatment) middle cerebral artery occlusion reduced the total infarcted volume by 20-70% in dose-dependent manner. Pretreatment or post-treatment of honokiol at concentration of 0.1 and 1.0 microg/kg significantly decreased the neutrophil infiltration in the infarcted brain. Time course of neutrophil infiltration was performed in parallel with the lipid peroxidation in infracted brain tissue during FCI/R injury. The results indicate that honokiol can protect brain tissue against lipid peroxidation and neutrophil infiltration during FCI/R injury and cerebral infarction induced by FCI/R is accompanied with a prominent neutrophil infiltration to the infarcted area during FCI/R course. In-vitro, honokiol (0.1-10 microM) significantly diminished fMLP (N-formyl-methionyl-leucyl-phenylalanine)- or PMA (phorbol-12-myristate-13-acetate)-induced neutrophil firm adhesion, a prerequisite step behind neutrophil infiltration, and ROS production in neutrophils. Intracellular calcium overloading activates calcium-stimulated enzymes and further exaggerates FCI/R injury. Honokiol (0.1-10 microM) impeded the calcium influx induced by fMLP (a receptor agonist), AlF(4)(-) (a G-protein activator) or thapsigargin (an intracellular calcium pool releaser). Therefore, we conclude that the amelioration of FCI/R injury by honokiol can be attributed to its anti-oxidative and anti-inflammatory actions through, at least in part, limiting lipid peroxidation and reducing neutrophil activation/infiltration by interfering firm adhesion, ROS production, and calcium overloading that may be primed/activated during FCI/R injury.

Animals↗

PubMed2002

A model system study of the inhibition of heterocyclic aromatic amine formation by organosulfur compounds.

Organosulfur compounds and sodium bisulfite significantly inhibited (P < 0.05) heterocyclic aromatic amine (HAA) formation in model systems containing phenylalanine, creatinine, and glucose. There was, however, no inhibition by the same compounds in a model system containing only phenylalanine and creatinine. Diallyl disulfide (DAD) and dipropyl disulfide (DPD) concentrations in the model systems were significantly decreased (P < 0.05) after heating for 10 min at 180 degrees C. Only very low concentrations of sulfhydryl groups (4.19 and 4.00 micromol) were produced on heating DAD and DPD for 30 min. Reaction of glucose and DAD produced several sulfur-containing compounds. After 10 min of heating at 180 degrees C, HAA formation in the control model systems was increased significantly, and DAD was an effective inhibitor during this heating period. Tetrahydrothiophene-3-one (THT) and tetrahydrothiophene (THP); two products resulting from the interaction of glucose and DAD, had no direct influence on HAA formation in the model systems.

Allyl Compounds↗

PubMed1996

Diallyl disulfide suppresses the growth of human colon tumor cell xenografts in athymic nude mice.

The present studies examined the anti-proliferative effects of diallyl disulfide (DADS) on the growth of human colon tumor cell line, HCT-15, xenografts in 6-wk-old female NCr nu/nu mice with an initial body weight of 20-22 g. Intraperitoneal injection of 1 mg DADS thrice weekly reduced tumor volume by 69% (P < 0.05) without apparent ill consequences such as altered growth of the host. Providing this quantity of DADS intragastrically also inhibited growth of the HCT-15 tumor. At equivalent DADS dosages, intraperitoneal treatment was proportionately more effective (P < 0.05) in reducing tumor growth than gastric intubation. Tumor inhibition caused by DADS (0.5 mg thrice weekly) was similar to that occurring with 5-fluorouracil (5-FU) treatment (0.5 mg thrice weekly). Combining DADS and 5-FU was no more effective in inhibiting tumor growth than using either compound alone. However, concurrent DADS treatment significantly (P < 0.05) inhibited the depression in leukocyte counts and spleen weight and prevented the elevated plasma urea caused by 5-FU treatment. These data suggest that DADS, a constituent of garlic oil, reduces the toxicity of 5-FU and is an effective antitumorigenic agent against xenografts resulting from an established human colon tumor cell line.

Administration, Oral↗

PubMed2005

Honokiol inhibits TNF-alpha-stimulated NF-kappaB activation and NF-kappaB-regulated gene expression through suppression of IKK activation.

Honokiol, a small molecular weight lignan originally isolated from Magnolia officinalis, shows anti-angiogenic, anti-invasive and anti-proliferative activities in a variety of cancers. In this study, we investigated whether honokiol affects the transcription factor nuclear factor-kappa B (NF-kappaB) which controls a large number of genes involved in angiogenesis, metastasis and cell survival. We observed that the tumor necrosis factor-alpha (TNF-alpha)-induced NF-kappaB activation was blocked by honokiol in four different cancer cell lines as evidenced by EMSA. Honokiol did not directly affect the NF-kappaB-DNA binding. Immunoblot experiments demonstrated that honokiol inhibited the TNF-alpha-stimulated phosphorylation and degradation of the cytosolic NF-kappaB inhibitor IkappaBalpha. Furthermore, honokiol suppressed the intrinsic and TNF-alpha-stimulated upstream IkappaB kinases (IKKs) activities measured by a non-radioactive kinase assay using immunoprecipitated IKKs, suggesting a critical role of honokiol in abrogating the phosphorylation and degradation of IkappaBalpha. In a HeLa cell NF-kappaB-dependent luciferase reporter system, honokiol suppressed luciferase expression stimulated by TNF-alpha and by the transient transfection and expression of NIK (NF-kappaB-inducing kinase), wild type IKKbeta, constitutively active IKKalpha and IKKbeta, or the p65 subunit. Honokiol was also found to inhibit the nuclear translocation and phosphorylation of p65 subunit of NF-kappaB. RT-PCR results showed that honokiol suppressed NF-kappaB-regulated inflammatory and carcinogenic gene products including MMP-9, TNF-alpha, IL-8, ICAM-1 and MCP-1. In line with the observation that NF-kappaB activation may up-regulate anti-apoptotic genes, it was shown that honokiol enhanced TNF-alpha-induced apoptotic cell death. In summary, our results demonstrate that honokiol suppresses NF-kappaB activation and NF-kappaB-regulated gene expression through the inhibition of IKKs, which provides a possible mechanism for its anti-tumor actions.

Antineoplastic Agents↗

PubMed1976

Metabolism of progesterone in uterine tissue of non-pregnant rats in vitro.

The metabolism of labelled progesterone was studied in vitro in uterine tissue of non-pregnant rats with particular emphasis on the influence of substrate concentration. Neither a qualitative nor quantitative difference was found for a steroid tissue ratio between 15 X 10(-6) and 4.2 X 10(-9) to 1 g (substrate amounts between 57.73 and 0.02 nmol); with both concentrations 42 to 44 per cent of progesterone was metabolized to about 35 per cent monohydroxymonoketonic steroids and 4-6 per cent dihydroxylated C21O2-compounds. In both sets of incubations we have isolated and identified the following steroids: 3alpha-hydroxy-5alpha-pregnan-20-one, 3beta-hydroxy-4-pregnen-20-one, 3alpha-hydroxy-4-pregnen-20-one, 20alpha-hydroxy-4-pregnen-3-one, 5alpha-pregnane-3alpha,20alpha-diol and 4-pregnene-3alpha,20alpha-diol. The most abundant metabolite formed in these incubations was 3alpha-hydroxy-4-pregnen-20-one which corresponds to about 30 per cent of the total activity recovered. It is the first time that the presence of 20alpha-hydroxysteroid-oxidoreductase activity is definitely established in this type of tissue. The identification of three allylic alcohols as progesterone metabolites in the rat uterus confirms that delta4-3-hydroxysteroids are important intermediates in the in vitro uterine metabolism of steroids.

20-alpha-Dihydroprogesterone↗

PubMed2003

Induction of multidrug resistance protein 3 in rat liver is associated with altered vectorial excretion of acetaminophen metabolites.

Treatment with the microsomal enzyme inducer trans-stilbene oxide (TSO) can decrease biliary excretion of acetaminophen-glucuronide (AA-GLUC) and increase efflux of AA-GLUC into blood. The hepatic canalicular multidrug resistance protein (Mrp) 2 and sinusoidal protein Mrp3 transport AA-GLUC conjugates into bile and blood, respectively. Thus, TSO-induced alterations in the vectorial excretion of AA-GLUC may occur via increased hepatic Mrp3 levels. The goal of this study was to determine whether TSO, diallyl sulfide (DAS), and oltipraz (OLT) treatments can up-regulate Mrp3 protein expression, and whether treatment with DAS and OLT can correspondingly increase hepatovascular efflux of AA metabolites. Rats were administered phenobarbital, TSO, DAS, OLT, or vehicle for 4 days. Interestingly, all of the chemicals increased the plasma concentration and urinary excretion of AA-GLUC and decreased its biliary excretion. In control animals, approximately 77% and 23% of AA-GLUC was excreted into bile or urine, respectively, whereas with inducer-pretreated animals, <32% of AA-GLUC was excreted into bile and >68% was excreted into urine. Correspondingly, all of the compounds increased hepatic Mrp3 mRNA levels by 13- to 37-fold and protein levels by 2- to 6-fold, respectively. In conclusion, these studies correlate increased Mrp3 protein levels in liver with increased hepatovascular excretion of AA-GLUC and suggest that induction of Mrp3 affects the route of drug excretion.

ATP Binding Cassette Transporter, Subfamily B↗

PubMed2003

Biofactors in the Mediterranean diet.

This Review covers the sources and the main effects on human health of well-known micronutrients such as minerals and vitamins and also of microconstituents contained in the Mediterranean diet. Vitamins were first identified because of deficiency diseases still present in certain parts of the world. Hydrosoluble vitamins, among them folic acid and vitamin C, also play a role in chronic degenerative diseases, not only the main cause of mortality in the Western world but also increasingly common in developing countries. Hydrosoluble vitamins are well represented in the Mediterranean diet, more so than vitamin A, a liposoluble vitamin obtained primarily from animal foods. Vitamin E is important for antioxidant and cellular functions. The Mediterranean diet is also rich in provitamins A, such as alpha- and beta-carotene and beta-cryptoxanthine. Microconstituents are non-nutritional compounds known to protect plants and more recently suspected to have a protective effect in humans. They play a role in the antioxidant defense of the organism, but their effect on various enzyme activities appears even more promising and is still under investigation. It is nevertheless difficult to isolate the effect of the numerous biofactors present in the Mediterranean diet from the foods themselves, especially because of the possible synergy between the various biofactors.

Allyl Compounds↗

PubMed1998

Effects of oil-soluble organosulfur compounds from garlic on doxorubicin-induced lipid peroxidation.

Clinical efficacy of doxorubicin is compromised due to free radical generation leading to cardiac toxicity. Oil-soluble organosulfur compounds, diallyl sulfide (DAS), diallyl disulfide (DADS), dipropyl sulfide (DPS) and dipropyl disulfide (DPDS), present in garlic were examined for their antiperoxidant effects. DADS inhibited liver microsomal lipid peroxidation induced by NADPH, ascorbate and doxorubicin. DAS, DPS and DPDS were ineffective inhibitors of liver microsomal lipid peroxidation. DADS could be used in combination with doxorubicin to protect oxidative injuries to improve the clinical efficacy of doxorubicin.

Allyl Compounds↗

PubMed2006

Phytochemistry and antifungal properties of the newly discovered tree Pleodendron costaricense.

Gas chromatography analysis of the essential oils of leaves and bark collected from the newly discovered tree Pleodendron costaricense identified alpha-pinene, beta-pinene, beta-myrcene, beta-thujene, and beta-caryophyllene as their major constituents. Phytochemical analysis of P. costaricense parts led to the isolation and identification of delta-tocotrienol, beta-sitosterol, four known drimane-type sesquiterpenes, cinnamodial (1), cinnamosmolide (2), polygodial (3), and mukaadial (4), and two new compounds, a drimane-type sesquiterpene, parritadial (5), and an eremophilane-type sesquiterpene, pleodendione (6). Antifungal assays with the two major compounds, 1 and 2, were carried out, and results showed a high activity of 1 against Alternaria alternata (MIC = 3.9 microg/mL), Candida albicans azole-resistant strain D10, and Wangiella dermatitides (MICs = 15.6 microg/mL). Compound 2 showed less potent antifungal activities than 1 but was more effective against Candida albicans azole-resistant strain CN1A (MIC = 23.4 microg/mL) and Pseudallescheria boydii (MIC = 78.1 microg/mL). A combination of the dialdehyde sesquiterpenes with dillapiol showed a synergistic antifungal effect with 1 and an additive effect with 4 and 5.

Allyl Compounds↗

PubMed2006

Diallylsulfide and allylmethylsulfide are uniquely effective among organosulfur compounds in inhibiting CYP2E1 protein in animal models.

Garlic is a popular culinary herb that is also used throughout the world as a traditional medicine for the prevention and treatment of disease. Epidemiologic studies have suggested that long-term consumption of garlic reduces risk for certain cancers, most notably stomach and colon cancer. This article summarizes the key findings behind one important mechanism explaining the anticarcinogenic effects of garlic-derived agents in animal models: the inhibition of cytochrome p4502E1 (CYP2E1), with some commentary on other aspects of carcinogen metabolism modified by these unique phytochemicals.

Allyl Compounds↗