Probiotic potential and wound-healing activity of Pediococcus pentosaceus strain AF2 isolated from Herniaria glabra L. which is traditionally used to make yogurt.

Probiotics have been a part of our lives for centuries, primarily through fermented foods. They find applications in various fields such as food, healthcare, and agriculture. Nowadays, their utilization is expanding, highlighting the importance of discovering new bacterial strains with probiotic properties suitable for diverse applications. In this study, our aim was to isolate new probiotic bacteria. Herniaria glabra L., a plant traditionally used for yogurt making in some regions and recognized in official medicine in many countries, was chosen as the source for obtaining probiotic bacteria. We conducted bacterial isolation from the plant, molecularly identified the isolated bacteria using 16S rRNA sequencing, characterized their probiotic properties, and assessed their wound-healing effects. As a result of these studies, we identified the bacterium isolated from the plant as Pediococcus pentosaceus strain AF2. We found that the strain AF2 exhibited high resistance to conditions within the gastrointestinal tract. Our reliability analysis showed that the isolate had γ-hemolytic activity and displayed sensitivity to certain tested antibiotics. At the same time, AF2 did not show gelatinase and DNase activity. We observed that the strain AF2 produced metabolites with inhibitory activity against E. coli, B. subtilis, P. vulgaris, S. typhimurium, P. aeruginosa, K. pneumoniae, E. cloacae, and Y. pseudotuberculosis. The auto-aggregation value of the strain AF2 was calculated at 73.44%. Coaggregation values against E. coli and L. monocytogenes bacteria were determined to be 56.8% and 57.38%, respectively. Finally, we tested the wound-healing effect of the strain AF2 with cell culture studies and found that the strain AF2 promoted wound healing.

Activation function 1 of progesterone receptor is required for progesterone antagonism of oestrogen action in the uterus.

BACKGROUND: Progesterone receptor (PGR) is a master regulator of uterine function through antagonistic and synergistic interplays with oestrogen receptors. PGR action is primarily mediated by activation functions AF1 and AF2, but their physiological significance is unknown. RESULTS: We report the first study of AF1 function in mice. The AF1 mutant mice are infertile with impaired implantation and decidualization. This is associated with a delay in the cessation of epithelial proliferation and in the initiation of stromal proliferation at preimplantation. Despite tissue selective effect on PGR target genes, AF1 mutations caused global loss of the antioestrogenic activity of progesterone in both pregnant and ovariectomized models. Importantly, the study provides evidence that PGR can exert an antioestrogenic effect by genomic inhibition of Esr1 and Greb1 expression. ChIP-Seq data mining reveals intermingled PGR and ESR1 binding on Esr1 and Greb1 gene enhancers. Chromatin conformation analysis shows reduced interactions in these genes' loci in the mutant, coinciding with their upregulations. CONCLUSION: AF1 mediates genomic inhibition of ESR1 action globally whilst it also has tissue-selective effect on PGR target genes.

Mitigative Potential of Novel Lactobacillus plantarum TISTR 2076 against the Aflatoxins-Associated Oxidative Stress and Histopathological Alterations in Liver and Kidney of Broiler Chicks during the Entire Growth Period.

Aflatoxins are the secondary metabolites produced by Aspergillus flavus and Aspergillus parasiticus and have severe pathological effects on the health of human and animals. The present study was designed to investigate the toxicopathological changes induced by aflatoxins and mitigative potential of Lactobacillus plantarum in broiler birds. One hundred and eighty broiler chicks at one day of age was procured from the local market, and chicks were equally divided into six groups with thirty birds in each group. These birds were treated with aflatoxins (300 and 600 µg/kg) and Lactobacillus plantarum (1 × 108 cfu/kg of feed) in different combinations. The first group was kept as the control, and only a basal diet was provided to birds (BD). In the second group (AF1), the first level of aflatoxins (300 µg/kg) was fed to the birds. In the third group (AF2), the second level of aflatoxins (600 µg/kg) was fed to birds. In the fourth group (AF1LP), Lactobacillus plantarum was given with first level of aflatoxins. In the fifth group (AF2LP), Lactobacillus plantarum was given with the second level of aflatoxins, and in the 6th group (BDLP), Lactobacillus plantarum alone was fed to the chicks. This experimental study was continued for 42 days. Birds were slaughtered after 42 days, and different parameters were assessed. Parameters studied were gain in body weight, organ weight along with some histopathological, hematological, biochemical parameters and residues of aflatoxins in liver and kidney. Lactobacillus plantarum improved the body weight gain and restored the relative organ weight. Hepatic and renal biomarkers returned to normal concentrations, serum proteins were restored in combination group AF1LP, and partial amelioration was observed in the AF2LP group. Red blood cells, white blood cells, hemoglobin centration and packed cell volume became normalized in the AF1LP group, while partial amelioration was observed in the AF2LP group. LP also reduced the concentration of aflatoxin residues in liver kidney and improved the TAC concentrations. The results of this study elucidated the mitigative potential of Lactobacillus plantarum against serum biochemical, histopathological, hematological and toxicopathological changes induced by aflatoxins in the chicks.

Fetal programming: in utero exposure to acrylamide leads to intergenerational disrupted ovarian function and accelerated ovarian aging.

In this study we investigated the effects of multigenerational exposures to acrylamide (ACR) on ovarian function. Fifty-day-old Wistar albino female rats were divided into the control and ACR-treated groups (2.5, 10, and 20 mg/kg/day) from day 6 of pregnancy until delivery. The obtained females of the first (AF1) and second generation (AF2) were euthanized at 4 weeks of age, and plasma and ovary samples were collected. We found that in utero multigenerational exposure to ACR reduced fertility and ovarian function in AF1 through inducing histopathological changes as evidenced by the appearance of cysts and degenerating follicles, oocyte vacuolization, and pyknosis in granulosa cells. TMR red positive cells confirmed by TUNEL assay were mostly detected in the stroma of the treated groups. Estradiol and IGF-1 concentrations significantly decreased as a result of decreased CYP19 gene and its protein expression. However, ACR exposure in AF2 led to early ovarian aging as evidenced by high estradiol and progesterone levels among all treated groups compared to control group, corresponding to the upregulation of the CYP19 gene and protein expression. The apoptotic cells of the stroma were greatly detected compared to that in the control group, whereas no significant difference was reported in ESR1 and ESR2 gene expression. This study confirms the developmental adverse effects of ACR on ovarian function and fertility in at least two consecutive generations. It emphasizes the need for more effective strategies during pregnancy, such as eating healthy foods and avoiding consumption of ACR-rich products, including fried foods and coffee.

Facile synthesis of 4-O-ß-N-acetylchitooligosyl 2-acetamido-2,3-dideoxydidehydro-gluconolactone based on the transformation of chitooligosaccharide and its suppressive effects against the furylfuramide-induced SOS response.

A facile synthesis method is described for transforming the reducing-end residue of chitooligosaccharides (DP 2-4) into lactone. The desired 4-O-ß-N-acetylchitooligosyl lactones (GN(n)L) were conveniently prepared from chitooligosaccharides by consecutive dehydration and oxidation reactions to afford 4-O-ß-tri-N-acetylchitotriosyl 2-acetamido-2,3-dideoxydidehydro-gluconolactone (GN(3)L), 4-O-ß-di-N-acetylchitobiosyl 2-acetamido-2,3-dideoxydidehydro-gluconolactone (GN(2)L), and 4-O-ß-2-acetamido-2-deoxy-D-glucopyranosyl 2-acetamido-2,3-dideoxydidehydro-gluconolactone (GNL). The resulting lactone derivatives exhibited considerable suppression (42.6-54.3% at a concentration of 400 µM) in umu gene expression of the SOS response in Salmonella typhimurium TA1535/pSK1002 against the mutagen, 2-(2-furyl)-3-(5-nitro-2-furyl)acrylamido (AF-2). Lactonization of the chitooligosaccharides was found to be essential for their suppression of the SOS-inducing activity.

The antimutagenic effect of mistletoe lectin (Viscum album L. var. coloratum agglutinin).

A galactose- and N-acetyl-D-galactosamine-specific lectin (Viscum album L. var. coloratum agglutinin, VCA), which is known for its anticancer activity, was isolated from mistletoe. In this study, we investigated the antimutagenic potentials of VCA by using the pre-incubation method of the Ames test (Salmonella typhimurium TA98 and TA100) in the presence or absence of S9 mixture. Viscum album L. var. coloratum agglutinin was assessed for its antimutagenic properties against the mutagens 2-aminoanthracene (2AA) and furylfuramide (AF-2) for strain TA98, and sodium azide (NaN(3) ) and 2-aminoanthracene (2AA) for strain TA100. The concentrations used for this test compound were 100, 200 and 400 µg per plate. Viscum album L. var. coloratum agglutinin showed moderate, but not negligible, protective effects regarding the antimutagenic properties against the direct-acting mutagens NaN(3) and AF-2. Furthermore, VCA was more effective in preventing the mutagenicity of the indirect-acting mutagen 2-AA (in the presence of S9) when tested with both TA98 and TA100. In conclusion, this report has shown broad ranging antimutagenic effects of VCA to numerous mutagens in TA98 and TA100 Salmonella typhimurium strains. Although the data presented here cannot be applied in vivo, they can support other antimutagenic and anticarcinogenic findings for VCA.

Suppression of SOS-inducing activity of chemical mutagens by metabolites from microbial transformation of (-)-isolongifolene.

In this study, biotransformation of (-)-isolongifolene (1) by Glomerella cingulata and suppressive effect on umuC gene expression by chemical mutagens 2-(2-furyl)-3-(5-nitro-2-furyl)acrylamide (furylfuramide) and aflatoxin B(1) (AFB(1)) of the SOS response in Salmonella typhimurium TA1535/pSK1002 were investigated. Initially, 1 was carried out the microbial transformation by G. cingulata. The result found that 1 was converted into (-)-isolongifolen-9-one (2), (-)-(2S)-13-hydroxy-isolongifolen-9-one (3), and (-)-(4R)-4-hydroxy-isolongifolen-9-one (4) by G. cingulata, and their conversion rates were 60, 25, and 15%, respectively. The metabolites suppressed the SOS-inducing activity of furylfuramid and AFB(1) in the umu test. Comound 2 showed gene expression by chemical mutagens furylfuramide and AFB(1) was suppressed 54 and 50% at <0.5 mM, respectively. Compound 2 is the most effective compound in this experiment.

Levamisole and ryanodine receptors. I: A contraction study in Ascaris suum.

Cholinergic anthelmintics (like levamisole) are important drugs but resistance with reduced responses by the parasite to these compounds is a concern. There is a need to study and understand mechanisms that affect the amplitude of the responses of parasites to these drugs. In this paper, we study interactions of levamisole and ryanodine receptors on contractions of Ascaris suum body muscle flaps. In our second paper, we extend these observations to examine electrophysiological interactions of levamisole, ryanodine receptors (RyRs) and AF2. We report that the maximum force of contraction, g(max), was dependent on the extracellular concentration of calcium but the levamisole EC(50) (0.8 microM) was not. The relationship between maximum force of contraction and extracellular calcium was described by the Michaelis-Menten equation with a K(m) of 1.8mM. Ryanodine inhibited g(max) without effect on EC(50); ryanodine inhibited only 44% of the maximum contraction (K(i) of 40 nM), revealing a ryanodine-insensitive component in the levamisole excitation-contraction pathway. Dantrolene had the same effect as ryanodine but was less potent. The neuropeptide AF2 (1 microM) decreased the levamisole EC(50) to 0.2 microM without effect on g(max); 0.1 microM ryanodine and 100 microM dantrolene, inhibited the g(max) of the AF2-potentiated levamisole response. High concentrations of caffeine, 30 mM, produced weak contraction of the body-flap preparation. Caffeine behaved like ryanodine in that it inhibited the maximum force of contraction, g(max), without effects on the levamisole EC(50). Thus, RyRs play a modulatory role in the levamisole excitation-contraction pathway by affecting the maximum force of contraction without an effect on levamisole EC(50). The levamisole excitation-contraction coupling is graded and has at least two pathways: one sensitive to ryanodine and one not.

Levamisole and ryanodine receptors. II: An electrophysiological study in Ascaris suum.

Resistance to antinematodal drugs like levamisole has increased and there is a need to understand what factors affect the responses to these anthelmintics. In our previous study, we examined the role of ryanodine receptors in muscle contraction pathways. Here we have examined interactions of levamisole receptors, ryanodine receptors (RyRs), the excitatory neuropeptide AF2, and coupling to electrophysiological responses. We examined the effects of a brief application of levamisole on Ascaris suum body muscle under current-clamp. The levamisole responses were characterized as an initial primary depolarization, followed by a slow secondary depolarizing response. We examined the effects of AF2 (KHEYLRFamide), 1 microM applied for 2 min. We found that AF2 potentiated the secondary response to levamisole and had no significant effect on the primary depolarization. Further, the reversal potentials observed during the secondary response suggested that more than one ion was involved in producing this potential. AF2 potentiated the secondary response in the presence of 30 microM mecamylamine suggesting the effect was independent of levamisole sensitive acetylcholine receptors. The secondary response, potentiated by AF2, appeared to be dependent on cytoplasmic events triggered by the primary depolarization. Ion-substitution experiments showed that the AF2 potentiated secondary response was dependent on extracellular calcium and chloride suggesting a role for the calcium-activated anion channel. Caffeine mimicked the AF2 potentiated secondary response and 0.1 microM ryanodine inhibited it. 1.0 microM ryanodine increased spiking showing that it affected membrane excitability. A model is proposed showing ryanodine receptors mediating effects of AF2 on levamisole responses.

Novel mutation assay with high sensitivity based on direct measurement of genomic DNA alterations: comparable results to the Ames test.

Almost all of the methodologies developed to date to assay the potential mutagenicity of chemical substances are based on detection of altered phenotypic traits. The alternative approach of directly screening the whole genome for mutations is not feasible because of the logistics of carrying out mass sequencing of genes. Here we describe a novel and highly sensitive mutation assay, which we term the 'genome profiling-based mutation assay' (GPMA) that directly detects mutations generated in genomic DNA. We used GPMA to detect mutations caused by known mutagens such as AF2 and ethidium bromide even at concentrations of 30 ppb. The number of mutations detected was dependent on the number of generations in culture and the concentrations of the mutagens. Almost complete agreement was observed between GPMA and the Ames test in the discrimination of mutagens (63 out of 64). Owing to the high sensitivity of GPMA, the effects of long-term and low-dose exposures and the influence of chemicals of low solubility can also be screened. Thus, genotype-based GPMA can complement the Ames test, which is the standard technology in this field and is based on phenotypic traits.

Enhancement of ligand-dependent vitamin D receptor transactivation by the cardiotonic steroid bufalin.

Bufalin, a bufadienolide type cardiotonic steroid that is one of the major components of the toad venom-prepared traditional Chinese medicine called Ch'an Su or Senso, exhibits a cardiotonic action by inhibiting the membranous Na(+),K(+)-ATPase. Bufalin also induces differentiation of leukemia cells alone or in combination with other differentiation inducers including 1alpha,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)]. In this study, we performed a transient cotransfection assay using a vitamin D receptor (VDR) expression vector and a luciferase reporter and found that although bufalin did not transactivate the VDR, it effectively enhanced VDR activity induced by 1,25(OH)(2)D(3). Bufalin also augmented VDR activation by bile acid ligands, such as lithocholic acid and 3-ketocholanic acid. Other cardiotonic steroids including ouabain, digitoxigenin and cinobufagin did not enhance VDR activation. Bufalin did not bind directly to VDR but did modulate the interaction of VDR and cofactors, such as steroid receptor coactivator-1 and nuclear receptor corepressor. Bufalin treatment significantly increased the expression of an endogenous VDR target gene, CYP24, in kidney- and monocyte-derived cell lines treated with 1,25(OH)(2)D(3). The data indicate that bufalin-mediated cellular mechanisms such as interaction with Na(+), K(+)-ATPase may affect VDR transcriptional activity. Bufalin may be a useful tool in the investigation of VDR regulation by membrane-originating cellular signals and of pathophysiological mechanisms linking VDR to cardiovascular dysfunction.

Brief application of AF2 produces long lasting potentiation of nAChR responses in Ascaris suum.

Resistance of parasitic nematodes to the cholinergic anthelmintic levamisole is associated with a reduction in the proportion of time that acetylcholine receptor ion-channels are in the open state decreasing the response of nematode parasites to the drug. Here we examine electrophysiological and contractile responses to acetylcholine and the cholinergic agonist, levamisole, in Ascaris suum muscle looking for a pharmacological approach that may be developed to increase the response to cholinergic agonists. We found that short application of the FMRFamide, AF2, produced modulation (long lasting potentiation) of the peak membrane potential response to acetylcholine but not to levamisole. Since levamisole preferentially activates L-type acetylcholine receptors, we also tested the effect of nicotine (selective activator of N-type acetylcholine receptors) and bephenium (selective activator of B-type acetylcholine receptors) and found again no effect of AF2 on peak membrane potential responses. We then tested atropine on the AF2 potentiation of acetylcholine and found it to inhibit the peak potentiation suggesting that AF2 receptors interact with muscarinic receptors to produce the potentiation of acetylcholine. We saw similar atropine sensitive potentiation of acetylcholine responses in our muscle contraction experiments. The potentiation of the acetylcholine responses shows that nematode acetylcholine receptors are capable of a level of plasticity. A model involving calcium release from the sarcoplasmic reticulum, CaM Kinase, calcineurin, muscarinic receptors and AF2 receptors is proposed to explain our observations. These observations are important because they point to a pharmacological approach that may be developed to counter resistance to cholinergic anthelmintics.

Biotransformation of nobiletin by Aspergillus niger and the antimutagenic activity of a metabolite, 4'-hydroxy-5,6,7,8,3'-pentamethoxyflavone.

Biotransformation of nobiletin (1) by Aspergillus niger has been investigated, and the product obtained was determined as 4'-hydroxy-5,6,7,8,3'-pentamethoxyflavone (2). Antimutagenic activity of compound 2 was found, which showed suppressive effects on umu gene expression of the SOS response to DNA damage in Salmonella typhimurium TA1535/pSK1002, induced by the chemical mutagens furylfuramide, MeIQ, and Trp-P-1.

Prenylated flavanones isolated from flowers of Azadirachta indica (the neem tree) as antimutagenic constituents against heterocyclic amines.

Four prenylated flavanones were isolated from the methanol extract of the flowers of Azadirachta indica (the neem tree) as potent antimutagens against Trp-P-1 (3-amino-1,4-dimethyl-5H-pyrido[4,3-b]indole) in the Salmonella typhimurium TA98 assay by activity-guided fractionation. Spectroscopic properties revealed that those compounds were 5,7,4'-trihydroxy-8-prenylflavanone (1), 5,4'-dihydroxy-7-methoxy-8-prenylflavanone (2), 5,7,4'-trihydroxy-3',8-diprenylflavanone (3), and 5,7,4'-trihydroxy-3',5'-diprenylflavanone (4). All isolated compounds were found for the first time in this plant. The antimutagenic IC(50) values of compounds 1-4 were 2.7 +/- 0.1, 3.7 +/- 0.1, 11.1 +/- 0.1, and 18.6 +/- 0.1 microM in the preincubation mixture, respectively. These compounds also similarly inhibited the mutagenicity of Trp-P-2 (3-amino-1-methyl-5H-pyrido[4,3-b]indole) and PhIP (2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine). All of the compounds 1-4 strongly inhibited ethoxyresorufin O-dealkylation activity of cytochrome P450 1A isoforms, which catalyze N-hydroxylation of heterocyclic amines. However, compounds 1-4 did not show significant inhibition against the direct-acting mutagen NaN(3). Thus, the antimutagenic effect of compounds 1-4 would be mainly based on the inhibition of the enzymatic activation of heterocyclic amines.

Antimutagenic activity of 8-hydroxyisoflavones and 6-hydroxydaidzein from soybean miso.

The antimutagenic activity of four isoflavones isolated from soybean miso toward three kinds of mutagens, AF-2, MNNG, and Trp-P-1, was evaluated by the Ames test. 8-Hydroxyisoflavones had greater suppressive potency than that of daidzein, and 6-hydroxydaidzein had almost the same activity as daidzein. These results indicated the number of hydroxy and methoxy groups and the position of these functional groups were important for antimutagenic activity.

The effect of the anthelmintic emodepside at the neuromuscular junction of the parasitic nematode Ascaris suum.

Here we report on the action of the novel cyclo-depsipeptide anthelmintic, emodepside, on the body wall muscle of the parasitic nematode, Ascaris suum. Emodepside caused (i) muscle relaxation, (ii) inhibition of muscle contraction elicited by either acetylcholine (ACh), or the neuropeptide, AF2 (KHEYLRFamide) and (iii) a rapid relaxation of muscle tonically contracted by ACh. The inhibitory action of emodepside on the response to ACh was not observed in a denervated muscle strip, indicating that it may exert this action through the nerve cord, and not directly on the muscle. Electrophysiological recordings showed emodepside elicited a Ca(++)-dependent hyperpolarization of muscle cells. Furthermore, the response to emodepside was dependent on extracellular K+, similar to the action of the inhibitory neuropeptides PF1 and PF2 (SDPNFLRFamide and SADPNFLRFamide). Thus emodepside may act at the neuromuscular junction to stimulate release of an inhibitory neurotransmitter or neuromodulator, with a similar action to the PF1/PF2 neuropeptides.

Antimutagenic activity of isoflavone from Pueraria lobata.

A methanol extract from Pueraria lobata showed a suppressive effect on umu gene expression of the SOS response in Salmonella typhimurium TA1535/pSK1002 against the mutagen 2-(2-furyl)-3-(5-nitro-2-furyl)acrylamide (furylfuramide). The methanol extract from P. lobata was re-extracted with hexane, dichloromethane, ethyl acetate, butanol, and water, respectively. A suppressive compound in the dichloromethane and ethyl acetate extract fractions was isolated by SiO(2) column chromatography and identified as tectorigenin (1) by EI-MS and (1)H and (13)C NMR spectroscopy. Compound 1 and its methylated derivative [7,4'-di-O-methyltectorigenin (2)] had the suppressive effects on umu gene expression of the SOS response in Salmonella typhimurium TA1535/pSK1002 against furylfuramide, 4-nitroquinoline-1-oxide, N-methyl-N'-nitrosoguanidine, and activated Trp-P-1, which do not require live metabolic activation by S9. These compounds also showed suppression of SOS-inducing activity against Trp-P-1 and AfB(1), which requires liver metabolizing enzymes. In addition to the antimutagenic activities of these compounds against furylfuramide, Trp-P-1 and activated Trp-P-1 were also assayed by an Ames test using S. typhimurium TA100.

Suppression of the furylfuramide-induced SOS response by monoterpenoids with a p-menthane skeleton using the Salmonella typhimurium TA1535/pSK1002 Umu test.

Suppression of the furylfuramide-induced SOS response by 25 kinds monoterpenoids (hydrocarbons, alcohols, ketones, and aldehydes) with a p-menthane skeleton was studied. Suppression of the SOS-inducing activity by monoterpenoids was determined in the umu test using Salmonella typhimurium TA1535/pSK1002. The terpene alcohols, ketones, and aldehydes had potent suppressive effects, but the hydrocarbons did not. Especially, (+)-menthol, (+)-pulegone, piperitenone, and cuminaldehyde were shown to have the most potent suppressive effects, and the ID(50) (dose for 50% inhibition) was 0.52 micromol/mL.

Suppression of furylfuramide-induced SOS response by acetophenones using Salmonella typhimurium TA1535/pSK1002 umu test.

The recently isolated paeonol (2-hydroxy-4-methoxyacetophenone), as one of the antimutagenic compounds from Discorea japonica, was used as a lead compound for detailed structure-activity relationship studies. Nine acetophenones (2-hydroxy-4-methoxy, 2-hydroxy-5-methoxy, 2-hydroxy-6-methoxy, 4-hydroxy-3-methoxy, o-methoxy, m-methoxy, p-methoxy, and 2,5-dimethoxyacetophenone and acetophenone) were investigated for their ability of suppression of furylfuramide-induced SOS response using Salmonella typhimurium TA1535/pSK1002 in the umu test, against the mutagen, 2-(2-furyl)-3-(5-nitro-2-furyl)acrylamide (furylfuramide). The results showed that 2-hydroxy-6-methoxyacetophenone displayed the strongest activity (EC(50) = 0.6 micromol/mL), and a hydroxyl group at C-2 is necessary feature for acetophenone derivatives to show the suppressive effects of furylfuramide-induced SOS response.

Antimutagenic effect of resveratrol against Trp-P-1.

The methanol extract of Yucca schidigera (YE) showed a suppressive effect on umu gene expression of the SOS response induced by 3-amino-1,4-dimethyl-5H-pyrido[4,3-b]indole (Trp-P-1) in Salmonella typhimurium TA1535/pSK1002. The suppressive effect of YE was also observed for 2-aminoanthracene and activated Trp-P-1, without a significant effect on bacterial growth. The extract exhibited a weak suppressive effect on SOS-induction by N-methyl-N'-nitro-N-nitrosoguanidine, but not by furylfuramide or 4-nitroquinoline-1-oxide. The antimutagenic activity of YE against Trp-P-1 was demonstrated by Ames assay using Salmonella typhimurium TA98. Isolation and purification of the active component of YE was carried out using SiO2 column chromatography, and 275 mg of antimutagenic compound was isolated from 2.5 kg of dried chips of yucca roots and branches. The compound was identified as 3,4',5-trihydroxystilbene (THS). The SOS suppression and antimutagenicity of THS against Trp-P-1 was determined by umu test and Ames test.