SEARCH · PubMed Health

Results for “GLUCOSIDES”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 91 records · Page 5Linked to original sources

PubMed2006

beta-Glucosidase catalyzing specific hydrolysis of an iridoid beta-glucoside from Plumeria obtusa.

An iridoid beta-glucoside, namely plumieride coumarate glucoside, was isolated from the Plumeria obtusa (white frangipani) flower. A beta-glucosidase, purified to homogeneity from P. obtusa, could hydrolyze plumieride coumarate glucoside to its corresponding 13-O-coumarylplumieride. Plumeria beta-glucosidase is a monomeric glycoprotein with a molecular weight of 60.6 kDa and an isoelectric point of 4.90. The purified beta-glucosidase had an optimum pH of 5.5 for p-nitrophenol (pNP)-beta-D-glucoside and for its natural substrate. The Km values for pNP-beta-D-glucoside and Plumeria beta-glucoside were 5.04+/-0.36 mM and 1.02+/-0.06 mM, respectively. The enzyme had higher hydrolytic activity towards pNP-beta-D-fucoside than pNP-beta-D-glucoside. No activity was found for other pNP-glycosides. Interestingly, the enzyme showed a high specificity for the glucosyl group attached to the C-7' position of the coumaryl moiety of plumieride coumarate glucoside. The enzyme showed poor hydrolysis of 4-methylumbelliferyl-beta-glucoside and esculin, and did not hydrolyze alkyl-beta-glucosides, glucobioses, cyanogenic-beta-glucosides, steroid beta-glucosides, nor other iridoid beta-glucosides. In conclusion, the Plumeria beta-glucosidase shows high specificity for its natural substrate, plumieride coumarate glucoside.

Apocynaceae↗

PubMed1967

Inducible system for the utilization of beta-glucosides in Escherichia coli. II. Description of mutant types and genetic analysis.

Two types of mutants obtained by treating beta-gl(+) cells with nitrosoguanidine are described. One type, beta-gl(+)c, is constitutive for the biosynthesis of the aryl beta-glucoside splitting enzyme(s) and for the beta-glucoside permease; the other (beta-gl(+)sal(-)) has lost the capacity to ferment salicin, but has retained the capacity to ferment arbutin and other aryl beta-glucosides. By two successive mutational steps, beta-gl(+)sal(-)c double mutants can be obtained. Determinations of the enzymatic splitting of salicin and p-nitrophenyl beta-glucoside by beta-gl(+)sal(-) cells and extracts showed that these mutants have lost the capacity to split salicin but do split p-nitrophenyl beta-glucoside; they possess the beta-glucoside permease, and in them salicin is a gratuitous inducer for enzyme and permease biosynthesis. Studies on a beta-gl(+) strain, which splits salicin as well as p-nitrophenyl beta-glucoside, have shown that the splitting of salicin is more temperature-sensitive than that of p-nitrophenyl beta-glucoside and other beta-glucosides. Other properties of the two activities are similar. Interrupted mating experiments and cotransduction with P1kc phage showed that the genetic determinants of the beta-glucoside system map between the pyrE and ile loci. Three distinct mutational sites were found and are presumed to have the following functions: beta-glA, a structural gene for an aryl beta-glucoside splitting enzyme; beta-glB, either the structural gene for the beta-glucoside-permease or a regulatory gene; and beta-glC, a regulatory gene (or site). Escherichia coli wild-type strains are of the genotype A(+) B(-) C(+). The beta-gl(+) mutation determining the ability to ferment beta-glucosides is considered to be a permease or regulatory mutation, and the resulting genotype is A(+) B(+) C(+). The beta-gl(+)sal(-) phenotype results from a mutation in the beta-glA gene (genotype A' B(+) C(+)), and the constitutive phenotype results from a mutation in the beta-glC gene, the genotypes A(+) B(+)C(a) and A' B(+)C(a) corresponding to the phenotypes beta-gl(+)c and beta-gl(+)sal(-)c.

Bacterial Proteins↗

PubMed1985

Molecular characterization of the human erythrocyte anion transport protein in octyl glucoside.

Band 3 protein, the anion transport protein of the human erythrocyte membrane, was purified in the presence of the nonionic detergent octyl glucoside. A molecular characterization was carried out to investigate whether the native structure of the protein was retained in the presence of this detergent. Band 3 bound octyl glucoside below the critical micelle concentration (cmc) of the detergent, approaching saturation above the cmc. At 40 mM octyl glucoside, close to saturating concentrations, 0.64 g of octyl glucoside is bound per gram of band 3 protein, corresponding to 208 molecules of detergent bound per monomer of band 3. Sedimentation velocity and gel filtration studies, performed at 40 mM octyl glucoside, indicated that the band 3-octyl glucoside complex had an average molecular weight of 1.98 X 10(6), which corresponds to a dodecamer. Sedimentation equilibrium experiments confirmed that band 3 in octyl glucoside exists in a heterogeneous and high oligomeric state. This high oligomeric state did not change dramatically over octyl glucoside concentrations ranging from 6 to 60 mM. The circular dichroism spectrum of band 3 changed only slightly over this range of octyl glucoside concentrations. The alpha-helical and beta-sheet contents of band 3 in 2 mM octyl glucoside were calculated to be 40% and 27%, respectively, indicating that no gross alteration in the secondary structure of the protein had occurred in octyl glucoside. The ability of band 3 to bind 4-benzamido-4'-aminostilbene-2,2'-disulfonate (BADS), a potent inhibitor (Ki = 1 microM) of anion transport, was measured to assess the integrity of the inhibitor binding site of the protein in octyl glucoside.(ABSTRACT TRUNCATED AT 250 WORDS)

Anion Exchange Protein 1, Erythrocyte↗

PubMed1997

Pyridoxine-5'-beta--glucoside exhibits incomplete bioavailability as a source of vitamin B-6 and partially inhibits the utilization of co-ingested pyridoxine in humans.

This research was conducted to investigate 1) the bioavailability of pyridoxine-5'-beta-D-glucoside (PN-glucoside) relative to that of pyridoxine (PN) in human subjects, and 2) the competitive effect of PN-glucoside on the metabolism of co-ingested PN. To evaluate PN-glucoside bioavailability, the subjects were administered a single oral dose of either deuterium-labeled ([2H2]) PN (Trial 1) or [2H2] PN-glucoside (Trial 2), and the urinary excretion rates of labeled 4-pyridoxic acid (4PA) were measured. The [2H2]4PA derived from [2H2] PN or [2H2]PN-glucoside was excreted mainly in the first 8 h after the dose. Excretion of [2H2]4PA during the 48-h postdose period indicated that the bioavailability of PN-glucoside was approximately 50% relative to PN, which is consistent with our previous report of 58% bioavailability determined using a different protocol and fewer subjects. To assess the effects of PN-glucoside on PN utilization, the subjects were administered different ratios of nonlabeled PN-glucoside with [2H2]PN in Trials 3 and 4. Comparing Trial 1 with Trials 3 and 4, the quantity of nonlabeled PN-glucoside, as a fraction of total vitamin B-6 administered, ranged from 0 to 40% (on the basis of pyridoxine equivalents), with a constant dose of [2H2]PN in each. In these trials, the rate but not the total extent of the excretion of [2H2]4PA derived from [2H2]PN was inversely related to the proportion of co-ingested nonlabeled PN-glucoside. Thus, antagonistic effects of PN-glucoside on PN metabolism do occur in humans, although the effect is less pronounced than that seen previously in rats. Such interactive effects must be considered in evaluating the net bioavailability of dietary forms of vitamin B-6.

Administration, Oral↗

PubMed2004

Liquid chromatography coupled to nuclear magnetic resonance spectroscopy for the identification of isoflavone glucoside malonates in T. pratense L. leaves.

Previous studies revealed that the main isoflavones in extracts of leaves of T. pratense L. are biochanin A and formononetin, their 7-O-glucosides, and two glucoside malonate isomers of each of them. Since LC-MS(/MS) did not provide sufficient information to distinguish the glucoside malonate isomers, in the present paper LC-NMR as well as off-line two-dimensional NMR were used to obtain further structural information. Matrix solid-phase dispersion (MSPD) was applied to obtain sufficiently high analyte concentrations to perform LC-NMR. Stop-flow reversed-phase LC-NMR was performed using a gradient of deuterated water and deuterated acetonitrile. Offline COSY and NOESY experiments were carried out to determine the positions of the glucose moiety on the flavonoid aglycone, and of the malonate moiety on the glucose. Based on the fragmentation patterns in MS/MS and the NMR spectra, the two formononetin glucoside malonate isomers were identified as 7-O-beta-D-glucoside 6"-O-malonate and 7-O-beta-D-glucoside 4"-O-malonate; i.e. they only differ in the substitution position of the malonate group on the glucoside ring. The biochanin A glucoside malonate isomers, however, have quite different structures. The main and later eluting isomer is biochanin A 7-O-beta-D-glucoside 6"-O-malonate, and the minor and earlier eluting isomer is 5-hydroxy-7-methoxyisoflavone 4'-O-beta-D-glucoside 4"-O-malonate: the positions of the methoxy group and the glucoside 6"-O-malonate group on the flavonoid skeleton are interchanged.

Chromatography, Liquid↗

PubMed2005

Masked mycotoxins: determination of a deoxynivalenol glucoside in artificially and naturally contaminated wheat by liquid chromatography-tandem mass spectrometry.

Conjugated mycotoxins, in which the toxin is usually bound to a more polar substance like glucose, are referred to as masked mycotoxins, as these substances escape routine detection methods but can release their toxic precursors after hydrolysis. This is the first report on the natural occurrence of a glucoside of deoxynivalenol (DON) in Fusarium-infected wheat and maize. To obtain appropriate standards, we chemically synthesized deoxynivalenol-3-beta-D-glucopyranoside (DON-3-glucoside) and deoxynivalenol-15-beta-D-glucopyranoside (DON-15-glucoside). The synthesis products were characterized by liquid chromatography-tandem mass spectrometry. The DON-glucosides showed different collision-induced dissociation (CID) fragmentation behaviors and could therefore be distinguished. Wheat plants were either treated with DON (n = 52) or with Fusarium spp. (n = 4) at anthesis, and after harvest, wheat ears were analyzed for DON and DON-glucosides. All 56 treated wheat samples contained DON and a DON-glucoside with the same retention time, molecular mass, and CID fragmentation behavior as the synthetic DON-3-glucoside. Moreover, the DON-glucoside was also found in two out of three analyzed naturally DON-contaminated maize and in five out of five naturally contaminated wheat samples, in a range from 4 to 12% of the DON concentration. To further confirm the identity of the DON-glucoside, the compound was isolated from wheat extracts and characterized as DON-3-glucoside with NMR. The results of this study indicate the importance to consider both DON and DON-3-glucoside with regard to food and feed safety.

Chromatography, Liquid↗

PubMed2000

Effects of naturally occurring stilbene glucosides from medicinal plants and wine, on tumour growth and lung metastasis in Lewis lung carcinoma-bearing mice.

Stilbene glucosides are naturally occurring phytoalexins, found in a variety of medicinal plants. Among the stilbene derivatives, resveratrol 3-O-D-glucoside (piceid) is found in grapes and wine. We studied the effects of stilbene glucosides isolated from medicinal plants and grapes on tumour growth and lung metastasis in mice bearing highly metastatic Lewis lung carcinoma (LLC) tumours. We also studied the inhibitory effects of stilbene glucosides on differentiation of human umbilical vein endothelial cells (HUVECs) to form a capillary network. Tumour growth in the right hind paw and lung metastasis were inhibited by oral administration of the stilbene glucosides, piceid and 2,3,5,4'-tetrahydroxystilbene-2-O-D-glucoside for 33 consecutive days, in LLC-bearing mice. As the number of CD8+ and NK1.1+ T cells in the spleen was not affected, the inhibitory effects of these stilbene glucosides on tumour growth and lung metastasis could not be explained by natural killer or cytotoxic T lymphocyte activation. Piceid inhibited the DNA synthesis in LLC cells at a concentration of 1000 microM, but not at lower concentrations (10-100 microM). 2,3,5,4'-Tetra-hydroxystilbene-2-O-D-glucoside also inhibited DNA synthesis in LLC cells (IC50 81 microM). In addition, both stilbene glucosides inhibited the formation of capillary-like tube networks (angiogenesis) of HUVECs at concentrations of 100 to 1000 microM. We suggest that the antitumour and antimetastatic activity of the stilbene glucosides, piceid and 2,3,5,4'-tetrahydroxystilbene-2-O-D-glucoside, might be due to the inhibition of DNA synthesis in LLC cells and angiogenesis of HUVECs.

Animals↗

PubMed1991

Urinary excretion of bile acid glucosides and glucuronides in extrahepatic cholestasis.

Recently the formation of bile acid glucosides has been described as a novel conjugation mechanism in vitro and in vivo. In 10 patients with extrahepatic cholestasis caused by carcinoma of the head of the pancreas we investigated excretion rates and profiles of urinary bile acid glucosides. Urinary bile acid glucosides and, for comparison, bile acid glucuronides were extracted and characterized according to established methods. In controls total urinary bile acid glucoside excretion was 0.22 +/- 0.03 mumol/24 hr (mean +/- S.E.M.)-in the range of bile acid glucuronide excretion (0.41 +/- 0.06 mumol/24 hr; mean +/- S.E.M.). A gas chromatography-mass spectrometry-characterized trihydroxy bile acid glucoside of still-unknown hydroxyl positions accounted for 65% of total urinary bile acid glucosides. In extrahepatic cholestasis total urinary bile acid glucoside excretion was 0.52 +/- 0.13 mumol/24 hr (mean +/- SEM), yet significantly lower than bile acid glucuronide excretion (1.53 +/- 0.13 mumol/24 hr; mean +/- SEM; p less than 0.001). In cholestasis the primary bile acid derivatives cholic and chenodeoxycholic acid glucosides amounted to 90%, whereas the trihydroxy bile acid glucoside had decreased to 5% of total bile acid glucoside excretion, indicating its alteration during enterohepatic circulation. The data establish the composition and quantity of urinary bile acid glucosides in healthy controls and cholestasis and constitute a quantitative comparison with another glycosidic conjugation reaction, bile acid glucuronidation.

Aged↗

PubMed1986

Basal-lateral transport and transcellular flux of methyl alpha-D-glucoside across LLC-PK1 renal epithelial cells.

The characteristics of methyl alpha-D-glucoside transport by the LLC-PK1 cell line are extended by a study of the interaction of this glucose analog with the basal-lateral membrane of these cells: 1 mM methyl alpha-D-glucoside enters LLC-PK1 cells across the basal-lateral membrane 10-times more slowly than when entering across the apical membrane; neither 10 mM glucose nor 10 mM methyl alpha-D-glucoside affect the rate of methyl glucoside uptake at the basal lateral membrane; 0.1 mM phlorizin in the apical hemichamber significantly decreases the rate at which methyl glucoside enter the cell when methyl glucoside is present in the basal-lateral hemichamber; the methyl glucoside transcellular flux ratio, Ja/Jb (apical to basal vs. basal to apical) is 15, whereas Ja/Jb for D-mannitol equals 1; and basal-lateral to apical fluxes (Jb) of mannitol consistently exceed those of methyl glucoside. These results demonstrate that methyl glucoside, unlike glucose, is accumulated within these cells to a high degree because of the limited ability of methyl glucoside to exit the cells by a carrier-mediated pathway. They also raise the important caveat for any studies with glucose (and other low-molecular-weight substrates) by showing that a monosaccharide presented to one surface of these cells will traverse the cell sheet (in part) by the intercellular route and will enter the cell at the unintended cell surface. The ability of the tight junctions of this intercellular route to discriminate between open-chain molecules, such as mannitol, vs. closed ring structures, like methyl glucoside, is also described.

Animals↗

PubMed2000

Cellular uptake of dietary flavonoid quercetin 4'-beta-glucoside by sodium-dependent glucose transporter SGLT1.

Although it has been suggested that the intestinal glucose transporter may actively absorb dietary flavonoid glucosides, there is a lack of direct evidence for their transport by this system. In fact, our previous studies with the human Caco-2 cell model of intestinal absorption demonstrated that a major dietary flavonoid, quercetin 4'-beta-glucoside, is effluxed by apically expressed multidrug resistance-associated protein-2, potentially masking evidence for active absorption. The objective of this study was to test the hypothesis that quercetin 4'-beta-glucoside is a substrate for the intestinal sodium-dependent D-glucose cotransporter SGLT1. Cellular uptake of quercetin 4'-beta-glucoside was examined with Caco-2 cells and SGLT1 stably transfected Chinese hamster ovary cells (G6D3 cells). Although quercetin 4'-beta-glucoside is not absorbed across Caco-2 cell monolayers, examination of the cells by indirect fluorescent microscopy as well as by HPLC analysis of cellular content revealed cellular accumulation of this glucoside after apical loading. Consistent with previous observations, the accumulation of quercetin 4'-beta-glucoside in both Caco-2 and G6D3 cells was markedly enhanced in the presence of multidrug resistance-associated protein inhibition. Uptake of quercetin 4'-beta-glucoside was greater in SGLT1-transfected cells than in parental Chinese hamster ovary cells. Uptake of the glucoside by Caco-2 and G6D3 cells was sodium-dependent and was inhibited by the monovalent ionophore nystatin. In both Caco-2 and G6D3 cells, quercetin 4'-beta-glucoside uptake was inhibited by 30 mM glucose and 0.5 mM phloridzin. These results demonstrate for the first time that quercetin 4'-beta-glucoside is transported by SGLT1 across the apical membrane of enterocytes.

Animals↗

PubMed2004

C-terminus loop 13 of Na+ glucose cotransporter SGLT1 contains a binding site for alkyl glucosides.

Recently, we identified the extramembranous C-terminus loop 13 of SGLT1 as a binding site for the aromatic glucoside phlorizin, which competitively inhibits sodium D-glucose cotransport. Alkyl glucosides are also competitive inhibitors of the transport. Therefore, in this study, we searched for potential binding sites for alkyl glucosides in loop 13. To this end, we synthesized a photoaffinity label (2'-Azi-n-octyl)-beta-D-glucoside and analyzed the region of attachment using MALDI mass spectrometry, producing wild-type recombinant truncated loop 13. Furthermore, we prepared four single-Trp mutants of the loop and determined their fluorescence, its change in the presence of alkyl glucosides, and their accessibility to acrylamide. Photolabeling of truncated loop 13 with (2'-Azi-n-octyl)-beta-D-glucoside revealed an attachment of the C2 group of the alkyl chain to Gly-Phe-Phe-Arg (amino acid residues 598-601). In the presence of n-hexyl-beta-D-glucoside, all mutants (R601W, D611W, E621W, and L630W) exhibited a significant decrease in Trp fluorescence with an apparent binding affinity of 8-14 microM. Only L630W exhibited a significant blue shift, and only in R601W was a change in acrylamide quenching (protection) observed. No quenching or protection was found for D-glucose; however, 1-hexanol produced the same results as n-hexyl-beta-D-glucoside. The interaction shows stereoselectivity for n-hexyl-beta-D-glucoside binding; the beta-configuration of the sugar moiety at C1, the cis conformation of the unsaturated alkenyl side chain in the C3-C4 bond, and the alkyl chain length of six to eight carbon atoms lead to an optimum interaction. A schematic two-dimensional model was derived in which C2 interacts with the region around residue 601, C3 and C4 interact with the region between residues 614 and 619, and C6-C8 interact with the region between residues 621 and 630. The data demonstrate that loop 13 provides binding sites for alkyl glucosides as well as for phlorizin; thus, loop 13 of SGLT1 seems to be a major binding domain for the aglucone residues of competitive D-glucose transport inhibitors.

Acrylamide↗

PubMedDate not supplied

Downstream processing of enzymatically produced geranyl glucoside.

Geraniol plays an important role in the fragrance and flavor industry. The corresponding glucoside has interesting properties as a "slow release" aroma compound. Therefore, the enzymatic production and downstream processing of geranyl glucoside were investigated. Geranyl glucoside was produced in a spray column reactor with an initial production rate of 0.58 mg x U(-1) x h(-1). A pretreated hydrophobic microfiltration membrane was used to prevent migration of the aqueous, enzyme-containing phase to the downstream process. No retention of the glucoside, which accumulated in the geraniol phase, was found. On the basis of examples from the literature, four downstream processes were tested on their viability for this system. Extraction with water and foaming were not suitable to recover geranyl glucoside from geraniol. In the first case, the glucoside selectivity for the geraniol phase was found to be high, which made extraction with water unsuccessful. In the second case it was possible to obtain a stable foam, but significant enrichment of the foam with glucoside did not occur. Adsorption on alumina and distillation under reduced pressure were applied successfully and tested in-line with the bioreactor. A maximum glucoside adsorption of 7.86 mg x g(-1) was achieved on alumina. After desorption and evaporation of the extractant the pure glucoside was obtained quantitatively. A pure product could not be obtained after distillation because a small amount of glucose was present in the permeate as well, which accumulated in the bottom fraction. It was shown that with this reactor system a production of 1 kg of geranyl glucoside in 2 days is possible using an initial amount of 50,000 units of enzyme.

Acyclic Monoterpenes↗

PubMed1991

Bioavailability of pyridoxine-5'-beta-D-glucoside determined in humans by stable-isotopic methods.

Stable-isotopic methods were employed to evaluate the utilization of dietary pyridoxine-5'-beta-D-glucoside (PN-glucoside), a major form of vitamin B-6 in plant-derived foods, as a source of available vitamin B-6 for adult men (20-35 y old, n = 5). Deuterium-labeled forms of free pyridoxine (PN) and PN-glucoside were compared using the urinary excretion of labeled forms of the vitamin B-6 metabolite 4-pyridoxic acid as the main index of absorption and metabolism. When comparing orally administered, isotopically labeled PN and PN-glucoside in separate groups of subjects, similar bioavailability was observed although within-group variability was high. A dual-label study designed to examine the bioavailability of these compounds when administered simultaneously indicated that the utilization of deuterated PN-glucoside was 58 +/- 13% (mean +/- SEM) relative to that of deuterated PN. PN-glucoside was detected in all urine samples, which provided additional evidence of incomplete metabolic utilization. In contrast, intravenously administered PN-glucoside underwent approximately half the metabolic utilization of oral PN-glucoside. These studies indicate that the bioavailability of dietary PN-glucoside, although incomplete, is substantially greater in humans than previously found in rats. In addition, the difference between oral and intravenous routes suggests a role of beta-glucosidase(s) of the intestinal mucosa, microflora, or both in the release of free PN from dietary PN-glucoside.

Administration, Oral↗

PubMed1995

Pyridoxine and pyridoxine-5'-beta-D-glucoside exert different effects on tissue B-6 vitamers but similar effects on beta-glucosidase activity in rats.

Pyridoxine glucoside is a partially available form of vitamin B-6 present in plant-derived foods. In this set of three studies, rats were fed diets containing different concentrations of either pyridoxine or pyridoxine glucoside in the presence or absence of a fixed concentration of pyridoxine for 2 wk. The distribution of B-6 vitamers and beta-glucosidase activity in tissues was examined to determine the metabolic effects of chronic consumption of pyridoxine glucoside. Rats fed pyridoxine glucoside either with or without pyridoxine exhibited a significant increase in the amount of hepatic pyridoxine 5'-phosphate (not detected in rats fed pyridoxine alone), whereas hepatic pyridoxal 5'-phosphate was decreased with increasing dietary pyridoxine glucoside. The activity of cytosolic beta-glucosidases in small intestine and kidney was affected by the dietary concentration of both pyridoxine and pyridoxine glucoside. Enzymatic activity capable of hydrolyzing pyridoxine glucoside was found in mucosal and intraluminal fractions of small intestine and in the kidney. Other tissues examined, including liver, spleen and stomach, did not hydrolyze pyridoxine glucoside in detectable quantities. These findings indicate that microbial and mucosal enzymes can participate in the intestinal hydrolysis of pyridoxine glucoside and that the kidney may contribute to postabsorptive hydrolysis. These findings further support the observations that dietary pyridoxine glucoside influences vitamin B-6 metabolism.

Animals↗

PubMed2002

Leucine-derived cyano glucosides in barley.

Barley (Hordeum vulgare) seedlings contain five cyano glucosides derived from the amino acid L-leucine (Leu). The chemical structure and the relative abundance of the cyano glucosides were investigated by liquid chromatography-mass spectrometry and nuclear magnetic resonance analyses using spring barley cultivars with high, medium, and low cyanide potential. The barley cultivars showed a 10-fold difference in their cyano glucoside content, but the relative content of the individual cyano glucosides remained constant. Epiheterodendrin, the only cyanogenic glucoside present, comprised 12% to 18% of the total content of cyano glucosides. It is proposed that the aglycones of all five cyano glucosides are formed by the initial action of a cytochrome P450 enzyme of the CYP79 family converting L-Leu into Z-3-methylbutanal oxime and subsequent action of a less specific CYP71E enzyme converting the oxime into 3-methylbutyro nitrile and mediating subsequent hydroxylations at the alpha-, as well as beta- and gamma-, carbon atoms. Presence of cyano glucosides in the barley seedlings was restricted to leaf tissue, with 99% confined to the epidermis cell layers of the leaf blade. Microsomal preparations from epidermal cells were not able to convert L-[(14)C]Leu into the biosynthetic intermediate, Z-3-methylbutanal-oxime. This was only achieved using microsomal preparations from other cell types in the basal leaf segment, demonstrating translocation of the cyano glucosides to the epidermal cell layers after biosynthesis. A beta-glucosidase able to degrade epiheterodendrin was detected exclusively in yet a third compartment, the endosperm of the germinating seed. Therefore, in barley, a putative function of cyano glucosides in plant defense is not linked to cyanide release.

Anti-Bacterial Agents↗

PubMed2006

Comparison of the effects of a new conjugated oral estrogen, estradiol-3beta-glucoside, with oral micronized 17beta-estradiol in postmenopausal women.

The objective of this article is to evaluate the pharmacokinetics of serum estrone and estradiol levels in women who were taking either 17beta-estradiol-3beta-glucoside (E(2)-3beta-glucoside) or 17beta-estradiol (E(2)) daily and to examine the effects of E(2)-3beta-glucoside and E(2) on postmenopausal symptoms, gonadotropins, hepatic metabolism, and coagulation factors. Healthy postmenopausal women on estrogen who had undergone a hysterectomy were recruited. Subjects were randomly assigned to receive equivalent doses of either E(2)-3beta-glucoside or micronized E(2) for 28 days. Pharmacokinetic studies of estrone and estradiol were performed on days 1, 2, 28, and 29. Gonadotropin levels and Kupperman Index (KI) scores were determined at baseline and on treatment day 28. Mean serum estradiol and estrone concentrations in those taking E(2)-3beta-glucoside were comparable with those taking E(2). Mean baseline follicle stimulating hormone (FSH) levels were 84 +/- 27 mIU/mL and 71 +/- 24 mIU/mL in the E(2)-3beta-glucoside and E(2) groups, respectively, with significant decreases (P < 0.01) of 54 +/- 21 mIU/mL and 38 +/-18 mIU/mL, respectively, by treatment day 28. Baseline KI scores in the E(2)-3beta-glucoside group were 10 +/- 6 compared with 5 +/- 4 on treatment day 28, which is equivalent to a 50% reduction in menopausal symptoms (P = 0.003). The change in KI scores in the E(2) group was not statistically significant. Total serum estradiol and estrone levels in women taking E(2)-3beta-glucoside are comparable with those in women taking E(2). E(2)-3beta-glucoside reduces serum gonadotropin levels to the premenopausal range and is effective at reducing postmenopausal symptoms. E(2)-3beta-glucoside is a novel synthetic estrogen that is well tolerated and has promise as a hormone replacement therapy.

Administration, Oral↗

PubMed1995

Uptake and metabolism of riboflavin-5'-alpha-D-glucoside by rat and isolated liver cells.

The effect of riboflavin alpha-D-glucoside, isolated from rat liver, on the uptake of riboflavin was studied using freshly isolated rat liver cells. The transport characteristics and metabolic fate of the glucoside were also determined using the radioactive compound. The initial (1-min) uptake of 1 mumol/L [3H]riboflavin glucoside (2.90 +/- 0.29 pmol/10(6) cells) was higher than that of 1 mumol/L [3H]riboflavin (1.35 +/- 0.30 pmol/10(6) cells). However, the accumulation of glucoside after 60 min was significantly lower than that of riboflavin. The presence of up to 30 mumol/L glucoside had no significant effect on the initial uptake of [3H]riboflavin (3 mumol/L, 10(9) cells/L). Measurement of the kinetic parameters for glucoside gave an apparent Kt value of 83.4 +/- 12.4 mumol/L and a Vmax of 208.6 +/- 17.9 pmol/(10(6) cells.min). Decreases in the temperature of incubation decreased uptake rate. Replacement of Na+ with other monovalent cations did not affect uptake. The presence of D-glucose (1 mumol/L to 5.5 mmol/L) had no inhibitory effect on uptake of 1 mumol/L [3H]riboflavin glucoside. The results indicate that the transport of riboflavin glucoside may not involve the transport mechanisms for riboflavin or D-glucose. Metabolic studies with isolated hepatocytes showed that the glucoside was hydrolyzed to yield riboflavin upon entry into the cell. The vitaminic efficiency of this compound was tested by feeding it to growing male rats. These experiments indicate that the glucoside and free riboflavin are comparable sources of the vitamin.

Administration, Oral↗

PubMed1988

Inotropic activity of digitoxigenin glucoside and related glycosides.

The cardiovascular effects of digitoxigenin glucoside and two derivatives, digitoxigenin glucoside tetraacetate and 4',6'-isopropylidene digitoxigenin glucoside were studied in pentobarbital-anaesthetized dogs. Digoxin (0.112 mumol/kg) and digitoxigenin glucoside (0.056 mumol/kg) produced similar increases in myocardial contractility, although digitoxigenin glucoside was faster in onset of action and had a shorter duration of action. Digitoxigenin glucoside caused a significantly greater increase in blood pressure than digoxin. Digitoxigenin glucoside tetraacetate (0.056 mumol/kg) and isopropylidene digitoxigenin glucoside (0.112 mumol/kg) also increased myocardial contractility. Time to peak effect and duration of action were similar to those of digitoxigenin glucoside. The tetraacetate derivative of digitoxigenin glucoside was less hypertensive than the parent compound. The results suggest that the rapid onset and short duration of effect are a function of the glucose moiety. The rapid onset and, what appears to be, a reduced tendency to accumulate may confer clinical potential for these analogues.

Animals↗