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PubMed1995

Effect of amiloride on the taste of NaCl, Na-gluconate and KCl in humans: implications for Na+ receptor mechanisms.

Sodium-salt transduction in many species may be mediated by both apical and submucosal ion channels on the taste receptor cell membrane. The apical ion channel is blockable by the diuretic amiloride, whereas the submucosal pathway is not. Sodium salts with small anions, such as NaCl, can stimulate submucosal as well as apical ion channels; sodium salts with large anions, such as Na-gluconate, activate primarily the apical channels. In humans, reports on the effects of amiloride on the taste of NaCl are conflicting and no data exist on the effects of amiloride on organic sodium salts. In the present experiment, subjects gave magnitude estimates of the total intensity and of each of the basic taste qualities for NaCl, Na-gluconate and KCl. Five concentrations of each of these stimuli were presented to the anterior tongue following distilled water adaptation and after amiloride treatment. There was a significant decrease in the total taste intensity of NaCl and Na-gluconate after amiloride, but no effect on KCl. The saltiness of all three salts was unaffected, but amiloride decreased the perceived sourness of the sodium salts. KCl sourness was unaffected by amiloride. There was a proportionately larger effect of amiloride on Na-gluconate than on NaCl, which is consistent with a larger role for the apical ion channel in Na-gluconate transduction. However, an appreciable amiloride-insensitive component is present for both NaCl and Na-gluconate, suggesting that an amiloride-insensitive pathway also plays a role in the transduction of both sodium salts. These data support the hypothesis that an amiloride-sensitive transduction component exists in humans, but suggest that it is considerably smaller than in many other species.

Amiloride↗
PubMedDate not supplied

A biochemical and histologic rationale for the treatment of hydrofluoric acid burns with calcium gluconate.

Hydrofluoric acid has unique properties that make it attractive for a variety of industrial and household uses. Exposure to dilute and concentrated solutions of hydrofluoric acid can lead to severe pain and tissue necrosis. Local treatment with topical calcium gluconate and subdermal injections of 0.5 ml 10% solution of calcium gluconate per cm2 of affected tissue has been advocated but frequently fails to relieve the patient of pain. Intraarterial infusion of calcium gluconate has been advocated for these patients, but several reports have been made of massive soft-tissue loss associated with such therapy. The purpose of this study was to show what, if any, were the microscopic effects on the distal arterial tree of intraarterial infusion of calcium gluconate. By studying 1 micron-thick cuts of distal rat aortas after proximal infusion of concentrated (10%) and dilute (2%) calcium gluconate, we were able to show that the incidence of microperforations in the intima and media of the rat aorta increased with the concentration of calcium gluconate. We conclude that intraarterial infusions should be reserved for only the most severe cases of hydrofluoric acid burns unresponsive to local therapy.

Animals↗
PubMed1975

Genes involved in the uptake and catabolism of gluconate by Escherichia coli.

The isolation and properties of a mutant of Escherichia coli K12 that is totally unable to take up and utilize gluconate are described. Genetical analysis shows this phenotype to be associated with two lesions. One phenotype, designated GntM-, is the result of a mutation in a gene co-transducible with malA; the other, designated GNTS-, is the result of a mutation in a gene (GntS) co-transducible with fdp. The GntS--phenotype differs little from that of wild-type cells, but GntM- GntS+ organisms grow on gluconate only after a prolonged lag and form a gluconate uptake system that is strongly repressed by pyruvate. Moreover, such GntM- mutants readily give rise to further mutants that form a gluconate uptake system, gluconate kinase and 6-phosphogluconate dehydratase consititutively; in partial diploids, this constitutivity is recessive to the inducible character. It is postulated that the GntM- phenotype is due to malfunction of a negative control gene gntR, and that gntS+ specifies the activity of a gluconate uptake system.

Biological Transport, Active↗
PubMed1991

Analysis of the gluconate (gnt) operon of Bacillus subtilis.

The gluconate (gnt) operon of Bacillus subtilis includes the gntR, gntK, gntP, and gntZ genes, respectively encoding the transcriptional repressor of the operon, gluconate kinase, the gluconate permease, and an unidentified open reading frame (Fujita and Fujita, 1987). We have compared the proteins encoded by the gnt operon of B.subtilis with published sequences and showed that (i) the gluconate repressor is homologous to several putative regulatory proteins in Escherichia coli, (ii) the gluconate kinase of B. subtilis is homologous to xylulose kinase, glycerol kinase and fucose kinase in E. coli (20-26% identity; 12-59 S.D.), (iii) the gluconate permease exhibits a C-terminal domain which is homologous to a hydrophobic protein encoded by an unidentified open reading frame (dsdAp) which precedes the dsdA gene of E. coli (39% identity; 19 S.D.), and (iv) the gntZ gene product is homologous to 6-phosphogluconate dehydrogenases of other bacteria and of animals (48-56%; 82-178 S.D.), thereby suggesting that the B. subtilis gntZ encodes 6-phosphogluconate dehydrogenase. Several conserved regions of the sequenced 6-phosphogluconate dehydrogenases can serve as signature patterns of this protein. Computer analyses have indicated that the previously reported sequences of the porcine and ovine 6-phosphogluconate dehydrogenases, as well as the hypothetical DsdAp protein, are probably erroneous. The probable reasons for the errors are reported along with the proposed revised sequences.

Amino Acid Sequence↗
PubMed2004

The Bacillus subtilis yqjI gene encodes the NADP+-dependent 6-P-gluconate dehydrogenase in the pentose phosphate pathway.

Despite the importance of the oxidative pentose phosphate (PP) pathway as a major source of reducing power and metabolic intermediates for biosynthetic processes, almost no direct genetic or biochemical evidence is available for Bacillus subtilis. Using a combination of knockout mutations in known and putative genes of the oxidative PP pathway and 13C-labeling experiments, we demonstrated that yqjI encodes the NADP+-dependent 6-P-gluconate dehydrogenase, as was hypothesized previously from sequence similarities. Moreover, YqjI was the predominant isoenzyme during glucose and gluconate catabolism, and its role in the oxidative PP pathway could not be played by either of two homologues, GntZ and YqeC. This conclusion is in contrast to the generally held view that GntZ is the relevant isoform; hence, we propose a new designation for yqjI, gndA, the monocistronic gene encoding the principal 6-P-gluconate dehydrogenase. Although we demonstrated the NAD+-dependent 6-P-gluconate dehydrogenase activity of GntZ, gntZ mutants exhibited no detectable phenotype on glucose, and GntZ did not contribute to PP pathway fluxes during growth on glucose. Since gntZ mutants grew normally on gluconate, the functional role of GntZ remains obscure, as does the role of the third homologue, YqeC. Knockout of the glucose-6-P dehydrogenase-encoding zwf gene was primarily compensated for by increased glycolytic fluxes, but about 5% of the catabolic flux was rerouted through the gluconate bypass with glucose dehydrogenase as the key enzyme.

Amino Acid Sequence↗
PubMed1967

Gluconate metabolism in Escherichia coli.

On the basis of information available in the literature, gluconate dissimilation in Escherichia coli is thought to occur via the hexose monophosphate pathway. Evidence is presented in this study that gluconate is catabolized in this organism via an inducible Entner-Doudoroff pathway. This evidence is based on chromatographic examination of end products produced from (14)C-labeled gluconate or glucose, distribution of (14)C in the carbon atoms of pyruvate formed from specifically labeled (14)C-glucose and (14)C-gluconate, and the ability of cell-free extracts to produce pyruvate from 6-phosphogluconate. Degradation of gluconate by an Entner-Doudoroff pathway occurred simultaneously with a glycolytic cleavage of glucose. A relationship between gluconate-induced, Entner-Doudoroff pathway activity and catabolism of glucose in Escherichia coli and other bacterial species is discussed.

Alcohol Oxidoreductases↗
PubMed1980

D-glucose and D-gluconate transport in vesicles from Pseudomonas putida.

Vesicles prepared from glucose-grown cells of Pseudomonas putida (ATCC, 12633) retain glucose oxidase (GOX) and gluconate dehydrogenase (GADH) activity and actively transport D-glucose, 2-deoxy-D-glucose (2DOG), 3-deoxy-3-fluoro-D-glucose (3FG), and D-gluconate by saturable processes. The transport of these substrates is stimulated by the addition of L-malate or reduced phenazine methosulphate (PMS). Vesicles prepared from succinate-grown cells of P. putida lose their capacity to transport D-glucose, 2DOG, and 3FG by a saturable process. The transport and accumulation of D-gluconate, however, is retained with a KX value of 65 microM and a Vmax of 1.0 nmol . mg protein-1 . min-1. The rate of D-gluconate transport is stimulated by the addition of reduced PMS of L-malate with a reduction in the KX value to 42.0 microM. Respirometric studies with these vesicles indicate the presence of an active GOX and L-malate dehydrogenase but a defective GADH. Thus a reductase activity is detected in the presence of D-gluconate and either 2,6-dichloroindophenol (DCIP) or ferricyanide, as measured by a decrease in absorbance at 500 and 420 nm, respectively. Measurements on these vesicles with the oxygen electrode, however, indicate that no electron transfer from GADH to oxygen occurs. This is in contrast to the results with glucose-grown vesicles or with L-malate or D-glucose as substrates in the succinate-grown vesicles. A comparison between glucose and gluconate oxidase activity in native and detergent-treated vesicles is made. The significance of these results in relation to the presence of a glucose carrier in P. putida and other pseudomonads is presented.

Ascorbic Acid↗
PubMed2001

Optimisation of fermentation conditions for gluconic acid production by a mutant of Aspergillus niger.

Aspergillus niger ORS-4, isolated from the sugarcane industry waste materials was found to produce notable level of gluconic acid. From this strain, a mutant Aspergillus niger ORS-4.410 having remarkable increase in gluconic acid production was isolated and compared for fermentation properties. Among the various substrates used, glucose resulted into maximum production of gluconic acid (78.04 g/L). 12% concentration led to maximum production. Effect of spore age and inoculum level on fermentation indicated an inoculum level of 2% of the 4-7 days old spores were best suited for gluconic acid production. Maximum gluconate production could be achieved after 10-12 days of the fermentation at 30 degrees C and at a pH of 5.5. Kinetic analysis of production indicated that growth of the mutant was favoured during initial stages of the fermentation (4-8 days) and production increased during the subsequent 8-12 days of the fermentation. CaCO3 and varying concentrations of different nutrients affected the production of gluconic acid. Analysis of variance for the factors evaluated the significant difference in the production levels.

Aspergillus niger↗
PubMed2001

Gluconic acid production by Aspergillus niger mutant ORS-4.410 in submerged and solid state surface fermentation.

Aspergillus niger ORS-4.410, a mutant of Aspergillus niger ORS-4 was produced by repeated irradiation with UV rays. Treatments with chemical mutagnes also resulted into mutant strains. The mutants differed from the parent strain morphologically and in gluconic acid production. The relationship between UV treatment dosage, conidial survival and frequency of mutation showed the maximum frequency of positive mutants (25%) was obtained along with a conidial survival of 59% after second stage of UV irradiation. Comparison of gluconic acid production of the parent and mutant ORS-4.410 strain showed a significant increase in gluconic acid production that was 87% higher than the wild type strain. ORS-4.410 strain when transferred every 15 days and monitored for gluconic acid levels for a total period of ten months appeared stable. Mutant ORS-4.410 at 12% substrate concentration resulted into significantly higher i.e. 85-87 and 94-97% yields of gluconic acid under submerged and solid state surface conditions respectively. Further increase in substrate concentration appeared inhibitory. Maximum yield of gluconic acid was obtained after 6 days under submerged condition and decreased on further cultivation. Solid state surface culture condition on the other hand resulted into higher yield after 12 days of cultivation and similar levels of yields continued thereafter.

Aspergillus niger↗
PubMed1994

Development of a mutant strain of Aspergillus niger and optimization of some physical factors for improved calcium gluconate production.

In the course of mutation studies of Aspergillus niger strain AB with ethylene imine (1:4000), a mutant A. niger AB 501, produced greater amount of calcium gluconate in the culture broth (88.0 g/lit) as against the parent strain (36.0 g/lit) by the surface culture method of fermentation. This mutant was then exposed to UV-rays and a mutant, A.niger AB 1801, was found to produce high calcium gluconate in the culture broth (120 g/lit). The optimum cultural conditions for the production of calcium gluconate by A.niger AB 1801 were pH, 6.5; period of incubation, 9 days; volume of medium in 1 litre flask, 150 ml; temperature, 30 degrees C, volume of inoculum, 7.5 ml of cell suspension containing 2.6 x 10(7) spores and age of inoculum, 6 days old spores of A. niger AB 1801. The maximum yield of calcium gluconate to the above conditions was 168 g/lit. The cultural conditions that support maximum cultural growth did not, however, give optimal yield of calcium gluconate because after having yielded the maximum of calcium gluconate the growth of organism continued to increase further.

Aspergillus niger↗
PubMed1998

Zinc gluconate and the common cold. Review of randomized controlled trials.

OBJECTIVE: To examine the evidence of seven randomized controlled trials (RCT) on the therapeutic effectiveness of zinc gluconate lozenges for treating the common cold. DATA SOURCES: Using the MeSH headings common cold and zinc gluconate, MEDLINE was searched from 1966 on for all published RCTs evaluating use of zinc gluconate for treating the common cold. STUDY SELECTION: For this study, only double-blind RCTs were included. SYNTHESIS: Fair evidence suggests that zinc gluconate lozenges have a therapeutic effect in treating the common cold. Starting therapy with zinc gluconate lozenges within 24 to 48 hours of onset of cold symptoms reduces the duration and severity of the cold. Patients must suck lozenges every 2 hours while awake during the cold. Minimum effective dose appears to be 13.3 mg of elemental zinc per lozenge. Evidence suggests that compounds such as citric acid, sorbitol, and mannitol bind the free zinc ion in the mouth, and this could account for variations in therapeutic benefit. Bad taste and nausea are important side effects of zinc lozenges. CONCLUSION: Evidence supports use of zinc gluconate lozenges for reducing the symptoms and duration of the common cold, but the side effects, bad taste, and therapeutic protocol might limit patient compliance.

Adult↗
PubMed2001

A randomized, controlled parallel-group trial on efficacy and safety of iron sucrose (Venofer) vs iron gluconate (Ferrlecit) in haemodialysis patients treated with rHuEpo.

BACKGROUND: The objectives of the present trial were to compare the efficacy and safety of two i.v. iron preparations with respect to haemoglobin levels, iron status and recombinant human erythropoetin (rHuEpo) dosage requirements in stable, rHuEpo-treated haemodialysis patients (maintenance phase of iron treatment) over 6 months. METHODS: A total of 59 patients were randomized and assigned to one of two treatment groups and 55 patients were analysed (iron sucrose n=27; iron gluconate n=28). Iron sucrose was administered in a dose of 250 mg iron diluted in 100 ml normal saline given over 60 min once per month, while 62.5 mg iron as iron gluconate was given once per week in a slow push injection (5 min). RESULTS: --Efficacy parameters: Haemoglobin levels could be maintained from baseline to endpoint in both groups. There were, however, more patients in the iron sucrose group than in the iron gluconate group for whom treatment was discontinued because their haemoglobin values exceeded 12.5 g/dl or ferritin values exceeded 1000 ng/ml (five vs two and three vs one patient, respectively). Transferrin saturation and serum ferritin increased significantly in both groups (+255.7 ng/ml with iron sucrose and +278.5 ng/ml with iron gluconate), while rHuEpo dosage did not change significantly throughout the study. --Safety parameters: There were a total of 174 infusions of iron sucrose and 720 injections of iron gluconate during the trial; all of them were well tolerated. In particular, we did not observe anaphylactoid reactions or any events suggestive of iron toxicity such as hypotension, dizziness, or nausea. CONCLUSIONS: High doses of iron sucrose (Venofer((R)) at a dose of 250 mg/month) was equally effective in maintaining haemoglobin and equally well tolerated as low doses of iron gluconate (Ferrlecit((R)) at a dose of 62.5 mg once per week) in stable, rHuEpo treated haemodialysis patients.

Drug Administration Schedule↗
PubMed1998

0.25% chlorhexidine gluconate gel. A protective topical microbicide.

BACKGROUND AND OBJECTIVES: An estimated 4 million new cases of chlamydial infection occur each year. This experiment assessed the effects of a vaginally applied gel formulation of 0.25% chlorhexidine gluconate on chlamydial infection and on the vaginal ecosystem. STUDY DESIGN: Twelve monkeys were treated with a single application of 0.25% chlorhexidine gluconate. These animals were assessed for changes in vaginal flora before and at 30 minutes, 1 day, and 2 days postapplication by microbiologic analysis. Cervical and vaginal tissues were assessed by colposcopy at each time point. Five monkeys received a single application of 0.25% chlorhexidine gluconate gel followed (30 minutes) by a cervical inoculation with Chlamydia trachomatis. Four monkeys were inoculated with Chlamydia only. Cervicovaginal tissues were assessed via modified colposcopy, vaginal swabs were collected for assessment of vaginal flora, and cervical swabs were collected for detection of Chlamydia (culture/ligase chain reaction) at baseline and days 1, 2, and 7 postinoculation. RESULTS: Changes in vaginal flora were minimal in all monkeys. Application of 0.25% chlorhexidine gluconate did not affect adversely vaginal colonization by lactobacilli. All chlamydial infection control monkeys were infected, whereas none of the five monkeys pretreated with chlorhexidine gluconate were positive for C. trachomatis by culture or ligase chain reaction. Colposcopic observations remained largely unchanged in all groups. CONCLUSIONS: A 0.25% chlorhexidine gluconate gel was protective against chlamydial infection in all animals tested, had no adverse effect on the vaginal flora, and had minimal effect on cervicovaginal tissues after a single application.

Administration, Intravaginal↗
PubMed1980

Elimination pattern and tissue distribution of intravenous iron-poly (sorbitol-gluconic acid) complex in the rat.

The elimination pattern and tissue distribution in rats of intravenous [14C-gluconic acid]-poly(sorbitol-gluconic acid) and 59Fe-iron-poly(sorbitol-gluconic acid) complex, glusoferron (Ferastral) have been examined. Twenty-four hours after injection of 20 or 200 mg/kg of [14C-gluconic acid]-poly(sorbitol-gluconic acid), 5%-6% of the injected dose of radiolabel was eliminated as 14CO2 and about 85% in the urine and faeces. Administration of 59Fe-iron-poly(sorbitol-gluconic acid) complex (10 and 100 mg of iron/kg) resulted in a urinary and faecal excretion of about 18% and 40% of the given dose, respectively, during the first 4 days. Biliary excretion was low. The mean molecular weight of the biliary product after the iron complex was lower than that of the parent compound. Radiocarbon in tissues after 24 hours was negligible. Liver and bones accounted for most of the retained radioiron following 100 mg of iron/kg bodyweight of the 59Fe-iron complex with maximum levels of 27% and 12% of the injected dose, respectively, 4 days after dosing. Red cell incorporation of 59Fe attained a level of 16% at the end of 28 days.

Animals↗
PubMed2005

Acute hypersensitivity reaction to ferric gluconate in a premedicated patient.

OBJECTIVE: To report a case of an acute hypersensitivity reaction to ferric gluconate in a patient premedicated with dexamethasone, diphenhydramine, and prochlorperazine. CASE SUMMARY: A 38-year-old female with persistent iron deficiency anemia was initiated on parenteral iron therapy with ferric gluconate 125 mg intravenously over 10 minutes. The patient initially tolerated this first dose well; however, she later experienced nausea, dizziness, and minor tongue swelling. On her second course of therapy, the woman was premedicated with dexamethasone, diphenhydramine, and prochlorperazine prior to the same dose of ferric gluconate infused over 30 minutes. Subsequently, the patient developed epigastric pain, nausea, swelling of her lips and tongue, and hypotension. The symptoms abated after administration of diphenhydramine, dexamethasone, morphine, cimetidine, intravenous fluids, and oxygen. She was discharged after a short stay in the emergency department observation unit. DISCUSSION: Data are limited on the relative safety of ferric gluconate compared with iron dextran. Ferric gluconate does not appear to be associated with severe life-threatening events; however, the possibility of an acute hypersensitivity reaction with this product does exist. In this case, use of the Naranjo probability scale indicated a probable relationship between the hypersensitivity reaction and ferric gluconate. CONCLUSIONS: Healthcare professionals should be aware of this serious but rare event and encouraged to further document and report these events.

Adult↗
PubMed1998

[Anaphylactoid shock caused by chlorhexidine gluconate].

We report two cases of anaphylactoid shock caused by chlorhexidine gluconate. Both patients had skin flare, severe hypotension and increased airway pressure during cannulation of an antibacterial IVH catheter containing chlorhexidine gluconate after skin sterilization with chlorhexidine gluconate. In case 1, we did not identify the mechanism and causative drugs. In case 2, an intradermal test to chlorhexidine gluconate was positive 2 months later. Then we confirmed that the anaphylactoid shock was caused by chlorhexidine gluconate. We should bear in mind the risk of anaphylactoid shock when we use chlorhexidine gluconate or the IVH catheter containing the bactericide.

Adult↗
PubMed1984

Determination of calcium gluconate by selective oxidation with periodate.

A modified analytical method was developed which can accurately quantitate calcium gluconate and its pharmaceutical preparations in the presence of other calcium compounds or other cations able to complex with EDTA. The proposed method was based on the principle of the Malaprade reaction, according to which gluconic acid is selectively and quantitatively oxidized by sodium periodate. The content of calcium gluconate was calculated from the amount of gluconic acid found. The selective oxidation proceeded at 50 degrees C for 10 min, yielding approximately 100% recovery of calcium gluconate. The proposed method was accurate, precise, and superior to the compendia EDTA- complexometric method in terms of specificity.

Calcium Gluconate↗
PubMed1990

Ionization and hemodynamic effects of calcium chloride and calcium gluconate in the absence of hepatic function.

Serial serum ionized calcium concentrations were measured before and after administration of either calcium chloride or calcium gluconate during the anhepatic stage of liver transplantation in 15 patients to determine the release of ionized calcium in the absence of hepatic function. When hypocalcemia (Ca++ less than 0.8 mM) occurred during the anhepatic stage, patients were randomly assigned to treatment with chemically equivalent doses of either calcium chloride (10 mg/kg, n = 8) or calcium gluconate (30 mg/kg, n = 7). Serum concentrations of ionized calcium and citrate, hematocrit, arterial blood gas tensions, acid-base state, and hemodynamic profiles were determined before and up to 10 min after calcium therapy. In both groups of patients initial similar and rapid increases in Ca++ (0.98 +/- 0.14 mM in the calcium chloride group and 1.05 +/- 0.10 mM in the calcium gluconate group) were followed by gradual decreases over the next 10 min. Measured hemodynamic values were similar in the two groups, and neither group showed improvement in cardiovascular function after calcium therapy, possibly because of the decrease in preload that occurred during the anhepatic stage. Equally rapid increases in Ca++ after administration of calcium chloride and gluconate in the anhepatic state suggest that calcium gluconate does not require hepatic metabolism for the release of Ca++ and is as effective as calcium chloride in treating ionic hypocalcemia in the absence of hepatic function.

Adult↗