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PubMed1976

Fluorescence densitometric method for the determination of gluconic and lactobionic acids ("sugar acids") in pharmaceutical preparations.

An in situ fluorimetric method has been developed for the quantitation of gluconic and lactobionic acids and their salts in tablet formulations. The method is based on glycol cleavage with lead tetraacetate followed by treatment with dichlorofluorescein. Calcium gluconate and lactobionate were determined in Calcium-Sandoz and Ca-C 1000 Sandoz effervescent tablets. The reproducibility corresponded to relative standard deviations between 0.7 and 3.5% (usually below 2%). Detection limits of 0.2 mug per spot can be obtained. Interfering compounds such as citric acid, sugars and ascorbic acid can be separated from the "sugar acids". The linearity of the calibration graphs between 0.5 and 5 mug per spot is satisfactory (r = 0.994-0.999). The method is simple and could be applied to the routine analysis of suitable pharmaceutical formulations. Other compounds with glycol structures should also be adaptable to this technique.

Chromatography, Thin Layer↗
PubMed1987

The problems of taste in placebo matching: an evaluation of zinc gluconate for the common cold.

A recently published randomized, controlled, double-blind, study has reported efficacy of zinc gluconate lozenge treatment of the common cold. Because of a higher rate of side effects in the zinc group and the lack of any confirmatory evidence of blinding efficacy, we are concerned about the possible contribution of bias to the study result. Unflavored zinc gluconate tablets can be easily distinguished from the relatively tasteless, unflavored calcium lactate tablets, which were used as placebo in the cited study, increasing our concern about bias. In order to be able to test zinc lozenges in a second trial of common cold therapy, we developed a matching placebo containing denatonium benzoate (a bitter substance used to prevent thumb sucking in children) and then undertook a formal evaluation of blinding efficacy. This article reports the results of this evaluation, encompassing two randomized, controlled taste trials; the first trial of the placebo matching showed zinc recipients to exhibit a higher rate of side effects and also a significantly higher proportion of subjects believing they were on "active" treatment. Alterations in dosage before the second taste trial yielded comparability of the placebo and zinc lozenges. This study illustrates the pitfalls which may sometimes be encountered in performing and publishing studies in which placebos are either not tested at all or tested in too small a subject population to detect a significant subjective difference between the placebo and the active medication.

Clinical Trials as Topic↗
PubMed1993

Lactobionic and gluconic acid complexes of FeII and FeIII; control of oxidation pathways by an organ transplantation preservant.

Lactobionic acid, [4-beta-(galactosido)-D-gluconic acid] = LBA, is the major component of the Wisconsin organ transplantation preservant fluid and may suppress oxygen radical-induced tissue damage upon reperfusion by the control of FeII autoxidation. FeII and FeIII complexes of LBA and the related gluconic acid (GLC) have been studied herein by titrimetric, infrared, and electrochemical methods (CV; DPP). FeII(GLC) forms quickly at pH 7, but FeII(LBA) reacts in two steps, the second requiring 4 hr. The initial complex lacks coordination of the LBA carboxylate (C-1) and is bound by the "2,3,5" hydroxyl groups. The slow rearrangement forms a "1,2,3,6" chelate which FeII(LBA) shares in common with the donor set of the FeIII(LBA) complex. Titration data shows the removal of three protons from LBA through pH 5 and an additional proton from pH 6 to 9 which is indicative of the [FeIII(LBA)(OH)(H2O)]- formulation with LBA donating at the "1,2,3,6" positions. The more stable, second form of FeII(LBA) has been investigated in its oxidation mechanisms with H2O2 and O2 using selected trapping agents for HO. and ferryl intermediates. Eighty-six percent of the oxidation events of FeII(LBA)/H2O2 occurs in steps involving formation and reduction of freely diffusible HO.. These pathways are altered by the known HO. traps t-butanol, dmso, ethanol, and methanol in the manner predictable for beta-oxidizing radicals (from t-butanol or dmso) and alpha-reducing radicals (from ethanol and methanol). Fourteen percent of the FeII(LBA)/H2O2 reaction occurs via FeIVO intermediates not trapped by t-butanol or dmso, but intercepted by primary and secondary alcohols. The HO. generating pathways are responsible for a competitive LBA ligand oxidation at the C-2 position via HO., formed from FeII(LBA) and H2O2 within the original reaction cage. Competitive ligand oxidation at C-2 is absent for the FeII(LBA)/O2 autoxidation, indicative of a different redox mechanism. The FeII(LBA)/O2 reaction rate is first-order in each component and is insensitive to the presence of t-butanol as an HO. trap. These observations support a ferryl intermediate in the autoxidation pathway and the absence of HO. or free H2O2 during autoxidation. Although chelation of FeII by hard ligand donors such as edta4-, Cl-, or HPO4(2-) accelerate the rate of autoxidation of FeII, chelation of carboxylate, alkoxy, and hydroxyl donors of LBA does not accelerate autoxidation. The implications of these findings, and the absence of an inner-sphere coordination role of the 4-beta-(galactosido) functionality toward the action of LBA in organ preservant fluids, are discussed.

Adenosine↗
PubMed1975

Roentgen patterns of extravasation of calcium gluconate in the tissues of the neonate.

Calcium gluconate is irritating to soft tissues and can produce tissue necrosis and slough; Radiographs of the part following extravasation initially show only soft tissue swelling. A variable pattern of soft tissue calcification then develops in one to three weeks, and gradually is completely resorbed over several months' time. The cause of the soft tissue calcifications may be quite puzzling, if the incident of calcium gluconate extravasation has been overlooked.

Arteriosclerosis↗
PubMed1976

Studies on some nutritional factors influencing the production of gluconic acid.

Investigations were carried out to formulate an economical medium that can give maximum yield of gluconic acid by the submerged culture technique, using Aspergillus niger NRRL3. It was found that the highest yield of acid could be secured when a medium of the following ingredients was used: 13.0% glucose syrup, 0.1% NaNO3, 0.025% calcium superphosphate, 0.007% KCl, 0.025% MgSO4-7H20, and 0.5% CaCO3. It was also found that glucose syrup, which represents an available and cheap carbohydrate source for gluconic acid production by fermentation, can replace glucose powder which is more expensive.

Aspergillus↗
PubMed1999

Bioconversion of glucose and fructose to sorbitol and gluconic acid by untreated cells of Zymomonas mobilis.

The bioconversion of glucose and fructose to gluconic acid and sorbitol, respectively, by the enzymes glucose-fructose oxidoreductase (GFOR) and glucono-delta-lactonase (GL), contained in untreated cells of Zymomonas mobilis ATCC 29191, was investigated in batch runs with glucose plus fructose concentrations (S0) varying from 100 to 750 g l-1 in equimolar ratio. When S0 was increased to 650 g l-1, the yields were improved, reaching a maximum of 91% for both products, with productivities of 1.6 and 1.5 g g-1 cell h-1 for gluconic acid and sorbitol, respectively. Above this level (S0 = 750 g l-1), no further improvement in yields was observed and productivities decreased due to the longer process time. The high yields of bioconversion runs with S0 > or = 650 g l-1 are a consequence of the sequential inhibition of the normal metabolism of Z. mobilis by substrates and products, resulting in preferential utilization of substrates via the GFOR/GL system.

Fermentation↗
PubMed2001

Novel degradable polymers combining D-gluconic acid, a sugar of vegetal origin, with lactic and glycolic acids.

To synthesize functionalized poly(lactic acid-co-glycolic acid)-based polyesters for biomedical and pharmaceutical applications such as controlled drug delivery, D-gluconic acid was considered as an interesting source of comonomer. Accordingly D-gluconic acid was used to synthesize novel 1,4-dioxane-2,5-diones with protected hydroxyl groups, namely 3-(1,2:3,4-tetraoxobutyl-di-O-isopropylidene)-dioxane-2,5-dione (5a) and 3-methyl-6-(1,2:3,4-tetraoxobutyl-di-O-isopropylidene)-dioxane-2,5-dione (5b). The ring-opening homopolymerization and copolymerization of these cyclic dilactones with DL-lactide provided novel degradable polyesters with higher glass transition temperatures than poly(lactic acid-co-glycolic acid) polymers.

Biocompatible Materials↗
PubMed2004

Effect of Schizosaccharomyces pombe on aromatic compounds in dry sherry wines containing high levels of gluconic acid.

Volatile compounds have been determined in control dry sherry wines and those supplemented with gluconic acid, which were inoculated with the Schizosaccharomyces pombe 1379 (ATCC 26760) yeast strain. These compounds were grouped, according to volatiles exhibiting the identical odor quality, into nine groups of the same odor character (aromatic series) as a way of establishing the aroma profile for the studied wines. Control and supplemented wines showed changes in the balsamic, spicy, roasty, and fruity aromatic series, and tasters judged the aroma as typical of wines subjected to biological aging. This fission yeast may be used as a treatment to reduce gluconic acid contents in wines obtained from rotten grapes, making feasible the incorporation of these wines into the biological aging process. In addition, this procedure may also help to accelerate the traditional biological aging in sherry winemaking due to the contribution of some specific compounds by S. pombe to the wine.

Gluconates↗
PubMed1985

The active transport of 2-keto-D-gluconate in vesicles prepared from Pseudomonas purida.

The transport of 2-keto-D-gluconate (alpha-D-arabino-2-hexulopyranosonic acid; 2KGA) in vesicles prepared from glucose-grown Pseudomonas putida occurs by a saturable process with a Km of 110.0 +/- 2.9 microM and a Vmax. of 0.55 +/- 0.04 nmol X min-1 X (mg of protein)-1. The provision of phenazine methosulphate/ascorbate or L-malate leads to an accumulation of intravescular 2KGA, a decrease in the Km value to 50 +/- 2.1 microM and 35 +/- 2.9 microM respectively and no change in the Vmax. In the presence of electron donors the transport of 2KGA is inhibited by the respiratory poisons antimycin A, rotenone and the uncoupler 2,4-dinitrophenol. 2KGA transport is also competitively inhibited by 4-deoxy-4-fluoro-2-keto- or 3-deoxy-3-fluoro-2-keto-D-gluconate with Ki values of 50 microM and 160 microM respectively. The carrier system for 2KGA is repressed in vesicles from cells grown on succinate. Such vesicles transport 2KGA by non-specific physical diffusion with a Km value of infinity in the absence or presence of electron donors. Vesicles from glucose or succinate grown cells, in the presence of phenazine methosulphate/ascorbate at pH 6.6, generate a proton-motive force (delta p) of approx. 140 mV. The delta p, composed of proton gradient (delta pH) and a membrane potential (delta psi), is collapsed in the presence of dinitrophenol. Based on the results obtained with valinomycin, nigericin and carbonyl cyanide m-chlorophenylhydrazone, the active transport of 2KGA at pH 6.6 is coupled predominately to the delta pH component of delta p.

2,4-Dinitrophenol↗
PubMed2004

Magnesium gluconate offers no more protection than magnesium sulphate following diffuse traumatic brain injury in rats.

OBJECTIVE: Previous studies have demonstrated that magnesium salts, including the sulphate and chloride forms, are neuroprotective following traumatic brain injury (TBI). Recently, studies in cardiac ischaemia/reperfusion injury have demonstrated that the gluconate salt of magnesium may provide superior protection against oxidative damage and postischaemic dysfunction than MgSO(4). We have therefore compared the efficacy of both MgSO(4) and magnesium gluconate (MgGl(2)) on outcome following diffuse TBI in rats. METHODS: Adult male Sprague-Dawley rats were injured using the 2-metre impact acceleration model of diffuse TBI. At 30 min after injury, animals were administered with either 250 micromoles/kg i.v. MgSO(4), MgGl(2), or equal volume saline vehicle. Thereafter, animals were assessed for motor and cognitive outcome using the rotarod and Barnes maze, respectively, or their brains removed at 3 days after TBI and used for histological examination. RESULTS: Treatment with either magnesium salt significantly improved functional outcome as compared to vehicle treated controls. Similarly, treatment with either magnesium salt attenuated the degree of histological dark cell change at 3 days after TBI relative to the vehicle treated animals. There were no significant differences between the magnesium treated groups. CONCLUSIONS: We conclude that MgSO(4) and MgGl(2) are equally neuroprotective following TBI. Our results suggest that MgGl(2) may only be more effective in conditions that produce ischaemia, where high concentrations of reactive oxygen species are generated.

Animals↗
PubMed2001

Ineffectiveness of intranasal zinc gluconate for prevention of experimental rhinovirus colds.

Zinc has generally been administered by the oral route in studies of prevention or treatment of the common cold. The purpose of these studies was to evaluate the effectiveness of intranasal zinc gluconate for prevention of experimental rhinovirus infection and illness. Ninety-one volunteers, 41 treated with active medication and 50 treated with placebo, received study medication for 3 days, were inoculated with rhinovirus, and then were treated with study medication for an additional 6 days. Rhinovirus infection was documented in 37 (74%) of the 50 placebo-treated volunteers and in 32 (78%) of the 41 volunteers treated with active medication. Zinc treatment had no effect on total symptom score, rhinorrhea, nasal obstruction, or the proportion of infected volunteers who developed clinical colds. These data do not support a role for intranasal zinc gluconate for prevention or treatment of the common cold.

Administration, Intranasal↗
PubMed1976

Respiratory insufficiency after intraperitoneal administration of Kanamycin: failure of calcium gluconate to reverse toxic effects.

A 47-year-old woman developed postanesthesia respiratory insufficiency five hours after an intramuscular injection of 0.5 gm of kanamycin and one hour and 40 minutes after peritoneal lavage with 1.0 gm of kanamycin. The respiratory insufficiency was not reversed by an intravenous infusion of 400 mg of calcium gluconate. This is the third reported instance of respiratory insufficiency after kanamycin lavage. Only one of the previously reported patients responded to intravenous infusion of calcium gluconate, despite the experimental evidence supporting its efficacy.

Anesthetics↗
PubMedDate not supplied

Topical treatment of experimental hydrofluoric acid skin burns by 2.5% calcium gluconate.

Topical therapy with 2.5% calcium gluconate gel is considered as the "first-aid" treatment of accidental hydrofluoric acid skin burns. The efficacy of three different gel formulations varying in the amount and/or nature of their gelling and moisturizing agents was experimentally evaluated. Thirty male Wistar-Han rats (250 g) were exposed to 60 mul of 40% hydrofluoric acid for 2 minutes on two spots (4 cm) of skin under pentobarbital anesthesia. One lesion was massaged with 1 g of gel (10 rats/type of gel) at 3 minutes; 30 minutes; 1 hour; 1 hour, 30 minutes; 2 hours; 3 hours; and 4 hours after injury. During the next 3 days, rats received a single daily application of gel. The other lesion for each rat remained untreated (control). From day 1 after injury to the end of the study (day 17), gel therapy reduced the number of extensive (-66%), severe (-44%), and moderate (-34%) lesions (P < .0001). It reduced (P < .001) the median Area Under the Curve day 0-17 of burn injury from 34.0 (25th to 75th percentile: 18.2-44.5; untreated lesions) to 17.7 (7.0-26.7); overall, there was three cases of treatment failure. At day 17, full wound recovery was obtained in 14 cases by gel therapy compared with 6 in the absence of treatment. The efficacy of the three gel formulations was comparable for all evaluated parameters. Repeated applications of a 2.5% calcium gluconate gel is an efficient treatment of experimental 40% hydrofluoric acid skin burn; few differences were observed between evaluated gel formulations.

Administration, Topical↗
PubMed2004

Structural alteration of cofactor specificity in Corynebacterium 2,5-diketo-D-gluconic acid reductase.

Corynebacterium 2,5-Diketo-D-gluconic acid reductase (2,5-DKGR) catalyzes the reduction of 2,5-diketo-D-gluconic acid (2,5-DKG) to 2-Keto-L-gulonic acid (2-KLG). 2-KLG is an immediate precursor to L-ascorbic acid (vitamin C), and 2,5-DKGR is, therefore, an important enzyme in a novel industrial method for the production of vitamin C. 2,5-DKGR, as with most other members of the aldo-keto reductase (AKR) superfamily, exhibits a preference for NADPH compared to NADH as a cofactor in the stereo-specific reduction of substrate. The application of 2,5-DKGR in the industrial production of vitamin C would be greatly enhanced if NADH could be efficiently utilized as a cofactor. A mutant form of 2,5-DKGR has previously been identified that exhibits two orders of magnitude higher activity with NADH in comparison to the wild-type enzyme, while retaining a high level of activity with NADPH. We report here an X-ray crystal structure of the holo form of this mutant in complex with NADH cofactor, as well as thermodynamic stability data. By comparing the results to our previously reported X-ray structure of the holo form of wild-type 2,5-DKGR in complex with NADPH, the structural basis of the differential NAD(P)H selectivity of wild-type and mutant 2,5-DKGR enzymes has been identified.

Circular Dichroism↗
PubMed1975

The energy-coupling controlled efflux of 2-keto-3-deoxy-D-gluconate in Escherichia coli K 12.

Experiments were devised to test the plausibility and the predictions of a efflux rate equation which was previously derived [10]9 1. 2-Keto-3-deoxy-D-gluconate transport system conforms with universal laws relating zero-trans influx, influx at steady-state, steady-state levels of accumulation to external and internal substrate concentrations. 2. Full-time-course uptake kinetics fit the linearized graphical representation that can be inferred from the integrated rate equation. 3. Influx does not depend upon internal substrate concentration nor upon energy-coupling. 4. Zero-trans outflux (leak inot empty medium) is a first-order process (rate constant: 0.02 min-1) and not mediated by the carrier. Absence of cis-competition with D-glucuronate is in agreement with a simple diffusion mechanism. 5. Outflux increases when external substrate concentration is raised (counterflow). Outflux at steady-state equilibrates influx, and is a first-order process (rate constant: 0.15 min-1). 6. Uncoupling with azide leads to accelerate zero-trans outflux by a factor of 2-3. No further acceleration is obtained when other classical uncouplers are used. The process remains first-order, independent of the amount of carrier, and is accelerated by the presence of internal D-glucuronate as a result from trans-inhibition of the recapture. 7. Exchange outflux is all the more accelerated by azide as the carrier is less saturated. The process is clearly carrier-mediated and the outflux rate obeys a Michaelis law with respect to internal concentration. V is equal to V for influx. 8. Homo and hetero-overshoot experiments are in agreement with the participation of the carrier for mediating influx as well as outflux. 9. The kinetics of D-glucuronate outflux in a strain lacking the specific hexuronate permease but carrying the 2-keto-3-deoxy-D-glucuronate permease are similar to those obtained with 2-keto-3-deoxy-D-gluconate. We draw the conclusion that energy-coupling promotes the adjustment of outflux without interfering with influx rate. It apparently acts by reducing, in a continuous range, the affinity of the carrier facing inwards. The discussion is focused on the comparison with previously published models and on possible molecular mechanisms.

Azides↗
PubMed1978

Use of chlorhexidine gluconate and povidone iodine mouthwashes in the treatment of acute ulcerative gingivitis.

A trial was conducted to compare the effectiveness of povidone iodine and chlorhexidine gluconate with buffered peroxyborate in the treatment of acute ulcerative gingivitis. After 20 patients had entered the trial and 11 had required additional therapy with metronidazole to control their symptoms, the study was terminated. Those patients receiving peroxyborate all showed a satisfactory improvement in clinical signs and symptoms. One patient each receiving povidone iodine or chlorhexidine reported a symptomatic improvement, although gingival ulceration was still apparent at 1 week. The remaining patients all required metronidazole therapy to control their symptoms. Povidone iodine and chlorhexidine gluconate therefore cannot be recommended for the treatment of acute ulcerative gingivitis.

Acute Disease↗
PubMedDate not supplied

Hemodynamic effects of calcium gluconate administered to conscious horses.

Calcium gluconate was administered to conscious horses at 3 different rates (0.1, 0.2, and 0.4 mg/kg/min for 15 minutes each). Serum calcium concentrations and parameters of cardiovascular function were evaluated. All 3 calcium administration rates caused marked increases in both ionized and total calcium concentrations, cardiac index, stroke index, and cardiac contractility (dP/dtmax). Mean arterial pressure and right atrial pressure were unchanged; heart rate decreased markedly during calcium administration. Ionized calcium concentration remained between 54% and 57% of total calcium concentration throughout the study. We conclude that calcium gluconate can safely be administered to conscious horses at 0.1 to 0.4 mg/kg/min and that administration will result in improved cardiac function.

Animals↗
PubMed1974

Genetic control of the 2-keto-3-deoxy-d-gluconate metabolism in Escherichia coli K-12: kdg regulon.

2-Keto-3-deoxy-gluconate (KDG), an intermediate of the hexuronate pathway in Escherichia coli K-12, is utilized as the sole carbon source only in strains derepressed for the specific KDG-uptake system. KDG is metabolized to pyruvate and glyceraldehyde-3-phosphate via the inducible enzymes KDG-kinase and 2-keto-3-deoxy-6-phosphate-gluconate (KDPG) aldolase. However, another inducible pathway, where the KDG is the branch point, has been demonstrated. Genetic studies of the KDG degradative pathway reported in this paper led to the location of KDG kinase-negative and pleiotropic constitutive mutations. The kdgK locus, presumably the structural gene of the kinase, occurs at min 69 and is co-transducible with xyl. The mutants, simultaneously constitutive for the uptake, kinase, and aldolase, define a kdgR locus at min 36 between the co-transducible markers kdgA and oldD. As to the nature of the control exerted by the kdgR product, we have shown the following. (i) Thermosensitive mutants of the kdgR locus are inducible at low temperature but derepressed at 42 C for the three operons-kdgT (transport system), kdgK, and kdgA (KDPG aldolase). (ii) The kdgR(+) allele is dominant to the kdgR constitutive allele. (iii) A deletion in kdgA extending into the regulatory gene, kdgR, leads to a constitutive expression of the nondeleted operons-kdgT and kdgK. These properties demonstrate that the kdg regulon is negatively controlled by the kdgR product. It is presumed that differences in operator and in promotor structures could explain the strong decoordination, respectively, in the induction and catabolic repression, of these three enzymes activities.

Aldehyde-Lyases↗