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At least 415 records · Page 23Linked to original sources
PubMed2006

Sodium antimony gluconate induces generation of reactive oxygen species and nitric oxide via phosphoinositide 3-kinase and mitogen-activated protein kinase activation in Leishmania donovani-infected macrophages.

Pentavalent antimony complexes, such as sodium stibogluconate and sodium antimony gluconate (SAG), are still the first choice for chemotherapy against various forms of leishmaniasis, including visceral leishmaniasis, or kala-azar. Although the requirement of a somewhat functional immune system for the antileishmanial action of antimony was reported previously, the cellular and molecular mechanism of action of SAG was not clear. Herein, we show that SAG induces extracellular signal-regulated kinase 1 (ERK-1) and ERK-2 phosphorylation through phosphoinositide 3-kinase (PI3K), protein kinase C, and Ras activation and p38 mitogen-activated protein kinase (MAPK) phosphorylation through PI3K and Akt activation. ERK-1 and ERK-2 activation results in an increase in the production of reactive oxygen species (ROS) 3 to 6 h after SAG treatment, while p38 MAPK activation and subsequent tumor necrosis factor alpha release result in the production of nitric oxide (NO) 24 h after SAG treatment. Thus, this study has provided the first evidence that SAG treatment induces activation of some important components of the intracellular signaling pathway, which results in an early wave of ROS-dependent parasite killing and a stronger late wave of NO-dependent parasite killing. This opens up the possibility of this metalloid chelate being used in the treatment of various diseases either alone or in combination with other drugs and vaccines.

Animals↗
PubMed1974

Isolation of specialized transducing bacteriophages for gluconate 6-phosphate dehydrogenase (gnd) of Escherichia coli.

Specialized transducing phages for gluconate 6-phosphate dehydrogenase (gnd), a constitutive enzyme in Escherichia coli, have been isolated using a method previously described for other genes. The gnd-his region, carried on an F' episome, was first transposed to tonB. Rare phages carrying gnd were selected, by transduction, from phi80 lysogens of these strains; one phage also carried his (phi80gndhis). From the transductants, high-frequency transducing lysates were obtained; low multiplicity of infection then yielded defective lysogens. tonB deletion analysis of the phi80dgndhis lysogen shows the order of genes in the prophage to be imm80...hisOGD...gnd; according to a marker rescue experiment most phage late genes have been replaced by bacterial deoxyribonucleic acid. A heat-inducible, lysis-defective lambda-phi80 hybrid derivative of phi80dgndhis has been prepared.

Chromosome Mapping↗
PubMed1977

Escherichia coli K-12 structural kdgT mutants exhibiting thermosensitive 2-keto-3-deoxy-D-gluconate uptake.

A specific method is described for selecting thermosensitive mutants of Escherichia coli K-12 able to grow on 2-keto-3-deoxy-D-gluconate (KDG) and D-glucuronate at 2, but not at 42 degrees C. The extensive analysis of one such mutant is consistent with the conclusion that the carrier molecule responsible for KDG and glucuronate uptake becomes thermolabile. (i) Growth on a variety of carbon sources is perfectly normal at 28 and 42 degrees C, whereas in the same temperature range it gradually diminishes on KDG and glucuronate. (ii) The apparent Km value for KDG is about twofold in the range 25 to 40 degrees C. In the same temperature range, the Vmax values for KDG influx are higher for the mutant compared with those of the wild-type strain, but the optimum temperature is 34 degrees C instead of 38 degrees C. On the contrary, the Vmax values for glucuronate influx are lower for the mutant than for the parental strain, and the optimum temperature for both strains is shifted beyond 40 degrees C. (iii) The activation energies for KDG and glucuronate uptake are about twofold higher in the mutant than in the wild-type strain. (iv) Kinetics of counterflow under deenergized conditions (overshoot) at different temperatures indicate that the defect is located in the translocation step rather than in the processes involved in energy coupling. (v) The first-order rate constants for thermal denaturation are, respectively, 2.5- and 5-fold higher at 40 and 30 degrees C in the mutant than in the wild-type strain, and the activation energy for thermal denaturation is lower. (vi) The carrier molecule in the mutant is also much more sensitive to denaturation by N-ethylmaleimide. (vii) Four independent thermosensitive mutations and one revertatn were located by transduction in or near the kdgT locus, defined previously as the site of nonconditional KDG transport-negative mutations. These results support the conclusion that kdgT represents the structural gene coding for the KDG transport system.

Biological Transport↗
PubMed1984

Construction and expression of hybrid plasmids containing the structural gene of the Escherichia coli K-12 3-deoxy-2-oxo-D-gluconate transport system.

The kdgT gene of Escherichia coli, which encodes for the 3-deoxy-2-oxo-D-gluconate transport system, was isolated as a ColE1-kdgT hybrid plasmid from the Clarke and Carbon bank. A restriction and genetic map of the min 88 region of the chromosome was established; by subcloning the restriction fragments into the plasmid vector pBR322, the kdgT gene was localized on a 1.4-megadalton PstI DNA fragment, and the direction of transcription of the gene was determined by making use of an in vitro gene fusion between kdgT and lacZ genes. Amplification of the gene product of kdgT was up to 14-fold the level found in a haploid strain. When plasmids bearing kdgT were expressed in an in vivo maxicell system, a specific polypeptide of 28,000 daltons appeared that was found to be associated with the membrane fraction.

Carrier Proteins↗
PubMed1977

Effects of oral calcium gluconate on gastric acid secretion and serum gastrin concentration in man.

A single oral dose of 4-46 mmol calcium gluconate at pH 5-6 was administered intragastrically to 15 male volunteers without gastrointestinal disease. There was a significant rise in acid output from 30-90 minutes after the calcium was given compared with the basal hourly collection. The serum gastrin level 30 minutes after calcium administration was significantly raised, but no correlation could be demonstrated between the acid and gastrin responses. Serum calcium levels were unchanged throughout. An equimolar dose of magnesium sulphate had no such effects. This study suggests that the intragastric administration of calcium results in independent release of gastric acid and gastrin from the gastric mucosa.

Administration, Oral↗
PubMed2005

Parenteral iron therapy in treatment of anemia in end-stage renal disease patients: a comparative study between iron saccharate and gluconate.

BACKGROUND: Anemia in hemodialysis patients is a complex syndrome. The impetus of this study was to assess the safety and efficacy of iron saccharate complex (ISC) and sodium ferric gluconate complex (SFGC) in treating anemia in hemodialysis patients. METHODS: Forty-eight adult anemic patients of both genders (33 males and 15 females) who had an adequate level of both hemodialysis and nutrition status and received neither EPO nor parenteral iron therapy during the preceding 6 months were randomized to 2 groups. The first group comprised 22 patients who were treated with parenteral ISC, 100 mg twice weekly for 2 months and once weekly thereafter. The second group included 26 patients who received SFGC, 62.5 mg twice weekly for 2 months and once weekly thereafter. The patients were followed up for 6 months. RESULTS: This head-to-head study showed that iron stores were adequately repleted by the use of both drugs. Repletion of iron stores was associated with a significant rise in both hemoglobin and hematocrit in both groups at the end of the follow-up period in comparison to their initial values at the start of the study (p < 0.001). Both parenteral iron therapy preparations were tolerated without a statistical difference between both groups. CONCLUSION: This head-to-head study confirmed that both parenteral iron preparations are effective for adequate repletion of iron stores and constituted a step forward in the management of anemic hemodialysis patients without noticeable adverse effects related to the administration of both iron preparations.

Adult↗
PubMed1979

Scintigraphy of induced myocardial infarcts with 99Tcm-gluconate.

A new isotope compound, 99Tcm-gluconate, for detection of myocardial infarction has been tested in dogs. A close correlation was found between the isotope uptake measured in vivo with a gamma camera and the infarct weight of early irreversible myocardial infarcts.

Animals↗
PubMed1982

Myocardial accumulation of 99Tcm-pyrophosphate and 99Tcm-gluconate compared with morphologic findings in daunorubicin treated rabbits.

In long-term daunorubicin treated rabbits increased myocardial accumulation of 99Tcm-pyrophosphate and 99Tcm-gluconate of a varying degree were recorded, visible at gamma camera examination in more than half of the animals. Chronic cardiomyopathy morphologically and topographically different from the ischemic myocardial injury was demonstrated in most animals at light microscopic examination. The myocardial abnormalities were classified in qualitative and quantitative scores and compared with the degree of isotope accumulation. The rabbits receiving a large single dose of daunorubicin had slightly increased isotope accumulation in the myocardium but no histopathologic changes.

Animals↗
PubMed1992

Zinc gluconate and the common cold: a controlled clinical study.

A report in 1984 on the success of zinc gluconate against common cold symptoms could not be confirmed in three subsequent studies, which are now known to have used formulations that inactivated zinc. A non-chelating formulation including glycine, which releases 93% of contained zinc into saliva, was tested in a randomized, placebo-controlled, double-blind trial in 73 young adults. Efficacy was recorded in symptom diaries using a symptom severity rating. Patients' symptoms first appeared 1.34 days prior to entry to the study in both groups. Disappearance of symptoms occurred after an additional 4.9 days for zinc-treated patients versus 6.1 days for placebo-treated patients. A difference was noted in the efficacy of treatment if it was started 1 day after symptom onset: cold duration was an additional 4.3 days in zinc-treated patients compared with 9.2 days for placebo-treated patients. Cough, nasal drainage and congestion were the symptoms most affected, and only mild side-effects were noted.

Adult↗
PubMed1997

The efficacy of calcium gluconate in ocular hydrofluoric acid burns.

1. Although calcium gluconate (CG) is recommended in the treatment of hydrofluoric acid (HF) eye burn its efficacy seems to be controversial, and controlled human or animal studies are limited. The study's objective is to compare the efficacy of 1% CG and normal saline irrigation for the treatment of HF eye injury in animals. 2. 0.05 ml 2% HF was instilled to anesthetized rabbit's eyes. One minute later, four treatment groups were studies: (1) irrigation with normal saline followed by topical antibiotics, corticosteroids and cycloplegics for 48 h (n = 10); (2) irrigation with 1% CG followed by the same topical treatment (n = 9); (3) as group 1 and 1% CG drops over 48 h (n = 10); (4) as group 3, and injection of 1% CG subconjunctivally after irrigation (n = 9). 3. Corneal erosion area, corneal haziness, conjunctival status, vascularization (pannus) and acidity were assessed before injury, immediately after initial treatment and 1, 2, 7 and 14 days thereafter by slit lamp aided by fluorescein staining. 4. Conjunctival pH dropped from 6.0-6.5 to 2.5-3 after injury and increased to 6-6.5 after irrigation. Corneal erosion: smaller in groups 2, 3, significantly so at 2 days, but not different at 14 days. Corneal haziness: more severe in group 4, at 14 days, insignificant. Conjunctival damage: significantly worse in group 4 at 2, 7 and 14 days. Pannus appeared in 2-4 eyes in each group. 5. It seems that for HF injury 1% CG did not have any significant advantage over saline irrigation and topical treatment only. It might have some initial and temporary effect on healing process especially that involving erosion. Given subconjunctivally, 1% CG may be toxic and worsens clinical outcome.

Administration, Topical↗
PubMed2005

Zinc gluconate in the treatment of dysgeusia--a randomized clinical trial.

In the treatment of dysgeusia, the use of zinc has been frequently tried, with equivocal results. The aim of the present randomized clinical trial, which involved a sufficiently large sample, was therefore to determine the efficacy of zinc treatment. Fifty patients with idiopathic dysgeusia were carefully selected. Zinc gluconate (140 mg/day; n=26) or placebo (lactose; n=24) was randomly assigned to the patients. The patients on zinc improved in terms of gustatory function (p <0.001) and rated the dysgeusia as being less severe (p <0.05). Similarly, signs of depression in the zinc group were less severe (Beck Depression Inventory, p <0.05; mood scale, p <0.05). With the exception of the salivary calcium level, which was higher in the zinc patients (p <0.05), no other significant group differences were found. In conclusion, zinc appears to improve general gustatory function and, consequently, general mood scores in dysgeusia patients.

Adult↗
PubMed2004

A comparative evaluation of amphotericin B and sodium antimony gluconate, as first-line drugs in the treatment of Indian visceral leishmaniasis.

In a study to evaluate the relative efficacies of sodium antimony gluconate (SAG) and amphotericin B (AMB), each drug was used to treat 60 Indian cases of visceral leishmaniasis (VL). At the time of treatment, each case had recently been parasitologically confirmed. The patients received either 20 mg SAG/kg daily, by intramuscular injection, for 4 weeks, or 1 mg AMB/kg daily, infused slowly over 2 h, with no incremental dosage, for 20 days. The response of the patients was followed clinically and by the microscopical examination of bone-marrow aspirates (BMA). The infected macrophages in subsamples of the BMA collected pre-treatment were cultured so that the drug sensitivities of the parasites, to 20 microg SAG or 1 microg AMB/ml medium, could be determined in vitro. Other subsamples of the BMA were used to set up promastigote cultures that were then used to infect BALB/c mice. The responses of the mice to 5 days of treatment with SAG or AMB (at the same daily dosages as used in the clinical trials) were subsequently explored. SAG only cured 46.6% of the patients given the drug, only cleared amastigotes from 38.3% of the macrophage cultures, and only cured 53.3% of the infected mice. The corresponding values for AMB - 100%, 100% and 100% - were markedly higher (P <0.001 for each comparison). Although nine patients had to be withdrawn from the SAG group (all because of cardiac toxicity), all of the patients given AMB completed their treatment without any serious adverse effects (P <0.01). Two of the patients withdrawn from the SAG arm died shortly after their withdrawal; earlier withdrawal may have saved them. At least in the setting of the present study, AMB appears far superior to SAG as a first-line drug against VL and should replace it.

Adolescent↗
PubMed2006

Calcium gluconate and sodium succinate for therapy of sodium fluoroacetate experimental intoxication in cats: clinical and electrocardiographic evaluation.

Sodium fluoroacetate (SFAC) or Compound 1080 is a potent rodenticide, largely used after 1946 for rodent and home pest control. The toxic effects of SFAC are caused by fluorocitrate action, a toxic metabolite, which has a competitive action with aconitase enzyme, leading to citrate accumulation and resulting in interference in energy production by Krebs cycle blockade. In the present study, domestic cats were intoxicated with oral doses of fluoroacetate (0.45 mg/kg). The intoxicated animals presented emesis, diarrhea with abdominal pain posture and an abdominal palpation, tachypnea, bilateral midriasis, hypothermia, hyperexcitability and convulsions. Blood gas analysis indicated decreased pH and bicarbonate levels. Serum ionized calcium was also decreased. ECG showed non-specific changes in ventricular repolarization and ventricular arrhythmias. The survival rate was 75% in the treated group with calcium gluconate and sodium succinate and 37.5% in the nontreated group.

Animals↗
PubMed2000

[In vivo toxicity, and glutathione, ascorbic acid and copper level changes induced in mouse liver and kidney by copper(II) gluconate, a nutrient supplement].

While copper(II) gluconate (CuGL) is generally used as a nutrient supplement for infant foods and as an oral deodorant, little information is available regarding a toxic effect of CuGL on mammals. In this article, we examined in vivo induction of toxicity and change of level of glutathione and ascorbic acid, major biological antioxidants, lipid peroxide and copper (Cu) in liver and kidney 4 h after single intraperitoneal administration of CuGL at 0.05 and 0.10 mmol/kg to mice. Serum glutamic pyruvic transaminase (SGPT) activity, an indicator of hepatotoxicity, significantly increased compared to control in proportion to doses of CuGL. Hepatic level of glutathione measured as nonprotein sulfhydryl was not proportional to CuGL doses, but enhanced after dosing of 0.05 mmol/kg and lowered by 0.10 mmol/kg. Like SGPT activity, serum urea nitrogen (SUN) concentration, an indicator of nephrotoxicity, significantly increased in proportion to doses of CuGL. Renal glutathione level was not different from control after dosing of 0.05 mmol/kg and lowered by 0.10 mmol/kg. In both organs, relative organ weight and lipid peroxide level were not affected by the treatment with CuGL; ascorbic acid level was elevated after dosing of 0.05 mmol/kg and was not different from control after treatment with 0.10 mmol/kg; like SGPT activity and SUN concentration, Cu level significantly increased in proportion to doses of CuGL. These results suggest that in the liver and kidney after the treatment with CuGL Cu accumulated may induce toxicity, leading to level changes of glutathione and ascorbic acid and to no induction of oxidative damage.

Animals↗
PubMed1986

Effect of potassium gluconate on potassium transport of rat erythrocytes.

Effect of potassium gluconate (K-GL) on K+ uptake of rat erythrocytes was investigated. K-GL produced a significant increase in active K+ transport of Na+-rich erythrocytes, while Na+,K+-ATPase activity of hemoglobin-free ghosts without a glycolytic system was unaffected. When the experiment was carried out in intact erythrocytes, K-GL increased the lactate production and ATP content, and it promoted the methemoglobin reduction rate. In Na+-rich erythrocytes, the glycolysis inhibitors which produced a marked reduction in lactate content abolished the K-GL-induced increase in K+ and ATP content without affecting the KCl-induced increase. These results suggest that K-GL enhances K+ transport of erythrocytes through acceleration of glycolytic process.

Adenosine Triphosphatases↗
PubMed2006

Alteration of gene expression in the colon of colorectal cancer model rat by dietary sodium gluconate.

Butyrate induces apoptosis of various cancer cell lines in a p53-independent manner and inhibits the proliferation of cancer cells. In a previous report, we reported a significant reduction in tumor incidence in rat colon as a result of dietary sodium gluconate (GNA). The stimulation of apoptosis through enhanced butyrate production in the large intestine was involved in the antitumorigenic effect of GNA. In the present study, a cDNA microarray analysis was performed to investigate the particular mechanism involved in the antitumorigenic effect of GNA. Some up-regulated genes suggested by microarray analysis were further evaluated using real-time PCR. A microarray revealed that GNA regulates the expression of retinoic acid receptor (RAR) and retinoid X receptor (RXR), and several genes known as the target of retinoids in cancer cells. In other words, the antitumorigenic effect of GNA may involve the regulation of the retinoid signaling pathway by butyrate in a retinoid-independent manner.

Animals↗