927 resultados para calcium gluconate
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To examine the efficacy of calcium gluconate (two doses of Ca-Glu 5 mg/kg i.v.) to alleviate the injurious effects of organophosphorus induced delayed neuropathy (OPIDN) in the presence or absence of phenylmethanesulfonyl fluoride (PMSF go mg/kg i.m.), 14 groups of four isabrown hens were used. To measure the lymphocyte neuropathy target esterase (LNTE)activity, groups receiving just distilled water (control), groups receiving just Tri-orto-cresyl phosphate (TOCP; 500 mg/kg p.o.) (Positive control), and other groups receiving TOCP and Ca-Glu or PMSF simultaneously or 12 hours later following intoxication by TOCP were used. They were sacrificed 12 and 24 hours after the administration of TOCP. To observe a 28-day time course of neurotoxicity scores and calcium plasma concentration, five groups were used. Regarding free Ca(2+)in the plasma, the positive control produced a characteristic profile time course up and down (luring 28 days, and some hens with maximum score of neurotoxicity in 28 days. The treatment, which prevented greater oscillation in free Ca(2+) in the plasma, presented a decrease in OPIDN in relation to the positive control. Twelve hours after the administration of TOCP, LNTE was 70-80% inhibited when compared with control, whereas the first decrease in the free Ca(2+) in the plasma was significantly different from the control only 24 hours after the administration of TOCP. In summary, the sooner the Ca-Glu is started, the less severe the neuropathy effects.
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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 non-treated group.
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Insoluble calcium salts were added to milk to increase total calcium by 30 mM, without changing properties influencing heat stability, such as pH and ionic calcium. There were no major signs of instability associated with coagulation, sediment formation or fouling when subjected to ultra high temperature (UHT) and in-container sterilisation. The buffering capacity was also unaltered. On the other hand, addition of soluble calcium salts reduced pH, increased ionic calcium and caused coagulation to occur. Calcium chloride showed the largest destabilising effect, followed by calcium lactate and calcium gluconate. Milk became unstable to UHT processing at lower calcium additions compared to in-container sterilisation.
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The effects of serum and brain calcium concentration on rat behavior were tested by maintaining animals on either distilled water (N = 60) or water containing 1% calcium gluconate (N = 60) for 3 days. Animals that were maintained on high calcium drinking water presented increased serum calcium levels (control = 10.12 ± 0.46 vs calcium treated = 11.62 ± 0.51 µg/dl). Increase of brain calcium levels was not statistically significant. In the behavioral experiments each rat was used for only one test. Rats that were maintained on high calcium drinking water showed increased open-field behavior of ambulation (20.68%) and rearing (64.57%). on the hole-board, calcium-supplemented animals showed increased head-dip (67%) and head-dipping (126%), suggesting increased ambulatory and exploratory behavior. The time of social interaction was normal in animals maintained on drinking water containing added calcium. Rats supplemented with calcium and submitted to elevated plus-maze tests showed a normal status of anxiety and elevated locomotor activity. We conclude that elevated levels of calcium enhance motor and exploratory behavior of rats without inducing other behavioral alterations. These data suggest the need for a more detailed analysis of several current proposals for the use of calcium therapy in humans, for example in altered blood pressure states, bone mineral metabolism disorders in the elderly, hypocalcemic states, and athletic activities.
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This work evaluated the potential of the isoforms of methamidophos to cause organophosphorus-induced delayed neuropathy (OPIDN) in hens. In addition to inhibition of neuropathy target esterase (NTE) and acetylcholinesterase (AChE), calpain activation, spinal cord lesions and clinical signs were assessed. The isoforms (+)-, (+/-)- and (-)-methamidophos were administered at 50 mg/kg orally; tri-ortho-cresyl phosphate (TOCP) was administered (500 mg/kg, po) as positive control for delayed neuropathy. The TOCP hens showed greater than 80% and approximately 20% inhibition of NTE and AChE in hen brain, respectively. Among the isoforms of methamidophos, only the (+)-methamidophos was capable of inhibiting NTE activity (approximately 60%) with statistically significant difference compared to the control group. Calpain activity in brain increased by 40% in TOCP hens compared to the control group when measured 24h after dosing and remained high (18% over control) 21 days after dosing. Hens that received (+)-methamidophos had calpain activity 12% greater than controls. The histopathological findings and clinical signs corroborated the biochemical results that indicated the potential of the (+)-methamidophos to be the isoform responsible for OPIDN induction. Protection against OPIDN was examined using a treatment of 2 doses of nimodipine (1 mg/kg, i.m.) and one dose of calcium gluconate (5 mg/kg, iv.). The treatment decreased the effect of OPIDN-inducing TOCP and (+)-methamidophos on calpain activity, spinal cord lesions and clinical signs. (C) 2012 Elsevier B.V. All rights reserved.
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This in vitro study evaluated the effect of 35 hydrogen peroxide (HP) bleaching gel modified or not by the addition of calcium and fluoride on enamel susceptibility to erosion. Bovine enamel samples (3 mm in diameter) were divided into four groups (n = 15) according to the bleaching agent: control-without bleaching (C); 35 hydrogen peroxide (HP); 35 HP with the addition of 2 calcium gluconate (HP + Ca); 35 HP with the addition of 0.6 sodium fluoride (HP + F). The bleaching gels were applied on the enamel surface for 40 min, and the specimens were subjected to erosive challenge with Sprite Zero and remineralization with artificial saliva for 5 days. Enamel wear was assessed using profilometry. The data were analyzed by ANOVA/ Tukey's test (P 0.05). There were significant differences among the groups (P = 0.009). The most enamel wear was seen for C (3.37 ± 0.80 μm), followed by HP (2.89 ± 0.98 μm) and HP + F (2.72 ± 0.64 μm). HP + Ca (2.31 ± 0.92 μm) was the only group able to significantly reduce enamel erosion compared to C. The application of HP bleaching agent did not increase the enamel susceptibility to erosion. However, the addition of calcium gluconate to the HP gel resulted in reduced susceptibility of the enamel to erosion. © 2012 Alessandra B. Borges et al.
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Recently was observed that pyrethroids decrease motor coordination and that calcium channels can be important targets for this effect. To contribute with this observation, this work studied the motor coordination and exploration (using hole-board apparatus), and locomotion (using open-field apparatus) of rats exposed to following treatments: permethrin (PM), PM plus calcium gluconate (CG) and PM plus amlodipine (AML). The results obtained show that CG or AML alone not changed the motor coordination while PM decreases it. CG kept the effect of permethrin; AML, however, decreased the values of permethrin to the control. Locomotor activity and exploration, which could confound results of motor coordination, were not modified by treatments. The concentration of PM in brain tissue was increased by the CG and AML. The neurosomatic index (weight brain/body weight) was increased by the PM and PM + CG. In conclusion, the combined results here obtained indicates that the calcium ion and the channels in which it is involved can be important targets for the toxic effect of pyrethroid insecticide permethrin on motor nerve activity of rats. (c) 2014 Elsevier B.V. All rights reserved.
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This in vitro study compared the effect of bleaching agents modified by the addition of calcium and/or fluoride and the application of a nano-hydroxyapatite paste after bleaching, on the susceptibility of enamel to erosion. Bovine enamel cylindrical samples (3 mm diameter) were assigned to six groups (n = 20 specimens/group) according to the bleaching agent: no bleaching (C-control), 7.5% hydrogen peroxide gel (HP), HP with 0.5% calcium gluconate (HP+Ca), HP with 0.2% sodium fluoride (HP+F), HP with calcium and fluoride (HP+Ca+F) and HP followed by the application of a nano-hydroxyapatite agent (HP+NanoP). The gels were applied on the enamel surface (1 h) followed by cyclic erosive challenges (Sprite Zero®-2 min), for 14 days. The paste was applied after bleaching for 5 min (HP+NanoP). The enamel surface alteration was measured by contact profilometry (µm) (after 7 and 14 days). C-control (mean ± SD: 2.29 ± 0.37 at 7 days/4.86 ± 0.72 at 14 days) showed significantly lower loss compared to the experimental groups. HP+Ca (3.34 ± 0.37/6.75 ± 1.09) and HP+F (4.49 ± 0.92/7.61 ± 0.90) presented significantly lower enamel loss than HP (4.18 ± 0.50/10.30 ± 1.58) only for 14 days and HP+Ca+F (4.92 ± 1.03/8.12 ± 1.52) showed values similar to the HP+F group. The HP+NanoP (5.51 ± 1.04/9.61 ± 1.21) resulted in enamel loss similar to the HP after 14 days. It was found that 7.5% hydrogen peroxide increased the susceptibility of enamel to erosion. The addition of calcium or fluoride to the bleaching gel reduced the erosion effect, while the nano-hydroxyapatite agent did not provide any protective effect.
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The purpose of this randomized, cross-over in situ study was to determine the effects of 4 chewing gums on artificial caries-like subsurface lesions. Two chewing gums (1 with zinc citrate and 1 without) contained dicalcium phosphate (3.9%), calcium gluconate (1.8%) and calcium lactate (0.45%), 1 chewing gum contained casein phosphopeptide-amorphous calcium phosphate nanocomplexes (0.7%), and another one contained no calcium. Fifteen subjects without current caries activity (7 male, 8 female; mean age: 27.5 +/- 2.5 years) wore removable buccal appliances in the lower jaw with 4 bovine enamel slabs with subsurface lesions. The appliances were inserted immediately before gum chewing for 20 min and then retained for an additional 20 min. This was performed 4 times per day. Every subject chewed 4 different chewing gums over 4 periods of 14 days each. During a fifth period (control) the subjects only wore the appliances without chewing gum. At completion of each period the enamel slabs were embedded, sectioned and subjected to transversal microradiography. With regard to change of mineral loss and of lesion depth no significant differences could be found between chewing gums containing calcium and calcium-free chewing gums. Moreover, the chewing gum groups and the control group did not differ significantly if adjustments were made for baseline values (p > 0.05; ANCOVA). Under the conditions of the present study it may be concluded that the use of chewing gum offers no additional remineralizing benefit to buccal tooth surfaces, even if the chewing gum contains calcium compounds.
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The effects of serum and brain calcium concentration on rat behavior were tested by maintaining animals on either distilled water (N = 60) or water containing 1% calcium gluconate (N = 60) for 3 days. Animals that were maintained on high calcium drinking water presented increased serum calcium levels (control = 10.12 ± 0.46 vs calcium treated = 11.62 ± 0.51 µg/dl). Increase of brain calcium levels was not statistically significant. In the behavioral experiments each rat was used for only one test. Rats that were maintained on high calcium drinking water showed increased open-field behavior of ambulation (20.68%) and rearing (64.57%). on the hole-board, calcium-supplemented animals showed increased head-dip (67%) and head-dipping (126%), suggesting increased ambulatory and exploratory behavior. The time of social interaction was normal in animals maintained on drinking water containing added calcium. Rats supplemented with calcium and submitted to elevated plus-maze tests showed a normal status of anxiety and elevated locomotor activity. We conclude that elevated levels of calcium enhance motor and exploratory behavior of rats without inducing other behavioral alterations. These data suggest the need for a more detailed analysis of several current proposals for the use of calcium therapy in humans, for example in altered blood pressure states, bone mineral metabolism disorders in the elderly, hypocalcemic states, and athletic activities.
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
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Pós-graduação em Pesquisa e Desenvolvimento (Biotecnologia Médica) - FMB