Sodium ascorbate 400mg capsules

BACKGROUND: Mega-dose sodium ascorbate (NaAscorbate) appears beneficial in experimental sepsis. However, its physiological effects in patients with septic shock are unknown. METHODS: We conducted a pilot, single-dose, double-blind, randomized controlled trial. We enrolled patients with septic shock within 24 h of diagnosis. We randomly assigned them to receive a single mega-dose of NaAscorbate (30 g over 1 h followed by 30 g over 5 h) or placebo (vehicle). The primary outcome was the total 24 h urine output (UO) from the beginning of the study treatment. Secondary outcomes included the time course of the progressive cumulative UO, vasopressor dose, and sequential organ failure assessment (SOFA) score. RESULTS: We enrolled 30 patients (15 patients in each arm). The mean (95% confidence interval) total 24-h UO was 2056 (1520-2593) ml with placebo and 2948 (2181-3715) ml with NaAscorbate (mean difference 891.5, 95% confidence interval [- 2.1 to 1785.2], P = 0.051). Moreover, the progressive cumulative UO was greater over time on linear mixed modelling with NaAscorbate (P < 0.001). Vasopressor dose and SOFA score changes over time showed faster reductions with NaAscorbate (P < 0.001 and P = 0.042). The sodium level, however, increased more over time with NaAscorbate (P < 0.001). There was no statistical difference in other clinical outcomes. CONCLUSION: In patients with septic shock, mega-dose NaAscorbate did not significantly increase cumulative 24-h UO. However, it induced a significantly greater increase in UO and a greater reduction in vasopressor dose and SOFA score over time. One episode of hypernatremia and one of hemolysis were observed in the NaAscorbate group. These findings support further cautious investigation of this novel intervention. Trial registration Australian New Zealand Clinical Trial Registry (ACTRN12620000651987), Date registered June/5/2020.

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Sepsis remains the leading cause of death in intensive care units globally, with catecholamine-resistant shock posing a persistent therapeutic challenge. Norepinephrine is the primary vasopressor used to treat hypotension in sepsis, but its efficacy is often limited by multifactorial loss of pressor responsiveness, including adrenergic receptor desensitisation, excess nitric oxide, systemic inflammation, and endothelial injury. Ascorbate (vitamin C) has emerged as a potential adjunct therapy because it supports endothelial function, reduces oxidative stress, activates the immune system and enhances endogenous vasopressor synthesis. Despite restoration of systemic hemodynamics with fluids and vasopressors, the frontal cortex remains particularly vulnerable to microcirculatory ischemia and hypoxia, contributing to sepsis-associated encephalopathy through hypoperfusion, hypoxia, hyperthermia, oxidative stress, neuroinflammation, and mitochondrial dysfunction, ultimately leading to neuronal injury and delirium. Plasma levels of ascorbate are profoundly depleted in sepsis and correlate with disease severity. Cerebral cortical neurons actively concentrate ascorbate at levels up to 250-fold higher than plasma, underscoring its importance in maintaining redox homeostasis and metabolism in the brain. While the conventional intravenous vitamin C formulation, ascorbic acid, has been associated with harm in clinical trials, emerging preclinical and early clinical data suggest that intravenous sodium ascorbate, a pH–neutral formulation of vitamin C, may restore noradrenaline sensitivity and re-establish frontal cortical microvascular perfusion and oxygenation. This review discusses the mechanistic rationale and therapeutic potential of sodium ascorbate in sepsis, including its ability to cross the blood-brain barrier. By stabilising cardiovascular and cerebrovascular function, sodium ascorbate may represent a promising adjunctive therapy to improve the management of sepsis.

Abstract licence: CC BY-NC-ND

The objective of this study was to evaluate different delaying times after bleaching and the use of different sodium ascorbate (SA) concentrations (10% and 35%) in the bond strength of adhesive cementation to enamel. This study used 54 sound bovine incisors, which were randomly assigned to the following groups: G1 (unbleached/control+ adhesive cementation (AC)); G2 (bleached + AC after 7 days); G3 (bleached + 10% SA + AC after 24 h); G4 (bleached + 10% SA + AC after 7 days); G5 (bleached + 35% SA + AC after 24 h); and G6 (bleached + 35% SA + AC after 7 days). After bleaching, G3, G4, G5, and G6 received an application of SA before the cylinders build up with RelyX Veneer cement. The samples were subjected to microshear test, and the results were analyzed by two-way ANOVA with Tukey’s post hoc test. Group one presented the highest mean bond strength (19.1 MPa) and G3 the lowest (16.96 MPa). There was no statistical difference between the groups tested (p ˃ 0.05). The fracture pattern observed was predominantly mixed. The adhesive cementation may be performed 24 h after bleaching when SA (10% or 35%) is used or after 7 days, without compromising bond strength.

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Background: The aim of this study was to investigate the effect of bleaching agent, sodium ascorbate as an antioxidant, and delay time on the shear bond strength (SBS) of orthodontic brackets to enamel using Transbond XT and universal adhesive. Materials and Methods: In this in vitro experimental study, 80 extracted maxillary premolars without any defect or decay were randomly divided into eight groups of 1: no bleaching + Transbond XT (NB/TX) bonding agent, 2: no bleaching + All-Bond Universal (NB/AB), 3: bleaching + Transbond XT (B/TX), 4: bleaching + All-Bond Universal (B/AB), 5: bleaching + sodium ascorbate + Transbond XT (B/SA/TX), 6: bleaching + sodium ascorbate + All-Bond Universal (B/SA/AB), 7: bleaching + Transbond XT after a 3-week delay (B/3W/TX), and 8: bleaching + All-Bond Universal after a 3-week delay (B/3W/AB). After thermocycling (1000 cycles, 5–55°C), the SBS was measured, and the adhesive remnant index scores were determined to assess the failure mode. Data were analyzed by one-way analysis of variance, Tamhane's post hoc test, Kruskal–Wallis, and Mann–Whitney U -test at the significance level of P &lt; 0.05. Results: The mean SBS range was 5.5–29.78 MPa. The highest SBS values were related to Group 2 (NB/AB) which were significantly higher than all groups ( P &lt; 0.05) and the lowest values were observed in Group 5 (B/SA/TX) which were significantly lower than all groups except Group 3 (B/TX) ( P &lt; 0.05). Conclusion: Bleaching with 40% hydrogen peroxide significantly decreased the SBS of orthodontic brackets, and 10% sodium ascorbate could not reverse the adverse effect of bleaching on SBS. Delaying the bonding procedure by 3 weeks using Universal adhesive considerably decreased the adverse effect of bleaching on SBS and increased the SBS to a clinically acceptable level for orthodontic treatment.

Abstract licence: CC BY-NC-SA

BACKGROUND: Megadose sodium ascorbate has shown promise as a treatment to reverse the pathophysiological effects of ovine Gram-negative sepsis. In human septic shock, lower doses of sodium ascorbate improved urine output and reduced vasopressor requirements compared with placebo. We sought to determine the minimum therapeutic dose of sodium ascorbate required to reverse sepsis-induced cardiovascular and renal dysfunction in sheep. METHODS: Healthy young adult sheep were instrumented with renal artery flow probes, and oxygen-sensing and laser Doppler probes in the kidneys. Non-anaesthetised animals were infused with live Escherichia coli for 31-h. At 23.5-h of sepsis, four groups (n = 7-8/group) received fluid resuscitation (30 mL/kg Hartmann's solution) and were randomized to intravenous sodium ascorbate (1.0, 2.0, or 3.0 g/kg) or vehicle, delivered as a bolus followed by 7-h infusion. Norepinephrine was titrated to maintain mean arterial pressure (MAP) at ~ 70 mmHg. RESULTS: At 23-h of sepsis, animals developed hypotension, hyperlactatemia, acute kidney injury, and renal medullary hypoxia. Vehicle-treated sheep required escalating doses of norepinephrine (from 0.4 to 0.8 ± 0.2 µg/kg/min) to restore MAP. Sodium ascorbate at 3.0 g/kg (achieving plasma ascorbate levels of ~ 10 mmol/L) rapidly restored MAP, allowing withdrawal of norepinephrine in half the animals (P = 0.007). Lower doses of sodium ascorbate (1.0 and 2.0 g/kg) had no significant effect on vasopressor requirements. The improvements in renal medullary oxygenation (25.2 ± 3.3 to 43.4 ± 4.5 mmHg, P = 0.04) and urine flow (from 0.5 ± 0.2 to 6.9 ± 2.4 ml/kg/h, P < 0.0001) were dose-dependent. Renal medullary tissue protein expression of nuclear factor kappa-light chain-enhancer B was significantly reduced with 3.0 g/kg of sodium ascorbate (to -52.9 ± 13.3%, P = 0.0005) and phosphorylated endothelial nitric oxide synthase at Ser-1177 was upregulated (to +219.5 ± 51.4%, P = 0.04) compared with vehicle-treated sheep. CONCLUSIONS: In established ovine Gram-negative sepsis, only 3.0 g/kg sodium ascorbate effectively restored cardiovascular and renal dysfunction, which was associated with suppression of renal inflammatory signalling and restoration of endothelial nitric oxide activity. These findings demonstrate a clear dose-dependent therapeutic threshold, where achieving plasma ascorbate concentrations of ~ 10 mmol/L is essential to elicit multi-organ protection.

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OBJECTIVES: To evaluate whether high-dose intravenous sodium ascorbate improves inflammatory markers in patients with sepsis. METHODS: A retrospective, observational, analytical, and comparative study was conducted on patients diagnosed with sepsis and admitted to the ICU at Clínica Estrios (Cartagena, Colombia) between July 1 and 30, 2024. Patients receiving standard treatment were compared with those who also received high-dose intravenous sodium ascorbate (>462 mg/kg/day), supplied by Biological Therapies, Australia. The main outcome was the duration of altered SIRS and SOFA scores. RESULTS: =9.00, p=0.003) compared to those who received standard therapy. CONCLUSIONS: High-dose sodium ascorbate may serve as an effective adjuvant therapy in sepsis.

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This study aimed to evaluate the effects of the application of 10% sodium ascorbate (SA) after in-office bleaching on the penetration of hydrogen peroxide (HP) into the pulp chamber, color change, and microtensile bond strength (µTBS) to the resin-enamel interface. Thirty premolars and thirty molars were randomly divided into three groups (n = 20 each). One group was exposed to deionized water (negative control). The other two groups were bleached with 35% HP in a single session for 3x15 minutes for each application. However, in only one of them, SA was applied for 10 minutes after bleaching. After, the concentration (µg/mL) of HP in each pulp chamber was evaluated by UV-Vis spectrophotometry. Color changes (ΔEab, ΔE00, and ΔWID) were evaluated with a digital spectrophotometer before and in the first week after bleaching. After treatment, molars were restored and sectioned to obtain resin-enamel interface sticks for µTBS at a crosshead speed of 1 mm/min until failure. The HP concentration and µTBS data were analyzed using one-way ANOVA and Tukey tests, and color changes were analyzed by t-tests (α = 0.05). SA application significantly improved the µTBS values and reduced the HP concentrations within the pulp chambers (p < 0.0001). The application of SA significantly interfered with the color changes after bleaching when compared to the control group (p < 0.05). Application of 10% SA after in-office bleaching successfully reduced the penetration of HP into the pulp chamber; however, it decreased color change.

Abstract licence: CC BY