About: Sodium ascorbate is a research topic. Over the lifetime, 869 publications have been published within this topic receiving 18589 citations. The topic is also known as: Sodium L-ascorbate & L-Ascorbic acid, monosodium salt.
TL;DR: This chapter presents microbiological assay for serum, plasma, and red cell folate, using cryopreserved, microtiter plate method, and the final working standard concentration of 500 ng/liter is presented.
Abstract: Publisher Summary This chapter presents microbiological assay for serum, plasma, and red cell folate, using cryopreserved, microtiter plate method. In the 500-ml beaker a solution of 0.5% (w/v) sodium ascorbate is prepared by dissolving 2.5 g of sodium ascorbate in 500 ml of water. This solution is used for preparing the working standard and for all assay dilutions. The working standard is prepared in the following way—a universal tube containing stock standard solution is brought to room temperature and a 50- μ l aliquot is taken and diluted to 100 ml with 0.5% (w/v) sodium ascorbate in a volumetric flask. This solution is mixed thoroughly, then 5 ml is taken and diluted to 100 ml with 0.5% (w/v) sodium ascorbate in a second volumetric flask to give a final working standard concentration of 500 ng/liter. Duplicate 50- μ l aliquots of serum or plasma or duplicate 25- μ l aliquots of whole-blood lysate are pipetted into labeled 4-ml polypropylene tubes. Using the adjustable repetitive sampling pipette the aliquots are diluted to a total of 1 ml with 0.5% (w/v) sodium ascorbate.
TL;DR: This procedure extends the application of this fastest of azide-based bioorthogonal reactions to the exterior of living cells to protect the cells from damage by oxidative agents produced by the Cu-catalyzed reduction of oxygen by ascorbate, which is required to maintain the metal in the active +1 oxidation state.
TL;DR: In vitro study tested the hypothesis that these oxidizing agents were responsible for dentin bond strength reductions by attempting to reverse the effect with sodium ascorbate, a reducing agent, and observed compromised bond strengths.
Abstract: The mechanism responsible for hydrogen-peroxide- or sodium-hypochlorite-induced reductions in dentin bond strength is unknown. This in vitro study tested the hypothesis that these oxidizing agents were responsible by attempting to reverse the effect with sodium ascorbate, a reducing agent. Human dentin was treated with these oxidants before or after being acid-etched and with or without post-treatment with sodium ascorbate. They were bonded with either Single Bond or Excite. Hydrogen peroxide reduced the bond strengths of both adhesives, while sodium hypochlorite produced reduction in adhesion of only Single Bond (p < 0.05). Following treatment with sodium ascorbate, reductions in bond strength were reversed. Transmission and scanning electron microscopy showed partial removal of the demineralized collagen matrix only by sodium hypochlorite. The observed compromised bond strengths cannot be attributed to incomplete deproteinization and may be related to changes in the redox potential of the bonding substrates.
TL;DR: AAcidS, AAcidG, SodAsS, SodasG and VitE presented the highest antioxidant activity among substances tested in this study, and the DPPH assay provides an easy and rapid way to evaluate potential antioxidants.
Abstract: The aim of this study was to assess, using the DPPH assay, the antioxidant activity of several substances that could be proposed to immediately revert the problems caused by bleaching procedures. The percentage of antioxidant activity (AA%) of 10% ascorbic acid solution (AAcidS), 10% ascorbic acid gel (AAcidG), 10% sodium ascorbate solution (SodAsS), 10% sodium ascorbate gel (SodAsG), 10% sodium bicarbonate (Bicarb), Neutralize(®) (NE), Desensibilize(®) (DES), catalase C-40 at 10 mg/mL (CAT), 10% alcohol solution of alpha-tocopherol (VitE), Listerine(®) (LIS), 0.12% chlorhexidine (CHX), Croton Lechleri (CL), 10 % aqueous solution of Uncaria Tomentosa (UT), artificial saliva (ArtS) and 0.05% sodium fluoride (NaF) was assessed in triplicate by 2,2-diphenyl-1-picryl-hydrazyl-hydrate (DPPH) free radical assay. All substances exhibited antioxidant activity, except for CL. AAcidS, AAcidG and VitE exhibited the highest AA% (p<0.05). On the contrary, CHX, NE, LIS and NaF showed the lowest AA% (p<0.05). In conclusion, AAcidS, AAcidG, SodAsS, SodAsG and VitE presented the highest antioxidant activity among substances tested in this study. The DPPH assay provides an easy and rapid way to evaluate potential antioxidants.
TL;DR: Ascorbic acid is effective when administered before, but not after, light exposure, suggesting that protection from light damage in the retina occurs during the light period, and the vitamin may act in an antioxidative fashion by inhibiting oxidation of membrane lipids during intense light.
Abstract: Cyclic light and dark-reared rats were exposed to intense visible light for various periods and then rhodopsin-measured following recovery in darkness for up to 14 days. Animals were injected with ascorbic acid or ascorbate derivatives at various doses prior to light exposure in green Plexiglas chambers. The results show that ascorbic acid administration elevates retinal ascorbate and reduces the loss of rhodopsin and photoreceptor cell nuclei resulting from intense light. When given in comparable doses, L-ascorbic acid, sodium ascorbate, and dehydroascorbate were equally effective in preserving rhodopsin. The ascorbate protective effect in the retina is also dose dependent in both cyclic light and dark-reared rats and exhibits a requirement for the L-stereoisomer of the vitamin. Ascorbic acid is effective when administered before, but not after, light exposure, suggesting that protection from light damage in the retina occurs during the light period. In some experiments, rod outer segments were isolated from rats immediately after light exposure, lipids extracted, and fatty acid composition determined. As judged by the preservation of rod outer segment docosahexaenoic acid in rats given ascorbate, the vitamin may act in an antioxidative fashion by inhibiting oxidation of membrane lipids during intense light.