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Sodium ascorbate

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.


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Book ChapterDOI
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.

435 citations

Journal ArticleDOI
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.

340 citations

Journal ArticleDOI
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.

297 citations

Journal ArticleDOI
TL;DR: It is demonstrated that both 5% NaOCl and RC-Prep produced significantly (p < 0.05) large reductions in resin-dentin bond strengths, and the reductions could be completely reversed by the application of either 10% ascorbic acid or 10% sodium asCorbate.

296 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
202311
202222
202120
202016
201919
201815