Effect Of Sodium Ascorbate Research Articles

The effect of sodium ascorbate on the mechanical properties of hyaluronan-based vascular constructs

Esterified hyaluronic acid (HYAFF) is routinely used for clinical tissue engineering applications such as skin and cartilage. In a previous study we developed a technique for in vitro generation of cylindrical constructs from cellularized HYAFF flat sheets. In the present investigation we studied the possibility to improve mechanical properties of this vascular construct by the addition of sodium ascorbate (SA). Non-woven HYAFF flat sheets were seeded with porcine aortic smooth muscle cells (SMCs) and cultured for 14 or 28 days with standard medium or medium additioned with SA. In selected experiments HYAFF sheets seeded with SMCs were wrapped to obtain cylindrical shape and then cultured in control medium or SA additioned medium for up to 28 days. We estimated cell viability for flat sheets, and performed histological examination, analysis of extracellular matrix (ECM) deposition and mechanical tests on tubular constructs. The number of viable cells and ECM deposition increased with time in constructs cultured in the presence of SA, as compared to control group. Moreover, SA improved mechanical properties of the vascular construct lowering material stiffness and increasing tensile strength as compared to untreated controls. The addition of SA to the medium improved cell proliferation and ECM synthesis on this biodegradable material, which leads to the formation of well organized, mechanical resistant tissue-engineered structure.

Effects of sodium ascorbate on microtensile bond strength of total-etching adhesive system to NaOCl treated dentine

The purpose of this study was to determine the microtensile bond strengths of total etching adhesive systems to pulpal chamber wall dentine after treated with various irrigants. Thirty extracted human third molars were cut horizontally to expose the pulp horn. The roof of the pulp chamber and pulp tissues were removed. The teeth were then divided into five groups of five specimens each to treat with various irrigants. Specimens in each group were treated as follows: group 1, with water for 10 min; group 2, with sodium hypochlorite for 10 min; group 3, with sodium hypochlorite for 10 min and water for 10 min; group 4, with sodium hypochlorite for 10 min and sodium ascorbate for 10 min; group 5, with sodium hypochlorite for 10 min, sodium ascorbate for 10 min and water 10 min. Treated specimens were dried, bonded with a total-etching adhesive system (single bond) and restored with a resin composite (Z250) then kept for 24 h before determination of the microtensile bond strengths. Group 2 (20.96+/-9.23 MPa) demonstrated significantly lower bond strengths than group 1 (30.06+/-10.44 MPa). No significant differences in bond strengths were found between group 3 (23.08+/-6.94) and group 2. Group 4 (40.55+/-8.99) demonstrated higher bond strengths than group 2. However, there were no significant differences between group 5 (24.55+/-9.73 MPa) and group 2. Sodium hypochlorite significantly reduced the bond strengths of the adhesive when a total-etching was applied. The application of sodium ascorbate on sodium hypochlorite treated dentine significantly improved the bond strengths.

Effect of Sodium Ascorbate on Nitrosamines Contents and Color of the Carotenoid in Red Pepper in Radish-Kimuchi

Effect of Sodium Ascorbate on Nitrosamines Contents and Color of the Carotenoid in Red Pepper in Radish-Kimuchi

The requirement for and mobilization of calcium during induction by sodium ascorbate and by hydrogen peroxide of cell death

The requirement for and mobilization of Ca 2+ ions during induction of cell death by sodium ascorbate were compared with those during induction of cell death by hydrogen peroxide. When HL-60 cells were incubated with sodium ascorbate, a rapid increase in the intracellular concentration of Ca 2+ ions and subsequent apoptotic cell death, characterized by cell shrinkage, nuclear fragmentation and cleavage of internucleosomal DNA to yield fragments that were multiples of 180–200 base pairs, were induced. However, these effects of sodium ascorbate were significantly reduced in Ca 2+-depleted medium. By contrast, hydrogen peroxide induced similar apoptosis-associated phenomena in the presence and in the absence of extracellular Ca 2+ ions. The intracellular concentration of the reduced form of glutathione was not significantly affected and glutathione disulfide was undetectable during the early stages of apoptosis. These data suggest that sodium ascorbate and hydrogen peroxide initiate cell death by different mechanisms.

Effects of sodium ascorbate, sodium saccharin and ammonium chloride on the male rat urinary bladder.

Sodium saccharin administered at high doses to male rats beginning after 5 weeks of age produces mild urothelial hyperplasia but does not result in a significant increase in incidence of bladder cancer unless it is administered after an initiating agent. However, if it is administered in a two-generation bioassay, a significant incidence of bladder tumors is produced. The hyperplastic and tumorigenic effects are inhibited by co-administration with high doses of NH4Cl. The present experiment was designed to evaluate the effects of another sodium salt, sodium ascorbate, administered through the neonatal time period. Sodium saccharin administered as 5% of the diet produced urothelial hyperplasia and increased labeling index, and this was inhibited by co-administration with 1.23% NH4Cl. Four doses of sodium ascorbate was evaluated. The lowest dose, 0.91%, was without effect on the urinary tract. A slight effect (not statistically significant) was observed at a dose of 2.73%, and a significant proliferative response was detected at 4.56 and 6.84%. Recent studies suggest that a calcium phosphate-containing amorphous precipitate forms in the urine of rats fed high doses of sodium saccharin, producing cytotoxicity of the urothelium and consequent regenerative hyperplasia. This precipitate was observed in the present experiment in the rats administered the high dose of sodium saccharin or the higher doses of sodium ascorbate. Formation of this precipitate and induction of urothelial proliferation were inhibited by co-administration of NH4Cl, but somewhat higher doses of ammonium chloride were required for doses of sodium ascorbate compared to sodium saccharin. These results demonstrate that sodium ascorbate administered through the neonatal time period of the male rat produces urothelial hyperplasia in the dose responsive manner, with a no-effect level of 0.91% of the diet. The formation of the calcium phosphate-containing amorphous precipitate and urothelial proliferation were inhibited by co-administration with NH4Cl.

Effects of sodium ascorbate (vitamin C) and 2-methyl-1,4-naphthoquinone (vitamin K3) treatment on human tumor cell growth in vitro. I. Synergism of combined vitamin C and K3 action.

The effects of sodium ascorbate (vitamin C) and 2-methyl-1,4-naphthoquinone (vitamin K3) administered separately or in combination on the in vitro cultured human neoplastic cell lines MCF-7 (breast carcinoma), KB (oral epidermoid carcinoma), and AN3-CA (endometrial adenocarcinoma) have been examined. When given separately, vitamin C or K3 had a growth inhibiting action only at high concentrations (5.10(3) mumol/1 and 10(5) nmol/l, respectively). Combined administration of both vitamins demonstrated a synergistic inhibition of cell growth at 10 to 50 times lower concentrations. At this level separately given vitamins are not toxic. The sensitivity to this treatment was somewhat different in the three cell lines, being slightly higher for KB line. This tumor cell growth inhibitory effect was completely suppressed by the addition of catalase to the culture medium containing vitamins C and K3, suggesting an excessive production of hydrogen peroxide as being implied in mechanisms responsible for the above-mentioned effects.

Ascorbate and cysteine-mediated selective neutralisation of extracellular oxidants during N-formyl peptide activation of human phagocytes.

The effects of sodium ascorbate and cysteine (2.5 X 10(-5) M-2.5 X 10(-4) M) on the intensity and profile of luminol-enhanced chemiluminescence, superoxide generation, extracellular myeloperoxidase (MPO) activity and auto-iodination were measured in purified human polymorphonuclear leukocytes activated by the leukoattractant FMLP in vitro. Chemiluminescence studies were also performed using a whole-blood method. Cysteine (10(-4) M-2.5 X 10(-4) M) and ascorbate (2.5 X 10(-5) M-2.5 X 10(-4) M) caused significant inhibition of the early extracellular peak of FMLP-activated chemiluminescence and increased the intensity of the later occurring intracellular peak in both PMNL and blood. At the same concentrations both agents scavenged superoxide released by FMLP-activated PMNL, inhibited oxidant generation by extracellular MPO and decreased FMLP-induced auto-oxidation of PMNL. Administration of a single 1 gram oral dose of ascorbate to adult human volunteers was associated with significant reduction and enhancement respectively of the extracellular and intracellular luminol-enhanced chemiluminescence responses of FMLP-activated blood. These results show that the water soluble anti-oxidants cysteine and especially ascorbate selectively neutralise the reactivity of harmful reactive oxidants released by phagocytes, whilst the intracellular generation of antimicrobial oxidants remains intact.

Antagonistic effect of sodium ascorbate on ethanol-induced changes in swimming of mice

Antagonistic effect of sodium ascorbate on ethanol-induced changes in swimming of mice

Effect of sodium ascorbate on tumor induction in rats treated with morpholine and sodium nitrite, and with nitrosomorpholine

Groups of male MRC Wistar rats were treated for 2 years either with morpholine (10 g/kg food) together with sodium nitrite (3 g/l drinking water) or with N-nitrosomorpholine (NM, 0.15g/l drinking water). In both cases, a group of rats was given sodium ascorbate (22.7 g/kg food) in addition to these treatments. When ascorbate was present, the liver tumors induced by morpholine and nitrite showed a 1.7-fold longer induction period, a slightly lower incidence, and an absence of metastases in the lungs, indicating that ascorbate had inhibited the in vivo formation of NM. Ascorbate did not affect liver tumor induction by the performed NM. The group treated with morpholine, nitrite, and ascorbate had a 54% incidence of forestomach tumors, including an 18% incidence of squamous cell carcinomas, possibly because ascorbate promoted NM action in this organ.

Effect of Sodium Ascorbate and Sodium Nitrite on Toxin Formation of Clostridium botulinum in Wieners

Toxin production by Clostridium botulinum was inhibited by sodium nitrite levels above 50 mug/g of wiener. Sodium ascorbate at levels of 105 and 655 mug/g of product did not decrease the effectiveness of the sodium nitrite inhibition, nor did sodium ascorbate potentiate it. The results indicate that the use of sodium ascorbate in vacuum-packaged wieners does not appreciably alter the inhibition of C. botulinum toxin formation by sodium nitrite.

Effect of Sodium Ascorbate on Egg Shell Thickness During Hot Weather

HEYWANG and Kemmerer (1955) reported that supplementing an all-mash laying diet with 454 mg. per pound of ascorbic acid did not improve shell quality, as measured by the ratio of dried shell weight to whole egg weight. The data were obtained during two summers under uncontrolled ambient temperatures with average maximums of 101 and 104 and average means of 90 and 91 degrees F.Thornton and Moreng (1958), however, reported that ascorbic acid at levels of 5, 10, and 20 mg. and sodium ascorbate at a level of 20 mg. per pound of diet had a favorable influence on shell thickness and strength under both “moderate” and “high” environmental temperatures. In another study, Thornton and Moreng (1959) found that shell thickness and strength were improved during “cool” and “warm” ambient temperatures when the diet was supplemented with 10 mg. ascorbic acid per pound of diet.In their 1958 report, Thornton…