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Results for “ASCORBIC ACID”

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PubMed1986

Effect of ascorbic acid on iron absorption from different types of meals. Studies with ascorbic-acid-rich foods and synthetic ascorbic acid given in different amounts with different meals.

The effect of ascorbic acid on the absorption of non-heme iron was studied in 299 subjects. Different meals in which the non-heme iron was labelled with two different radio-iron isotopes were served with and without ascorbic acid to the same subject. Other meals containing foods with a known high content of ascorbic acid were also studied. Studies were also made giving different amounts of ascorbic acid with different meals. Marked differences in the enhancement of iron absorption were seen when ascorbic acid was given in different meals. It is suggested that ascorbic acid promotes iron absorption from the diet by reducing the negative effect on iron absorption of certain ligands such as phytates and tannins present in the diet. This interpretation is supported by observations that the most pronounced effects of ascorbic acid were found in meals with a high content of ligands known to inhibit iron absorption. Crystalline ascorbic acid and native ascorbic acid in foods appeared to have the same effect in promoting absorption of iron. The results indicate that ascorbic acid has a key physiologic role in facilitating the absorption of non-heme iron from the diet and that about 50 mg of the vitamin in each main meal is desirable for optimum effect.

Adult↗
PubMed1990

Spontaneous decay of oxidized ascorbic acid (dehydro-L-ascorbic acid) evaluated by high-pressure liquid chromatography.

We applied high-pressure liquid chromatography to assess the decomposition of the oxidized form of vitamin C, dehydro-L-ascorbic acid. We selected experimental conditions that might represent a wide variety of clinical and research procedures. Decay of dehydro-L-ascorbic acid proceeded much more rapidly at high pH (7-8) than at low pH (3-5) and was more rapid at 37 or 45 degrees C than at 0 or 23 degrees C. When evaluated at pH 6.6, the percent decay was somewhat more rapid from an initial concentration of 1000 mumol/L than at 5-10 mumol/L. The analytical procedure (HPLC) provided useful information about the rate of decay under various conditions. This may facilitate future biological and clinical studies that require a distinction between the oxidized and reduced forms of vitamin C.

Ascorbic Acid↗
PubMed1997

Gas chromatographic/mass spectrometric measurement of ascorbic acid and analysis of ascorbic acid degradation in solution.

L-Ascorbic acid, DHA, and the oxidized products derived from AA can be accurately measured using GC/MS. Owing to the complex nature of the reactions through which AA proceeds, we believe that GC/MS is currently the procedure of choice in making AA-related measurements. The methods described are useful in defining reactions involving AA. The methods may indicate in vivo oxidative injury and may allow the use of AA-derived products to determine if antioxidant modulations are effective.

Animals↗
PubMed1986

Liquid chromatographic determination of uric acid and ascorbic acid in rat retinae after ophthalmic artery and optic nerve ligation.

Change of urate and ascorbate levels in retinae of rat left eyes after ophthalmic artery and optic nerve ligation was studied by reversed-phase high-performance liquid chromatography with electrochemical detection. The right eyes were used for sham operation. We found that uric acid levels in the retinae of the left eyes increased as a function of time after the operation, whereas those of the right eyes remained unchanged. In addition, we found that ascorbic acid levels in the retinae of the rat eyes decreased after the operation.

Animals↗
PubMed1992

Effect of acetylsalicylic acid, ascorbate and ibuprofen on the macrophage system.

The influence of ascorbic acid (CAS 50-81-7), acetylsalicylic acid (CAS 50-78-2) and ibuprofen (CAS 15687-27-1) on macrophages of C57BL/6 mice was investigated in vitro. It has been shown that ascorbic acid or acetylsalicylic acid alone did not stimulate or inhibit the production of interleukin-6, whereas a combination of both substances caused a significant stimulation. The viral replication in L929 fibroblasts was not affected by ascorbate and/or acetylsalicylic acid. In addition, the tumor-necrosis factor (TNF) synthesis of peritoneal macrophages was neither stimulated nor inhibited by both substances, alone or in combination. The oxygen radical production, however, was definitely inhibited by ascorbic acid, the effect of acetylsalicylic acid was far less marked, but at the high concentrations the inhibition was clearly discernible. Ibuprofen, a propionic acid derivate, was able to reduce the replication of vesicular stomatitis virus in L929 fibroblast cells. At the highest concentration of ibuprofen, 100 micrograms/ml, 34% of the fibroblast were able to survive. This protective effect declined as the ibuprofen concentration decreased. Ibuprofen could not stimulate peritoneal macrophages to secrete TNF, whereas the oxygen radical production was significantly reduced. In addition, ibuprofen activated mouse macrophages to produce interleukin-6 in a dose dependent way. The results of the in vitro experiments presented clearly show that ascorbic acid, acetylsalicylic acid in ibuprofen influenced the unspecific immune system.

Animals↗
PubMed2001

Diphenyl diselenide and ascorbic acid changes deposition of selenium and ascorbic acid in liver and brain of mice.

Sodium selenite (Na2SeO3) is the selenium form used in the composition of dietary supplements, and diphenyl diselenide (PhSe)2 is an important intermediate in organic synthesis, which increases the risk of human exposure to this chemical in the workplace. These compounds have been reported to inhibit the cerebral and hepatic aminolevulinic acid dehydratase (ALA-D) in vitro, and now we show that ascorbic acid can reverse some alterations caused by in vivo selenium exposure, but not ALA-D inhibition. The effect of Na2SeO3 or (PhSe)2 and ascorbic acid on selenium distribution, total non-protein thiol, ascorbic acid content (liver and brain) and haemoglobin was also examined. Mice were exposed to 250 micromol/kg (PhSe)2, or 18.75 micromol/kg Na2SeO3 subcutaneously, and to ascorbic acid, twice a day, 1 mmol/kg intraperitonially, for 10 days. Hepatic ALA-D of mice treated with (PhSe)2 was inhibited about 58% and similar results were observed in the animals that received ascorbic acid supplementation (P<0.01, for (PhSe)2-treated and (PhSe)2+ascorbic acid-treated mice). The haemoglobin content decreased after treatment with (PhSe)2 (P<0.01). However, the haemoglobin content of the (PhSe)2+ascorbic acid group was significantly higher than in the (PhSe)2-treated mice (P<0.05), and similar to control (P>0.10). Ascorbic acid treatment decreased significantly the hepatic and cerebral deposition of Se in (PhSe)2-exposed mice (P<0.01). Hepatic non-protein thiol content was not changed by treatment with (PhSe)2, ascorbic acid or (PhSe)2+ascorbic acid. Hepatic content of ascorbic acid was twice that in mice that received (PhSe)2, independent of ascorbic acid treatment (P<0.001). The results of this study suggest that vitamin C may have a protective role in organodiselenide intoxication.

Animals↗