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Results for “ascorbic acid”

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At least 55 records · Page 3Linked to original sources
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↗
PubMed1976

L-ascorbic acid, L-ascorbate 2-sulfate, and atherogenesis.

Rabbits on a high cholesterol diet were divided into three groups: one group received subcutaneous injections of physiological saline 3 times/day, 5 days/wk for 10 wk; another group received subcutaneous injections of L-ascorbic acid (0.37 mmole) according to the same timetable; and the third group was administered an equivalent amount of L-ascorbate 2-sulfate as outlined above. Each week the serum levels of total and free cholesterol and triglycerides were measured. At the end of 10 wk the animals were killed and the cholesterol content of the livers, spleens, and adrenal glands was measured. The aortas were examined for plaque deposition; the deposits were excised and pooled according to groups; and the total mass and cholesterol contents of the pooled plaques were determined. Administration of ascorbic acid or ascorbate 2-sulfate did not prevent hypercholesterolemia or elevated levels of serum triglycerides. No significant differences among the groups were found either in tissue cholesterol levels or in the extent or type of lesions found. Although plaque deposition appeared to be similar in the aortas of these animals, a marked difference was found in total mass and cholesterol content of the plaques: The plaques of the saline-treated group had a total mass and cholesterol content approximately 2.5 times that found in the group injected with ascorbic acid and about 1.5 times that found in the animals treated with ascorbate 2-sulfate. These results indicate that ascorbic acid, in particular, minimizes the total quantity of plaque deposition even though it is ineffective in preventing hypercholesterolemia, elevated serum triglycerides, and accumulation of cholesterol by several tissues.

Adrenal Glands↗
PubMedDate not supplied

Enzymatic formation of ascorbic acid in liver homogenate of mice fed dietary ascorbic acid.

The effect of exogenous ascorbic acid intake on enzymatic formation of ascorbic acid in mice has been studied. After the mice were on diets containing ascorbic acid for two months, the rates of ascorbic acid formation in mouse liver homogenates were measured in vitro using glucuronolactone and gulonolactone as substrate in their respective reaction systems. Exogenous ascorbic acid intake (1, 5 or 8% in the diet) was able to reduce activities of ascorbic acid synthesizing enzymes in mouse liver in either the glucuronolactone or gulonolactone system. The control mechanism for reaction of glucuronolactone to produce ascorbic acid is not stereospecific because large amounts of dietary erythorbic acid, a stereoisomer of ascorbic acid, could also reduce the rate of ascorbic acid formation when glucuronolactone was used as substrate. However, the regulation of ascorbic acid synthesis using gulonolactone as a precursor was apparently stereospecific. Dietary glucose or xylitol had no effect on activities of ascorbic acid synthesizing enzymes.

Animals↗
PubMed1979

Effects of ascorbic acid and sodium ascorbate on cyclic nucleotide metabolism in human lymphocytes.

L-ascorbic acid (LAA) augmented cGMP many-fold in highly purified human peripheral blood lymphocytes. The cGMP response occurred within 10 sec and persisted for at least 60 min. D-ascorbic acid (DAA) and dehydroascorbic acid (DHAA) were also equally active in enhancing cGMP concentrations but metabolic precursors of ascorbic acid and other inorganic acids did not increase cGMP levels. Determination of the amount of DHAA contaminating the LAA precluded the possibility that it was solely responsible for the enhanced cGMP levels. The sodium or calcium salts of ascorbic acid did not increase cGMP concentrations. If these neutralized preparations were acidified, increased cGMP concentrations were then noted. In broken cell preparations, LAA, DAA, and DHAA and to a lesser extent sodium ascorbate (NaA) enhanced guanylate cyclase activity while neither inhibited cAMP or cGMP phosphodiesterase (PDE) activity. The possible role of H2O2, fatty acid liberation, prostaglandin production, oxidizing-reducing agents, and free radical formation in mediating the effects of ascorbic acid on cGMP levels were evaluated, but none of these potential mechanisms were definitively proven to be a required intermediary for the cGMP enhancing activity of ascorbic acid. LAA, DHAA or NaA did not induce lymphocyte transformation or modulate lectin-induced mitogenesis.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗
PubMed1987

Hyaluronic acid degradation by ascorbic acid and influence of iron.

The effects of ascorbic acid, iron and ADP on hyaluronic acid, a compound present in inflamed joints, were investigated in an in vitro system. Ascorbic acid induces degradation of hyaluronic acid which increased in the presence of FeCl3 and which is additionally stimulated by ADP chelated ferric ions. The hyaluronic acid degrading reactions induced by the Fe-III/ADP/ascorbic acid system were inhibited by catalase and formate to various extents whereas the presence of superoxide dismutase did not exert any inhibitory effect. Desferrioxamine, a specific iron chelator, completely inhibited hyaluronic acid depolymerisation by ascorbic acid as well as in combination with FeCl3 or FeCl3/ADP, respectively. We suggest that the ultimate hyaluronic acid degrading species is OH, generated via the Fe-III/ADP catalysed Haber Weiss reaction. There is also an indication for the involvement of perferryl or/and ferryl species in the degradation process.

Adenosine Diphosphate↗
PubMed1985

The effect of synovial fluid proteins in the degradation of hyaluronic acid induced by ascorbic acid.

The degradation of hyaluronic acid induced by ascorbic acid and the effect of synovial fluid proteins, such as ceruloplasmin, transferrin, and albumin, were investigated on the basis of the elution volume and the molecular weight of hyaluronic acid using high-performance gel permeation chromatography. Hyaluronic acid was degraded to less than one-third of the original molecular weight in the range of the physiological concentrations of ascorbic acid. Synovial fluid proteins protected against the ascorbate-dependent degradation of hyaluronic acid at their physiological concentrations. It is suggested that the inhibitory activity of ceruloplasmin mainly depends on the ferroxidase activity and that of transferrin is probably due to iron binding property.

Albumins↗
PubMed1975

Effect of oral administration of large quantities of ascorbic acid on blood levels and urinary excretion of ascorbic acid in healthy men.

The influence of the daily ingestion of 1, 2, 3, and 5 grams of ascorbic acid on whole blood and plasma ascorbic acid levels and on the urinary excretion of ascorbic acid has been investigated. The ingestion of one gram of ascorbic acid per day for one week significantly increases plasma and whole blood levels over presupplementation levels, but larger amounts of ascorbic acid do not further increase plasma and whole blood ascorbic acid levels. Urinary excretion increases with intake, up to intakes of 3 grams per day but does not increase further when 5 grams of ascorbic acid is ingested per day. Upon discontinuing ascorbic acid supplementation the plasma and whole blood levels decline rapidly and the urinary excretion of ascorbic acid falls to presupplementation values within a few days. The results suggest that there is need for a detailed study of the routes of excretion of ascorbic acid at high levels of intake and that the safety of ingesting large quantities of ascorbic acid may be questioned.

Adult↗