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At least 199 records · Page 11Linked to original sources
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↗
PubMed1969

Ascorbic acid and copper in linoleate oxidation. II. Ascorbic acid and copper as oxidation catalysts.

Both ascorbic acid and copper were strong prooxidants in the oxidation of linoleate in a buffered (pH 7.0) aqueous dispersion at 37 degrees C. Minimum concentrations at which catalytic activity was detected were 1.3 x 10(-7) m for copper and 1.8 x 10(-6) m for ascorbic acid. For concentrations up to 10(-3) m, the increase in rate of oxidation with increase in concentration of catalyst was greater for ascorbic acid than for copper. Ascorbic acid had maximum catalytic activity at 2.0 x 10(-3) m, but was still prooxidant at the highest concentration tested (5.0 x 10(-2) m). Dehydroascorbic acid was a weaker prooxidant than ascorbic acid. Further degradation products of ascorbic acid were not prooxidant. In early stages of the oxidation autocatalytic behavior was observed with copper, but not with ascorbic acid. Ascorbic acid functioned as a true catalyst, i.e., it accelerated the reaction but it was not oxidized simultaneously with the linoleate. It is proposed that the dehydroascorbic acid radical initiates the linoleate oxidation reaction.

Alkenes↗
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↗
PubMed1995

Whole body X-ray irradiation to mice decreases ascorbic acid concentration in bone marrow: comparison between ascorbic acid and vitamin E.

The change in the ascorbic acid concentration in the bone marrow after whole body X-ray irradiation was compared with that in the vitamin E concentration. The ascorbic acid concentration in the bone marrow significantly decreased by 30% 1 h after exposure to 3 Gy of X-rays, whereas the vitamin E concentration in the bone marrow was significantly decreased 5 h after exposure, when the level of ascorbic acid was less than 10% of that in the control. At 24 h after exposure, the ascorbic acid concentration in the bone marrow was significantly decreased by 80% after exposure to 0.5 Gy, whereas the vitamin E concentration was significantly decreased after exposure to 1 Gy or more. In the bone marrow, the decrease in the ascorbic acid concentration was accompanied by a marked increase in the concentration of dehydroascorbic acid, an oxidized form of ascorbic acid. X-ray irradiation did not decrease either the ascorbic acid or vitamin E concentration in the serum or intestine. These findings suggest that the bone marrow is more highly susceptible to oxidative damage by radiation and that ascorbic acid plays an important defense role against it. On Day 8 after irradiation, the decreases in the vitamin E and ascorbic acid concentrations in the bone marrow showed recovery after exposure to 3 Gy, but not after the exposure to 6 Gy.

Animals↗
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↗