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At least 523 records · Page 29Linked to original sources
PubMed1998

Effect of naloxone on morphine-induced changes in striatal dopamine metabolism and glutamate, ascorbic acid and uric acid release in freely moving rats.

Recent findings have shown that systemic morphine increases extracellular dopamine (DA), dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), ascorbic acid (AA) and uric acid concentrations in the striatum of freely moving rats. The morphine-induced increase in DA oxidative metabolism is highly correlated with that of xanthine. In the present study, we evaluated the effects of subcutaneous (s.c.) naloxone (1 mg/kg) on morphine-induced changes in DA, DOPAC, HVA, 5-hydroxyindoleacetic acid (5-HIAA), AA, uric acid and glutamate in the striatum of freely moving rats using microdialysis. Dialysates were assayed by high performance liquid chromatography with electrochemical detection or (glutamate) ultraviolet detection. Morphine (5-20 mg/kg) given s.c. increased DA, DOPAC+HVA, 5-HIAA, AA and uric acid and decreased glutamate dialysate concentrations over a 3 h period after morphine. Morphine (1 mM), given intrastriatally, did not affect all the above parameters, with the exception of an early short-lasting decrease in AA concentration. Naloxone antagonised all morphine-induced changes with the exception of AA increase and glutamate decrease in dialysate concentrations. Systemic or intrastrial (0.2-2 mM) naloxone increased AA and decreased glutamate dialysate concentrations. When given intranigrally, morphine (1 mM) increased DOPAC+HVA, AA and uric acid and decreased glutamate dialysate concentrations over a 2 h period after morphine; DA and 5-HIAA concentrations were unaffected. These results suggest that: (i) morphine increases striatal DA release and 5-hydroxytryptamine oxidative metabolism by a micro-opioid receptor-mediated mechanism mainly at extranigrostriatal sites; (ii) morphine increases DA and xanthine oxidative metabolism and affects glutamate and AA release by a micro-opioid receptor mediated mechanism acting also at nigral sites; and (iii) a micro-opioid receptor-mediated mechanism tonically controls at striatal sites extracellular AA and glutamate concentrations.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1998

Studies of the cardioprotective effects of ascorbic acid in isolated rabbit hearts.

Ascorbic acid (CAS 50-81-7) might mediate cardioprotective effects by scavenging free oxygen radicals. The effects of exogenous ascorbic acid on acute myocardial ischemia (MI) was investigated in isolated electrically-driven rabbit hearts (Langendorff, constant pressure: 70 cm H2O, Tyrode solution, Ca2+ 1.8 mmol/l, 37 degrees C). Repetitive MI, separated by a reperfusion period of 50 min, was induced by coronary artery branch ligature and quantitated from epicardial NADH-fluorescence photography. Starting after a reperfusion period of 20 min, isolated hearts were treated with ascorbic acid (10(-5) or 10(-4) mol/l). Ascorbic acid had no significant influence on the left ventricular left ventricular pressure or the coronary flow (p > 0.05). Ascorbic acid had no significant effect on epicardial NADH-fluorescence area or intensity (p > 0.05). Free radical scavenging properties reported for ascorbic acid do not mediate cardioprotective effects at the concentrations used in isolated rabbit hearts.

Animals↗
PubMed1998

Dependence of growth, bone metabolism and functions of polymorphonuclear leukocytes on ascorbic acid in pigs.

Pigs with hereditary ascorbate deficiency (OD pigs) were depleted of, or supplemented with, ascorbic acid by respective diets. Depletion of young (i.e. 5-7 weeks old) animals for at least three weeks had a negative effect on growth, body temperature and levels of bone alkaline phosphatase and induced symptoms of scurvy. Doses of 5 mg ascorbic acid kg-1 body weight day-1 were sufficient to reverse these effects. The level of ascorbic acid sharply decreased in plasma within one week of depletion, whereas in leukocytes it declined more slowly and to a lower extent. Bone alkaline phosphatase levels substantially declined in ascorbic acid depleted animals. Supplementation with > 100 mg ascorbic acid kg-1 body weight day-1 did not improve growth. Dietary ascorbic acid was absorbed from the intestinal lumen into the blood within less than 1 hour and reached a peak 5-6 hours after the meal. The extent of this absorption depended on the systemic ascorbic acid level. Ascorbic acid influenced leukocyte function, since the production of reactive oxygen intermediates by polymorphonuclear leukocytes decreased in supplemented animals. Thus, this animal model permits to establish the level of dietary ascorbic acid that is critical for growth of pigs as well as to study its absorption into the blood and the associated alterations in polymorphonuclear leukocytes and bone metabolism.

Alkaline Phosphatase↗
PubMed1996

Oxidation of ascorbic acid by lipoxygenase: effect of selected chemicals.

The ability of soybean lipoxygenase to mediate ascorbic acid oxidation was examined. The oxidation of ascorbic acid was dependent on the concentration of linoleic acid, ascorbic acid and the enzyme. The optimal conditions to observe maximal enzyme velocity included the presence of 800 microM linoleic acid, 500 microM ascorbic acid and 25 nM soybean lipoxygenase in 50 mM Tris buffer, pH 8.3. The reaction displayed a K(m) value of 100 microM for ascorbic acid and an average specific activity of about 460 nmol/min/nmol enzyme under the optimal conditions. The effect of ascorbic acid on the lipoxygenase-catalysed co-oxidation of xenobiotics was also evaluated. Ascorbic acid markedly decreased the rate of oxidation of test xenobiotics by the lipoxygenase. In contrast, the rate of ascorbic acid co-oxidation was enhanced significantly by the presence of xenobiotics, which are co-oxidized simultaneously by lipoxygenase through the formation of free radicals. Superoxide generation was not observed during lipoxygenase-mediated ascorbic acid co-oxidation.

Ascorbic Acid↗
PubMed1978

[Examinations of aminoacids in aqueous humour after intravitreous injection of ascorbic acid (author's transl)].

The ascorbic acid concentration of the vitreous of rabbits was experimentally increased to about 20 times the normal value. 24 h after the intravitreal injection of ascorbic acid 13 out of 16 free amino acids were decreased, only Glutamicacid, Glycine and Alanine were increased. 48 h after the injection 13 amino acids were lowered. On the fourth day 8 amino acids were decreased in relation to normal values. After 4 weeks the concentrations of 5 amino acids were raised further compared to the normal values, but 10 amino acids were concentrated lower than the normal values. Also Glu-acid, Gly and Ala had fallen down to the range of the normal values. The total amino acids include the free amino acids and the amino acids, which we find after 6 h hydrolysis. On the first day 11 amino acids showed elevations, 7 amino acids were decreased. After 4 weeks Taurin, Lysine and Histidin were higher than the normal values, 15 amino acids were lower. In single cases the differences were statistically significant. We suppose, that the changes of amino acids are caused by the ascorbic acid or their derivates. There is an anterior drainage after intravitreal injection. We come to the conclusion, that there is a reversible disturbance of the diffusion and active transport of amino acids by ascorbic acid.

Animals↗
PubMed1976

Stability of vitamin C (ascorbic acid) in tablets.

Stability of ascorbic acid (vitamin C) in various tablet formulations and the nature and extent of formation of decomposition products (dehydroascorbic acid, diketogulonic acid, and oxalic acid) were determined under normal conditions of storage and in simulated use tests. IR spectrophotometric, colorimetric, fluorometric, titrimetric, polarographic, and chromatographic methods were applied. Recent implications concerning the instability of ascorbic acid in tablets and the potentially harmful nature of the breakdown products are shown to be unfounded. Under normal storage conditions, commerical-type ascorbic acid tablets are stable for over 5 years (greater than 95% potency retention). The amounts of all three breakdown products formed under the various storage conditions constitute a small percentage of the ascorbic acid content and pose no dietary hazard. IR spectroscopy was inadequate as a quantitative method for evaluating ascorbic acid potency in tablet formulations. The official titration methods and TLC, colorimetric, and polarographic determinations correlate well and define accurately the stability of ascorbic acid in these dosage forms.

Ascorbic Acid↗
PubMed1978

Leucocyte ascorbic acid and pregnancy.

1. Leucocyte ascorbic acid concentrations have been measured in 1147 females during early pregnancy and in smaller numbers of women before conception, throughout pregnancy and at 6 months post partum. 2. The leucocyte concentration in the 1st trimester was found to be affected by season, social class and smoking. Selecting individuals by extremes of social class, season and smoking produced two small populations with almost separate ascorbic acid distributions and mean concentrations of 21.7 and 45.1 microgram/10(8) leucocytes. 3. Early pregnancy had little effect on leucocyte ascorbic acid concentrations but values decreased in the second trimester. However, this was associated with a leucocytosis so that the total leucocyte ascorbic acid content of blood was unchanged. 4. Low ascorbic acid concentrations during the 1st trimester were not associated with subsequent spontaneous abortions, still-births or neonatal deaths, but there was an increased frequency of low values in women who gave birth to infants smaller than 3250 g. 5. The adequacy of ascorbic acid reserves in early pregnancy is discussed.

Adult↗
PubMed1996

The mechanism of uptake of ascorbic acid into osteoblasts and leukocytes.

Ascorbic acid is taken up into osteoblast cells by a saturable, stereospecific, Na(+)-dependent transporter, accumulating ascorbic acid to a level 100-fold that in the medium. The ascorbic acid uptake rate correlated with intracellular hydroxyproline synthesis. A second, distinct mechanism has also been described for accumulation of ascorbic acid into neutrophils and myeloid leukemia cells. This appears to be Na(+)-independent and relies on the glucose transporter GLUT1 to ferry dehydroascorbic acid (DHA) into cells and then to trap it as ascorbic acid to a high concentration.

Animals↗
PubMed2003

Ascorbic acid accumulates in cartilage in vivo.

BACKGROUND: Ascorbic acid plays an important role in collagen synthesis. Though ascorbic acid concentrations in many tissues and in plasma have been characterized, little is known about in vivo levels in cartilage. MATERIALS AND METHODS: To discern the role of ascorbic acid in cartilage, we conducted a dose-response study measuring ascorbic acid levels in various guinea pig tissues and fluids in response to this vitamin. To our knowledge, this is the first such study in cartilage. RESULTS: Ascorbic acid was higher in synovial fluid compared to paired plasma, and higher in cartilage than paired synovial fluid. Tissue levels were normalized to DNA to compare ascorbic acid concentrations relative to a measure of tissue cellularity. Normalized cartilage ascorbic acid concentrations were intermediate between liver (lowest) and adrenal (highest), two well-known concentrators of ascorbic acid. All tissues and fluids showed a saturation-effect characterized by large differences in ascorbic acid concentrations between low- and medium-dose groups and smaller concentration differences between medium- and high-dose groups. CONCLUSIONS: Cartilage, a tissue dependent on ascorbic acid for extracellular matrix production of collagen, concentrates ascorbic acid. This concentrating ability is consistent with the chondrocyte expression of SVCT2, a sodium-dependent ascorbic acid transporter.

Adrenal Glands↗
PubMed1996

Hormone induction of ascorbic acid transport in immature granulosa cells.

Ascorbic acid serves a vital role as an antioxidant, and like FSH, it inhibits apoptosis of granulosa cells in cultured follicles. In contrast, reactive oxygen species block the action of FSH and induce DNA damage in these cells. As the uptake of ascorbic acid by granulosa cells may be a site for regulation, we examined the nature of this process and whether uptake is under hormone control. Granulosa cells were isolated from immature rats pretreated with estradiol or diethylstilbestrol for 3-4 days and placed in culture. Culture of the cells with either FSH (50 ng/ml) or insulin-like growth factor I (IGF-I; 30 ng/ml) for 48 h increased ascorbic acid uptake by 2.7- and 1.9-fold (P < 0.05), respectively, and the response to FSH plus IGF-I was additive (4.5-fold; P < 0.05). The interval for maximum induction of ascorbic acid transport by FSH was between 4-8 h, whereas a significant response to IGF-I was not seen until 48 h. GnRH (1 microM), phorbol ester (phorbol 12-myristate 13-acetate; 1 microM), and 8-bromo-cAMP (8Br-cAMP; 1 mM) also induced ascorbic acid transport by 1.7-, 1.9-, and 2.3-fold (P < 0.05) within 24 h, and the response to maximal levels of phorbol ester and 8Br-cAMP was synergistic (4.8-fold; P < 0.05). Kinetic analysis showed a similar Michaelis constant (K(m); 50.8 +/- 5.3 microM) and maximum velocity (3.3 +/- 0.4 pmol/10(6) cells.min) for ascorbic acid transport in FSH-, 8Br-cAMP-, or phorbol ester-treated cells. Ouabain (100 microM) or removal of extracellular Na+ significantly inhibited ascorbic acid uptake, as did dinitrophenol (1 mM), an inhibitor of mitochondrial production of ATP. The induction of ascorbic acid transport by FSH, IGF-I, or GnRH was abolished by simultaneous incubation with tyrphostin (AG-18; 80 microM), a specific tyrosine kinase inhibitor, whereas induction was unaffected by an inactive, but chemically similar, compound (A-1; 80 microM). From these results we conclude that ascorbic acid uptake is energy and Na+ dependent and that the induction of ascorbic acid transporters in granulosa cells occurs through multiple hormones that ultimately influence tyrosine-specific protein kinases. The hormone-dependent induction of ascorbic acid accumulation in granulosa cells appears to be an essential process for the development and maintenance of a viable follicle.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1994

Effect of aldonic acids on the uptake of ascorbic acid by 3T3 mouse fibroblasts and human T lymphoma cells.

1. Previously, we reported that calcium L-threonate caused a dose-related increase in uptake of ascorbic acid (AA) by human T-lymphoma cells. Preincubation of mouse fibroblasts with calcium L-threonate also resulted in a dose-related augmentation in uptake of AA as compared to non-treated controls. 2. Potassium L-lyxonate increased AA uptake by lymphoma cells, but did not significantly affect uptake by fibroblasts. Tartaric acid decreased uptake of AA by both cell lines. 3. Ouabain and dinitrophenol had no effect on AA uptake nor on the ability of threonate to augment AA uptake by fibroblasts. However, in T-lymphoma cells ouabain and dinitrophenol reduced AA uptake and prevented augmentation of AA uptake by calcium L-threonate.

3T3 Cells↗
PubMed1980

Nutritional aspects of ascorbic acid: uses and abuses.

Ascorbic acid in physiological doses is essential for the normal functioning of the human body. Larger doses are required to treat a severe deficiency of vitamin C intake, as in the case of scurvy. Occasionally, massive doses may be required to treat a metabolic defect involving ascorbic acid. There has been some mention of megadose therapy with ascorbic acid for the prevention of colds, the improved healing of wounds and even the treatment of cancer, but no acceptable scientific data have been presented. In fact, in a few instances, such therapy has proved injurious.

Ascorbic Acid↗