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PubMed1995

Protective effect of seminal plasma proteins on the degradation of ascorbic acid.

The objectives of this study were to determine ascorbic acid stability and its effect on antiproteinase activity of seminal plasma in the presence of an oxidant. Effect of seminal plasma, and additives: glutathione, albumin, hydrogen peroxide and Tris buffer, on ascorbic acid degradation was investigated by UV absorbance. Antiproteinase against trypsin amidase activity was measured spectrophotometrically using N-benzoyl-DL-arginine-p-nitroanilide (BAPNA) as substrate. Ascorbic acid was destroyed much more rapidly with the addition of hydrogen peroxide than in Tris buffer at pH 8.2 alone. Seminal plasma protected ascorbic acid more efficiently than glutathione and albumin alone. The protective effect of seminal plasma on ascorbic acid degradation may closely relate to the function of ascorbic acid in reproductive system of scurvy-prone animals including teleost fish. Within the range of 1-8 mM concentrations, ascorbic acid had a pro-oxidant action on seminal plasma antiproteinase activity in vitro when they were incubated with hydrogen peroxide.

Animals↗

PubMed1979

Apparent effect of ascorbic acid medication on semen metal levels.

The apparent effect of ascorbic acid therapy for nonspecific spermagglutination on semen levels of ascorbic acid as well as macro- and micrometals was determined in 20 men (ages 25 to 38). Pretreatment diagnosis was based on infertility and relatively low ratings in sperm density, motility, motility index, and semen volume, and were associated with large numbers of abnormal sperm, sperm precursors, and leukocytes. The pretreatment levels of ascorbic acid, sodium, iron, potassium, zinc, manganese, lead, magnesium, and copper were measured in each patient's semen and compared with levels following 60 days of dietary vitamin C supplementation (1.0 gm/day). Analysis of the vitamin C preparation prescribed revealed that each subject was given an impure ascorbic acid medication to supplement a normal diet. Therefore, the significant increases in levels of ascorbic acid and metals in semen following therapy could not be attributed to ascorbic acid alone, nor, similarly, the improved physical parameters of each subject's semen following therapy; no apparent spermagglutination and restored fertility may be due to the interaction of ascorbic acid with cations found in semen.

Adult↗

PubMed1975

Ascorbic acid and blood lipid and uric acid levels of students.

Serum lipid and uric acid levels were investigated in two groups of healthy young students. Each member of the control group was given 1 g of citric acid, and each member of the experimental group 4 g of L-ascorbic aicd daily for 4 months. Blood samples were drawn every month and leucocyte ascorbic acid, serum ascorbic acid, cholesterol, free fatty acids, triglycerides and uric acid were determined. The ascorbic acid did not cause dramatic changes in lipid parameters, and no evidence could be found that ascorbic acid raises serum uric acid levels.

Adolescent↗

PubMed2000

Ascorbic acid and glutathione modulate the biological activity of S-nitrosoglutathione.

Ascorbic acid and glutathione (GSH) are important determinants of the intracellular redox state, and both are known to accelerate the decomposition of S-nitrosoglutathione (GSNO), an endogenous adduct of nitric oxide (NO). The implications of these observations for GSNO bioactivity are not yet clear. We investigated the effect of ascorbic acid and GSH on GSNO bioactivity by using a bioassay with isolated segments of guinea pig aorta suspended in organ chambers. Arterial segments demonstrated relaxation to GSNO (0.1 micromol/L) that was significantly enhanced by 300 micromol/L ascorbic acid (71+/-6% versus 53+/-6%, P<0.05) but not GSH. Both ascorbic acid and GSH significantly shortened the duration of arterial relaxation in response to 0.1 micromol/L GSNO (from >120 minutes to 22.5+/-3.5 and 36.3+/-4.3 minutes, respectively; P<0.05), consistent with accelerated decomposition of GSNO that was confirmed spectrophotometrically. The effect of ascorbic acid was abrogated by either DTPA or the copper(I)-specific agent bathocuproine but not deferoxamine, indicating a dependence on the availability of redox-active copper. Consistent with this notion, the action of ascorbic acid on GSNO bioactivity was also supported by copper-zinc superoxide dismutase, a physiologically relevant source of copper. In contrast, the effect of GSH on GSNO degradation and GSNO-mediated arterial relaxation was independent of transition metal ions, because DTPA had no effect. These data indicate that both ascorbic acid and GSH modulate GSNO bioactivity and suggest a distinction between the mechanism of GSNO degradation by ascorbic acid or GSH. Whereas both ascorbic acid and GSH accelerate the degradation of GSNO, only ascorbic acid is dependent on the presence of transition metal ions.

Animals↗

PubMed2006

Ascorbic acid contents of Pakistani fruits and vegetables.

Fresh fruits and vegetables are good sources of vitamin C which is known for its antioxidant and immune-enhancing effects. The objective of this study was to determine ascorbic acid (vitamin C) contents of regularly consumed fruits and vegetables available in Pakistani markets. Most commonly used fresh fruits and vegetables were homogenized in 5% trichloroacetic acid, and ascorbic acid contents in the extracts were determined using a spectrophotometric method. Banana, custard apple, orange, lemon, guava and papaya were found to be very rich in ascorbic acid. Among vegetables, capsicum (green sweet pepper), cauliflower, bittergourd, roundgourd, beetroot, spinach, cabbage and radish contained high concentrations of ascorbic acid. Chikoo, grapes, pear, apricot, peach, carrot, cucumber, lettuce and "kakri" were found to be poor sources of ascorbic acid. Several Pakistani fruits and vegetables (pear, melon, onion, sweet green pepper, spinach, cucumber) had ascorbic acid values similar to those reported by US Department of Agriculture in these fruits and vegetables in USA. However, wide differences in vitamin C contents were also observed in certain other fruits and vegetables from these two countries. This indicates that regional varieties of fruits and vegetables could vary in their ascorbic acid contents. Since subclinical deficiency of vitamin C appears to be quite common in developing countries like Pakistan, there is a need to develop awareness among masses to consume fresh fruits and vegetables with high contents of vitamin C.

Ascorbic Acid↗

PubMed1983

Serum ascorbic acid in patients undergoing chronic hemodialysis.

Serum presupplementation ascorbic acid levels were subnormal in 8 out of 10 patients undergoing chronic hemodialysis with capillary film and capillary flow dialyzers, the mean duration of treatment being 11 months. Supplementation with 100 mg ascorbic acid daily for two weeks raised the ascorbic acid values to normal in 9 out of 10 patients. After supplementation with 500 mg daily, all patients had ascorbic acid levels exceeding the normal upper limit, and 3 of them had gastrointestinal side-effects. The mean blood pH value, measured in 24 patients on chronic hemodialysis, showed a significant, though slight, decrease during supplementation with 500 mg daily as compared with the mean presupplementation value, but no statistically significant changes were observed in blood bicarbonate, base excess or PCO2 values.

Acid-Base Equilibrium↗

PubMed1991

Plant resistance mechanisms to air pollutants: rhythms in ascorbic acid production during growth under ozone stress.

Relationships between ozone (O3) tolerance and leaf ascorbic acid concentrations in O3-susceptible (O3-S) 'Hark' and O3-resistant (O3-R) 'Hood' soybean, Glycine max (L.) Merr., cultivars were examined with high-performance liquid chromatography (HPLC). Leaf samples were analyzed at 4 intervals during a 24 h period. Soybean cultivars grown in the greenhouse with charcoal filtered (CF) and nonfiltered (NF) air showed daily oscillations in ascorbic acid production. Highest ascorbic acid levels in leaves during light coincided with highest concentrations of photochemical oxidants in the atmosphere at 2:00 p.m. The resistant genotype produced more ascorbic acid in its trifoliate leaves than did the corresponding susceptible genotype. Under CF air (an O3-reduced environment) O3-S and O3-R cultivars showed rhythms in ascorbic acid production. In NF air (an O3 stress environment) the O3-R cultivar alone showed rhythms in ascorbic acid production. Results indicated that superior O3 tolerance in the Hood soybean cultivar (compared with Hark) was associated with a greater increase in endogenous levels of ascorbic acid. Ascorbic acid may scavenge free radicals and thereby protect cells from injury by O3 or other oxyradical products. Plants defend themselves against photochemical oxidant stress, such as O3, by several mechanisms. Experimental evidence indicates that antioxidant defense systems existing in plant tissues may function to protect cellular components from deleterious effects of photochemical oxidants through endogenous and exogenous controls.

Adaptation, Physiological↗

PubMed2002

Ascorbic acid status in postmenopausal women with hormone replacement therapy.

OBJECTIVES: Hormone oral contraceptives affected ascorbic acid status adversely in young women. In vitro, estrogens and progesterone inhibited ascorbic acid accumulation in intestinal cells. This is a pilot study to examine the relation between hormone replacement therapy (HRT) and plasma ascorbic acid levels among a group of healthy non-smoking postmenopausal women. METHODS: Healthy non-smoking postmenopausal women aged 48-72 years, 34 with HRT and 21 without HRT, were recruited in summer, 1997. Their fasting plasma ascorbic acid levels were measured and information on ascorbic acid intakes (diet and supplements) was collected through questionnaires. RESULTS: Women taking HRT in this study did not have significantly lower plasma ascorbic acid levels compared with non-HRT users. When subjects were further divided into groups based on ascorbic acid supplementation, HRT users without supplement had a lower mean plasma ascorbic acid level (54+/-16 microM, n=10) compared with non-HRT users (66+/-14 microM, n=12) (P=0.08 for the effect of therapy). HRT users and non-users taking ascorbic acid supplement had similar plasma levels (66+/-10 microM, n=24; 66+/-12 microM, n=9, respectively). CONCLUSION: HRT does not affect ascorbic acid status of healthy well-nourished non-smoking postmenopausal women that are using ascorbic acid supplement. Future larger case-control or supplement intervention study is needed.

Aged↗

PubMed1990

Millimolar concentrations of ascorbic acid in purified human mononuclear leukocytes. Depletion and reaccumulation.

Ascorbic acid (vitamin C) was found in isolated human mononuclear leukocytes and their purified components in millimolar concentration. Intracellular ascorbic acid was depleted greater than 96% during cell culture and was rapidly reaccumulated after addition of physiologic concentrations of ascorbic acid to the extracellular medium. Purified cells maintained concentration gradients of ascorbic acid as large as 100-fold across the plasma membrane. The ability to vary intracellular ascorbic acid concentrations over such a wide range makes it possible for the first time in these cells to study ascorbic acid function in direct relationship to intracellular concentration.

Ascorbic Acid↗

PubMed1990

Effect of Escherichia coli endotoxin on ascorbic acid transport in isolated adrenocortical cells.

The active uptake of ascorbic acid by isolated rat adrenocortical cells increases with ascorbic acid concentration, depends on time and calcium, and is inhibited by ACTH concentrations required for maximal steroidogenesis. Lipopolysaccharide of Escherichia coli 0111:B4 modifies the ascorbic acid uptake in a calcium-dependent manner. At low calcium concentrations, lipopolysaccharide exerts a stimulatory effect on ascorbic acid transport and at high concentrations lipopolysaccharide produces a dose-dependent inhibitory effect. This inhibition of the ascorbic acid transport by the endotoxin can alter the ascorbic acid accumulation in the adrenal gland during endotoxin shock.

Adrenal Cortex↗

PubMed1989

Haloperidol and reduced haloperidol concentrations and psychiatric ratings in schizophrenic patients treated with ascorbic acid.

Recent reports have suggested an augmentation by ascorbic acid of haloperidol treatment of schizophrenic patients. This study was designed to examine whether pharmacokinetic interactions between ascorbic acid and haloperidol occur in this population. Eight male inpatients diagnosed as having chronic schizophrenia by DSM-III-R criteria and stabilized on a fixed dose of haloperidol were given oral doses of ascorbic acid, 4.5 grams daily, for 2 weeks in an open trial. Serum concentrations of haloperidol and is metabolite, reduced haloperidol, were measured by high performance liquid chromatography. Psychiatric symptoms were monitored using the Psychiatric Symptom Assessment Scale performed by nursing staff blind to the haloperidol status but not to the ascorbic acid dosage. The addition of ascorbic acid was not associated with any change in psychopathology in this group of patients, nor was there any apparent pharmacokinetic interaction with haloperidol.

Ascorbic Acid↗

PubMed1990

Effects of dietary excess amino acids on the concentrations of cholesterol, alpha-tocopherol, ascorbic acid, and copper in serum and tissues of rats.

An experiment was conducted with growing rats to investigate the effects of feeding excessive specific L-amino acids for 8 days on serum and tissue cholesterol, alpha-tocopherol, ascorbic acid, and copper, and on liver microsomal cytochrome P-450. To a 10% casein diet were added 4% L-methionine, 5% L-cystine, 5% L-histidine, 5% L-threonine, 5% L-tryptophan, 5% L-phenylalanine, 5% L-tyrosine, 6% L-valine, 7% L-isoleucine, 7% L-lysine, or 8% L-leucine. Excessive cystine and histidine increased serum cholesterol and alpha-tocopherol. Excessive cystine and methionine increased liver and kidney alpha-tocopherol and ascorbic acid. Excessive tyrosine and phenylalanine caused a marked increase in serum copper and ceruloplasmin activity, whereas excessive cystine, methionine, and histidine caused a decrease in the ceruloplasmin activity. Excessive histidine increased liver cytochrome P-450, whereas excessive tyrosine markedly decreased liver cytochrome P-450.

Amino Acids↗

PubMed2000

Ascorbic acid enhances endothelial nitric-oxide synthase activity by increasing intracellular tetrahydrobiopterin.

Ascorbic acid enhances NO bioactivity in patients with vascular disease through unclear mechanism(s). We investigated the role of intracellular ascorbic acid in endothelium-derived NO bioactivity. Incubation of porcine aortic endothelial cells (PAECs) with ascorbic acid produced time- and dose-dependent intracellular ascorbic acid accumulation that enhanced NO bioactivity by 70% measured as A23187-induced cGMP accumulation. This effect was due to enhanced NO production because ascorbate stimulated both PAEC nitrogen oxide (NO(2)(-) + NO(3)(-)) production and l-arginine to l-citrulline conversion by 59 and 72%, respectively, without altering the cGMP response to authentic NO. Ascorbic acid also stimulated the catalytic activity of eNOS derived from either PAEC membrane fractions or baculovirus-infected Sf9 cells. Ascorbic acid enhanced bovine eNOS V(max) by approximately 50% without altering the K(m) for l-arginine. The effect of ascorbate was tetrahydrobiopterin (BH(4))-dependent, because ascorbate was ineffective with BH(4) concentrations >10 microm or in PAECs treated with sepiapterin to increase intracellular BH(4). The effect of ascorbic acid was also specific because A23187-stimulated cGMP accumulation in PAECs was insensitive to intracellular glutathione manipulation and only ascorbic acid, not glutathione, increased the intracellular concentration of BH(4). These data suggest that ascorbic acid enhances NO bioactivity in a BH(4)-dependent manner by increasing intracellular BH(4) content.

Animals↗

PubMed2000

Analysis of 3-morpholinosydnonimine and sodium nitroprusside effects on dopamine release in the striatum of freely moving rats: role of nitric oxide, iron and ascorbic acid.

The effects of intrastriatal infusion of 3-morpholinosydnonimine (SIN-1) or sodium nitroprusside (SNP) on dopamine (DA), 3-methoxytyramine (3-MT), dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), L-dihydroxyphenylalanine (L-DOPA), ascorbic acid and uric acid concentrations in dialysates from the striatum of freely moving rats were evaluated using microdialysis. SIN-1 (1 mM) infusion for 180 min increased microdialysate DA and 3-MT concentrations, while L-DOPA, DOPCA+HVA, ascorbic acid and uric acid levels were unaffected. Co-infusion with ascorbic acid (0.1 mM) inhibited SIN-1-induced increases in DA and 3-MT dialysate concentration. SNP (1 mM) infusion for 180 min increased greatly the dialysate DA concentration to a peak (2950% of baseline) at the end of the infusion, while increases in 3-MT were negligible. In addition, SNP decreased ascorbic acid and L-DOPA but increased uric acid concentration in the dialysate. Co-infusion with deferoxamine (0.2 mM) inhibited the late SNP-induced increase in DA dialysate concentration, but did not affect the decrease in ascorbic acid and increase uric acid dialysate concentrations. SNP (1 mM) infusion for 20 min moderately increased uric acid, DA and 3-MT, but decreased L-DOPA levels in the dialysate. Ascorbic acid concentration increased at the end of SNP infusion. Co-infusion with ascorbic acid (0.1 mM) inhibited the SNP-induced increase in DA and 3-MT, but did not affect the decrease in L-DOPA and increase in uric acid dialysate concentrations. These results suggest that NO released from SIN-1 may account for the increase in the dialysate DA concentration. NO released following decomposition of SNP may account for the early increase in dialysate DA, while late changes in microdialysate composition following SNP may result from an interaction between NO and the ferrocyanide moiety of SNP. Exogenous ascorbic acid inhibits the effect of exogenous NO on DA release probably by scavenging NO, suggesting that endogenous ascorbic acid may modulate the NO control of DA release from 300 striatal dopaminergic terminals.

Animals↗

PubMed1997

Evidence for the involvement of a muscarinic receptor in ascorbic acid secretion in the rat stomach.

It has been demonstrated that ascorbic acid is present in human gastric juice at a very high level even in the fasting state. In this study, we confirmed such a physiological event in pylorus-ligated rats and investigated the mechanism for gastric ascorbic acid secretion using the rat in vivo perfusion method. Gastric juice from fasting rats after a 4-hr ligation contained a 6-fold higher level of ascorbic acid than that in sera, indicating the presence of its active transport system across the gastric wall. To identify an endogenous mediator, four kinds of gastric stimulants were compared for their secretory abilities. Although all four secretagogues used stimulated acid secretion to comparable levels, ascorbic acid secretion was stimulated only by carbamylcholine chloride (carbachol). Carbachol-stimulated ascorbic acid secretion was abolished by atropine pretreatment, showing that it is mediated via a muscarinic cholinergic receptor. This cholinergic stimulation was also demonstrated in a rat mutant that genetically lacks the ability to synthesize ascorbic acid in the liver, similar to humans. In addition, a potent inhibitor of the gastric proton pump, which is a final regulatory component in the mechanism of acid secretion, caused no inhibition of ascorbic acid secretion in Osteogenic Disorder Shionogi (ODS) rats. These results are the first evidence indicating that ascorbic acid, the reduced form of vitamin C, is actively and independently secreted into the gastric juice under regulation of a cholinergic receptor system.

Animals↗

PubMed1980

Leukocyte ascorbic acid and its relationship to coronary artery disease in man.

The ascorbic acid level of the leukocytes in patients with coronary artery disease was compared to the ascorbic acid level of the leukocytes in patients without coronary artery disease as demonstrated by coronary arteriography. The leukocyte ascorbic acid level was found significantly lower in patients with coronary arteriography. The leukocyte ascorbic acid level was found significantly lower in patients with coronary atherosclerosis (P < 0.001). There was also significant difference in the leukocyte ascorbic acid levels among patients with abnormal coronary arteriograms who smoked compared to those who did not. The anatomical changes secondary to atherosclerotic disease, and mainly those changes related to the ground substance, have been shown to be the changes that have been observed in patients with ascorbic acid deficiency. From the present study, with its limitations, it is suggested that ascorbic acid may play a role in the pathogenesis of atherosclerosis, and although not implicated as an etiological factor in coronary artery disease, it suggests that a closer look at its possible role in the pathogenesis and progression of coronary artery disease is warranted.

Adult↗

PubMed2001

Plasma ascorbic acid: measurement, stability and clinical utility revisited.

AIMS: To compare plasma ascorbic acid results by the colorimetric FRASC (Ferric Reducing/Antioxidant and Ascorbic Acid) assay and a reference HPLC method; to re-examine plasma ascorbic acid stability, and anticoagulant effect. DESIGN AND METHODS: For method comparison, 31 plasma samples were tested by both methods. For stability, matching EDTA, heparin, citrate and fluoride/oxalate plasma, stored under different conditions of time and temperature, was measured. RESULTS: FRASC is an acceptable alternative to HPLC for plasma ascorbic acid: precision, limit of detection and recovery were similar, and results by the two methods were indistinguishable: mean (95% CI) difference:1.8 (-1.1-4.6; n = 31) micromol/L. Ascorbic acid was most stable in heparinized plasma. Marked loss (p < 0.05) in EDTA plasma occurred within 30 min of blood collection. CONCLUSIONS: FRASC offers a speedy and reliable alternative to HPLC for plasma ascorbic acid. Heparin is proposed as the anticoagulant of choice; loss of ascorbic acid is rapid in EDTA plasma ex vivo.

Adult↗

PubMed2001

Iron absorption from a breakfast cereal: effects of EDTA compounds and ascorbic acid.

Sodium iron ethylenediaminetetracetic acid (NaFeEDTA) has been recommended for food fortification programmes to improve iron status but its performance in commercial products has not been evaluated. The effect of EDTA on iron absorption from fortified cornflakes, given as part of a typical Western breakfast, was determined in a double-blind randomised study with 20 non-anaemic female volunteers, using experimentally prepared iron compounds, enriched with 58Fe, and faecal monitoring. Five meals were compared: hydrogen reduced iron, hydrogen reduced iron plus Na2EDTA (molar ratio EDTA:Fe 1:2), hydrogen reduced iron plus NaFe(III)EDTA at two different molar ratios (EDTA:total Fe 1:3 and 1:2), and hydrogen reduced iron plus 15 mg ascorbic acid (ascorbic acid:Fe 1.3:1). The iron and EDTA compounds were accurately weighed into gelatine capsules and taken with unfortified cornflakes, semi-skimmed milk and tea on two consecutive days; the iron dose per meal was 3.75 mg. Iron absorption from all five test meals was measured in each volunteer with a minimum wash-out period of 2 weeks between tests. Geometric mean iron absorption (%) from the 5 tests was 14.1, 17.6, 20.6, 24.4 and 17.5 respectively (equivalent to 0.5-0.9 mg absorbed iron). There was a significantly higher iron absorption from the mixture of reduced iron and NaFe(III)EDTA (EDTA:Fe 1:2) than from reduced iron alone (p = 0.014). It is not known whether the higher absorption was from reduced iron or NaFeEDTA or both. Absorption was not increased significantly with NaFe(III)EDTA (EDTA:Fe 1:3), Na2EDTA (EDTA:Fe 1:2) or ascorbic acid (15 mg).

Adult↗