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PubMed2001

Ascorbic acid loss in vegetables: adequacy of a hospital cook-chill system.

This research evaluates the ascorbic acid loss of vegetables prepared in a hospital cook-chill plated system. The ascorbic acid loss of three vegetable samples (carrots, peas and potatoes) were measured at various points in the cook-chill system and analysed using the DCPIP method. Substantial losses for all vegetables were identified at the cooking and regeneration stages. The ascorbic acid levels of the selected vegetables when raw ranged from 6 to 10 mg/100 g sample. At the end of the food service cycle the ascorbic acid content of the vegetables was reduced to 1.7-5.8 mg/100 g sample. The largest percentage loss of ascorbic acid, i.e. 76%, was found in mashed potatoes. Peas incurred the least percentage loss, i.e. 42%. This progressive deterioration during the cook-chill plated catering system causes an insubstantial presence of ascorbic acid in the food served to hospitalised patients.

Ascorbic Acid↗
PubMed2002

[Ascorbic acid consumption and serum levels in smokers and non-smokers adult men in Hermosillo, Sonora, México].

Ascorbic acid is one of the important antioxidant nutrients that can aid in the prevention of oxidative cellular damage. Adequate dietary intake is essential as humans can not synthesize this vitamin. It has been reported that smokers require higher dietary intakes to maintain their serum levels. The objective of this study was to determine serum levels of ascorbic acid in young male smokers and non smokers in the city of Hermosillo, Sonora, Mexico. In addition, their dietary intake of ascorbic acid was determined by a 24 h dietary recall. The dietary intake of ascorbic acid in 12 smokers was 64 +/- 11 mg/d and in 13 non smokers it was 70 +/- 12 mg/d. The smokers in this study did not meet the dietary recommendation of 100 mg/d. Serum ascorbic acid values in smokers and non smokers were 24.2 +/- 6.9 mumol/L and 30.9 +/- 3.7 mumol/L respectively. No significant difference was found among the 2 groups. Although the average serum ascorbic acid values fell within the range considered normal, 50% of the smokers had individual values that were below 23 mumol/L, indicating that these subjects have hipovitaminosis. A positive correlation between intake and serum levels was obtained for smokers (r = 0.71; p = 0.03). The results of this study suggest smokers may be at increased risk for chronic diseases due to their low intake and low serum levels of ascorbic acid.

Adolescent↗
PubMed1975

Studies on the fortification of cane sugar with iron and ascorbic acid.

1. The feasibility of improving iron nutrition by fortifying cane sugar with Fe and ascorbic acid was studied. 2. It was found to be possible to add a number of Fe salts together with ascorbic acid to sugar without affecting its appearance or storage properties. 3. The absorption of Fe from fortified sugar eaten with maize-meal porridge or made into jam or biscuits was measured in ninety-four volunteer multiparous Indian women using the 59-Fe erythrocyte utlization method. 4. The absorption of Fe from sugar fortified with ascorbic acid and ferrous sulphate and eaten with maize-meal porridge was increased about twofold in the ratio, ascorbic acid:Fe was 10:1 by weight. If the ratio was increased to 20:2, Fe absorption was increased a further threefold. 5. Sugar fortified with soluble Fe salts, including FeSO4.7H2O, discoloured both tea and coffee; sugar fortified with ferric orthophosphate did not have this effect. 6. Fe from FePO4.H2O was poorly absorbed when added with sugar to maize-meal porridge, and also when added with adequate quantities of ascorbic acid. This form of Fe was absorbed much less well than was the intrinsic Fe present in the maize. 7. When sugar fortified with FePO4.H2O and ascorbic acid was added to maize-meal porridge before cooling or was made into jam there was a several-fold increase in the amount of Fe absorbed.

Adult↗
PubMed2004

A change in gastric mucosal ascorbic acid status with the formation, progression, and recovery of compound 48/80-induced acute gastric mucosal lesions in rats.

We examined whether gastric mucosal ascorbic acid status changes with the formation, progression, and recovery of acute gastric mucosal lesions in rats treated with compound 48/80, a mast cell degranulator. Fasted Wistar rats received a single intraperitoneal injection of compound 48/80 (0.75 mg/kg). Apparent gastric mucosal lesions occurred 0.5 h after compound 48/80 treatment, progressed gastric mucosal lesions were observed at 3 h, and a partial recovery of the progressed lesions was found at 6 h. The gastric mucosal concentrations of total and reduced ascorbic acids in compound 48/80-treated rats decreased to approximately 60% of the levels of untreated rats at 3 h after the treatment but the decreased concentrations of total and reduced ascorbic acids were almost completely returned to the levels of untreated rats at 6 h. The gastric mucosal concentration of oxidized ascorbic acid in compound 48/80-treated rats showed little change. The serum concentrations of total and reduced ascorbic acids in compound 48/80-treated rats increased at 0.5 h after the treatment and further increased at 3 h but the increased concentrations of total and reduced ascorbic acids were almost completely returned to the levels of untreated rats at 6 h. The serum concentration of oxidized ascorbic acid in compound 48/80-treated rats increased transiently at 0.5 h after the treatment. The hepatic concentrations of total. reduced, and oxidized ascorbic acids in compound 48/80-treated rats increased 3 h after the treatment, but these increases were not observed at 6 h. These results indicate that gastric mucosal ascorbic acid status is disrupted with the progression of acute gastric mucosal lesions in rats treated with compound 48/80.

Animals↗
PubMed2005

Iron prevents ascorbic acid (vitamin C) induced hydrogen peroxide accumulation in copper contaminated drinking water.

Ascorbic acid (vitamin C) induced hydrogen peroxide (H(2)O(2)) formation was measured in household drinking water and metal supplemented Milli-Q water by using the FOX assay. Here we show that ascorbic acid readily induces H(2)O(2) formation in Cu(II) supplemented Milli-Q water and poorly buffered household drinking water. In contrast to Cu(II), iron was not capable to support ascorbic acid induced H(2)O(2) formation during acidic conditions (pH: 3.5-5). In 12 out of the 48 drinking water samples incubated with 2 mM ascorbic acid, the H(2)O(2) concentration exceeded 400 microM. However, when trace amounts of Fe(III) (0.2 mg/l) was present during incubation, the ascorbic acid/Cu(II)-induced H(2)O(2) accumulation was totally blocked. Of the other common divalent or trivalent metal ions tested, that are normally present in drinking water (calcium, magnesium, zinc, cobalt, manganese or aluminum), only calcium and magnesium displayed a modest inhibitory activity on the ascorbic acid/Cu(II)-induced H(2)O(2) formation. Oxalic acid, one of the degradation products from ascorbic acid, was confirmed to actively participate in the iron induced degradation of H(2)O(2). Ascorbic acid/Cu(II)-induced H(2)O(2) formation during acidic conditions, as demonstrated here in poorly buffered drinking water, could be of importance in host defense against bacterial infections. In addition, our findings might explain the mechanism for the protective effect of iron against vitamin C induced cell toxicity.

Ascorbic Acid↗
PubMed2000

The development of spectrophotometric and electroanalytical methods for ascorbic acid and acetaminophen and their applications in the analysis of effervescent dosage forms.

The electroanalytical study of ascorbic acid, acetaminophen and of several mixtures of these compounds in different ratios has been made by using a carbon paste electrode (CPE-graphite:solid paraffin 2:1) as working electrode and an Ag/AgCl reference electrode. The potential curves were recorded using different concentrations of ascorbic acid and acetaminophen by measuring samples between 10 and 50 microl. The oxidation reactions were studied in a potential range from -0.1 to +1.3 V with different sweep rates, at different current sensitivities, in stationary working conditions and stirring before each replicate. The oxidation of ascorbic acid occurs at +0.31 +/- 0.02 V and the oxidation of acetaminophen at +0.60 +/- 0.05 V; meanwhile, the current has a linear variation for the following concentration ranges: 10(-3)-10(-2) M for the ascorbic acid and 3 x 10(-6)-7.5 x 10(-3) M for acetaminophen (r2 = 0.999 for both ascorbic acid and acetaminophen). The mixtures of ascorbic acid and acetaminophen were made as follows: 1:1, 1:2, 1:3, 2:1, and 3:1. The studies revealed the alteration of the voltammograms processed according to the validation methodology. The best potential variation range for different current sensitivities, the influence of the sweep rate, of the solvent volume and of the pH were studied. The mutual interferences of the compounds in the mixtures and the electroactive compounds in the pharmaceutical dosage forms, especially effervescent ones, also made the object of the research. The same mixtures were studied using the direct spectrophotometric method that revealed a lot of spectral interferences. In order to solve this problem, an appropriate separation or an indirect spectrophotometric method (the apparent content curves method) were used. The spectrophotometric and voltammetric methods developed were used to determine ascorbic acid and acetaminophen in different dosage forms (vials, tablets, suppositories and effervescent dosage forms). The results were compared with those obtained by other techniques.

Acetaminophen↗
PubMed1995

The effects of ascorbic acid on free radical injury in cultured retinal pigment epithelial cells.

This study was conducted to investigate the effect of ascorbic acid on oxidative injury of cultured porcine retinal pigment epithelial (RPE) cells induced by t-butylhydroperoxide. The porcine RPE cells were cultured in Dulbecco's modified Eagle's medium and the culture medium was replaced with one containing 0.01 mM to 5 mM ascorbic acid and/or 0.2 mM t-butylhydroperoxide. After 2 hours incubation, the test medium was replaced with the control medium. The number of cells was counted with a Coulter counter after a 2-day incubation period. The medium was pretreated with 900 U/ml and the previous procedure was repeated to eliminate the toxic effects of hydrogen peroxide induced by ascorbic acid. Not only t-butylhydroperoxide (p < 0.01) but also ascorbic acid (p < 0.01) were found to have dose-dependent cytotoxicity on RPE cells. The cytotoxicity was more significant when both agents were added to the culture media. In the presence of catalase, the cytotoxicity of ascorbic acid became insignificant (p < 0.05). The cytotoxicity of t-butylhydroperoxide decreased when 1 mM and 5 mM of ascorbic acid was added to the culture media with catalase pretreatment (p = 0.0277). These results indicate that ascorbic acid was toxic to RPE cells in our culture model but this cytotoxicity was not detected in the presence of catalase. With catalase pretreatment, ascorbic acid in relatively high concentration provided protection against oxidative injury of t-butylhydroperoxide.

Animals↗
PubMed1980

Dietary ascorbic acid and muscle carnitine (beta-OH-gamma-(trimethylamino) butyric acid) in guinea-pigs.

Tissue ascorbic acid (AA) contents of approximately 12 and 100% saturation respectively were produced in two groups of guinea-pigs. The 'low-AA' group had a significantly lower muscle carnitine concentrations than the 'high-AA' group. There was no concomitant emergence of the symptoms customarily regarded as characteristic of hypovitaminosis C. It is concluded that muscle carnitine (beta-OH-gamma-(trimethyl-amino)butyric acid) is a highly-sensitive indicator of tissue AA contents; this could account for the lassitude and fatique reported to precede the emergence of frank scurvy in man.

Animals↗
PubMed2002

Plasmid DNA damage caused by methylated arsenicals, ascorbic acid and human liver ferritin.

Both dimethylarsinic acid (DMA(V)) and dimethylarsinous acid (DMA(III)) release iron from human liver ferritin (HLF) with or without the presence of ascorbic acid. With ascorbic acid the rate of iron release from HLF by DMA(V) was intermediate (3.37 nM/min, P<0.05) and by DMA(III) was much higher (16.3 nM/min, P<0.001). No pBR322 plasmid DNA damage was observed from in vitro exposure to arsenate (iAs(V)), arsenite (iAs(III)), monomethylarsonic acid (MMA(V)), monomethylarsonous acid (MMA(III)) or DMA(V) alone. DNA damage was observed following DMA(III) exposure; coexposure to DMA(III) and HLF caused more DNA damage; considerably higher amounts of DNA damage was caused by coexposure of DMA(III), HLF and ascorbic acid. Diethylenetriaminepentaacetic acid (an iron chelator), significantly inhibited DNA damage. Addition of catalase (which can increase Fe(2+) concentrations) further increased the plasmid DNA damage. Iron-dependent DNA damage could be a mechanism of action of human arsenic carcinogenesis.

Ascorbic Acid↗
PubMed1997

Ascorbic acid absorption in patients with systemic sclerosis.

OBJECTIVE: To investigate whether reduced circulating levels of ascorbic acid in patients with systemic sclerosis (SSc) are a result of malabsorption. METHODS: Eight patients with SSc, but with no evidence of bacterial overgrowth, and 8 healthy controls were recruited. On the first day of study, each subject was given orally an aliquot of [14C] ascorbic acid, which was then "flushed out" by oral intake of unlabeled ascorbic acid for the following 7 days. Plasma samples were collected at specified intervals and urine was collected continuously over the 8 day study period. [14C] content of plasma and urine were measured by scintillation counting. For each subject, a plasma [14C] decay curve was drawn. Each subject's ascorbic acid absorption was assessed using the area under the curve (AUC) and the apparent renal clearance (CLr[app]). Ascorbic acid intake was assessed using dietary history and food composition tables. RESULTS: There were no differences in the dietary intake of vitamin C (p = 0.16) and body mass indices (p = 0.91) between patients and controls. The plasma [14C] AUC and CLr(app) were similar between patients and controls [AUC patient mean (standard deviation, SD) = 37.1 (6.8), AUC control mean (SD) = 38.6 (9.9), p = 0.74; CLr(app) patient mean (SD) = 0.57 (0.24), CLr(app) control mean (SD) = 0.47 (0.27), p = 0.45]. CONCLUSION: There was no evidence of impaired absorption of ascorbic acid in patients with SSc without bacterial overgrowth compared to healthy controls.

Absorption↗
PubMed1983

Ascorbic acid and membrane ageing: critical determinants of the in-vitro binding of [3H]ADTN to rat striatal tissue.

Tritiated (+/-)-2-amino-6,7-dihydroxy-1,2,3,4-tetrahydronaphthalene [( 3H]ADTN), binding (0.125-4.0 nM) to rat striatal membranes was investigated using Tris-HCl buffer containing Na2EDTA, nialamide and varying concentrations of ascorbic acid. In the absence of ascorbic acid [3H]ADTN exhibited a high affinity (KD 1.26 nM) saturable binding (Bmax 138 fmol mg-1 protein) (Scatchard analysis). This was not modified by 10(-6) or 10(-5) M ascorbic acid used immediately or 60 min after preparation. However, 10(-4) M ascorbic acid added (within) 15 min after its preparation reduced the number of bindings sites and added 60 min after it also reduced affinity. Ascorbic acid 5.7 mM reduced affinity whether used within 15 min or 60 min of its preparation. When ascorbic acid 10(-4) M was used within 15 min of preparation, and membranes were used immediately, the binding of 2 nM [3H]ADTN was specifically displaceable by nM or sub-nM concentrations of dopamine agonists and antagonists. However, when membranes were used 1-2 h after their preparation there was an increasing loss of the high affinity binding sites displaceable by sub-nM concentrations of (+/-)-ADTN. Thus. [3H]ADTN can be shown to exhibit high affinity stereoselective binding to rat striatal membranes when these are freshly prepared and the assay is performed using Tris-HCl buffer containing nialamide. Na2EDTA and 10(-4) M ascorbic acid prepared within 15 min of use. The characteristics of this binding can be markedly modified if the concentration of ascorbic acid is increased, if its preparation time is extended, or if the membranes are allowed to 'age'.

Animals↗
PubMedDate not supplied

[Ontogenetic characteristics of ascorbic acid binding by nerve tissue proteins].

The highest ascorbic acid content has been found in a low-molecular fraction (m. w. less than 6000) of water-soluble proteins from brain tissue homogenates of rats, the lowest one--in a high-molecular fraction (m. w. about 65,000). The content of protein-bound ascorbic acid decreases during postnatal life. This process is accompanied by changes in the ratio of the reduced and oxidated forms of the ascorbic acid in favour of the latter.

Aging↗
PubMedDate not supplied

[Interaction of E. coli cells with ascorbic acid and sodium nitrite studied by ESR method].

Ascorbic acid, an effective modulator and regulator of cell metabolism, was shown to induce the production of nitric oxide in E. coli cells. This process was detected by EPR spectroscopy as the generation of a spectral signal typical of nitrosyl-iron-sulfur centers (Fe-S-NO) under anaerobic conditions. Incubation of E. coli cells in the presence of ascorbic acid under aerobic conditions was shown to be accompanied by sodium nitrite formation. It is suggested that ascorbic acid is capable of supporting the system of energy supply to cells in hypoxia caused by reduced oxygen content or treatment with sodium nitrite.

Ascorbic Acid↗
PubMedDate not supplied

The effects of ascorbic acid on in vitro heterophil function.

As a feed additive, ascorbic acid has been shown to have a protective effect against bacterial and viral diseases and to reduce the impact of detrimental stress in chickens. This study examined the effect of ascorbic acid treatment on in vitro heterophil function by examining random migration and phagocytosis and bacterial killing of Staphylococcus aureus. Heterophils were evaluated in broiler chickens ranging from 5 to 16 wk of age, and age differences were seen. Significant increases in bacterial killing were found in heterophils treated with ascorbic acid, and this difference tended to be greater in chickens from 5 to 10.5 wk of age. No significant differences were found in phagocytosis or random migration, but ascorbic acid tended to decrease random migration. The most significant effect on in vitro heterophil function was an increase in bacterial killing.

Animals↗
PubMed2001

Effect of ascorbic acid treatment on conduit vessel endothelial dysfunction in patients with hypertension.

Hypertension is associated with low plasma ascorbic acid levels and impaired endothelial function. Recent evidence suggests that increased vascular oxidative stress contributes to the pathophysiology of endothelial dysfunction and hypertension. We recently showed that chronic oral ascorbic acid therapy lowers blood pressure in hypertensive patients. We hypothesized that it would also improve endothelial vasomotor function. In a randomized, double-blind, placebo-controlled study, we examined the effect of acute (2 g po) and chronic (500 mg/day for 1 mo) ascorbic acid treatment on brachial artery flow-mediated dilation in 39 patients with hypertension. Compared with 82 age- and gender-matched normotensive controls, these patients had impaired endothelium-dependent, flow-mediated dilation of the brachial artery [8.9 +/- 6.1 vs. 11.2 +/- 5.7% (SD), P < 0.04]. After therapy, plasma ascorbic acid concentrations increased acutely from 50 +/- 12 to 149 +/- 51 micromol/l and were maintained at 99 +/- 33 micromol/l with chronic treatment (both P < 0.001). As previously reported, chronic ascorbic acid therapy reduced systolic and mean blood pressure in these patients. However, acute or chronic ascorbic acid treatment had no effect on brachial artery endothelium-dependent, flow-mediated dilation or on endothelium-independent, nitroglycerin-mediated dilation. These results demonstrate that conduit vessel endothelial dysfunction secondary to hypertension is not reversed by acute or chronic treatment with oral ascorbic acid. The effects of this treatment on resistance vessel vasomotor function warrant further investigation.

Adult↗
PubMed1992

Oxidation of ascorbic acid as an indicator of photooxidative stress in the eye.

When whole retinal pigmented epithelium (RPE) cells isolated from bovine eyes are incubated with 14C-labeled ascorbic acid and exposed to a visible laser, the ascorbic acid is oxidized to dehydro-L-ascorbic acid (DHA). The amount of ascorbic acid which is oxidized is proportional to the radiant exposure of the sample (i.e. the total amount of radiation per unit area delivered over the exposure time). Blue light is more effective than red light in driving the reaction. The amount of label appearing in the DHA fraction is increased if unlabeled DHA is present in the reaction mixture, indicating that some redox cycling of ascorbate is occurring in the RPE cells. The ascorbic acid oxidizing activity does not depend on intact cells, is not inactivated by heating the cells to 80 degrees C, and appears to reside mainly in the subcellular fraction which contains melanin pigment granules. The ascorbic acid oxidation may be caused by free radicals formed when melanin is illuminated with light. This reaction appears to be a useful method for quantifying the production of free radicals during photooxidative stress.

Animals↗
PubMed1982

Effect of oral contraceptive agents on ascorbic acid metabolism in the rhesus monkey.

Ascorbic acid (AA) metabolism was studied in six sexually mature female rhesus monkeys with normal menstrual cycles before and during oral contraceptive administration. The animals were fed a commercial monkey stock diet (15% protein) containing no AA and given a 100 mg AA tablet daily throughout the study. After an initial adaptation period and a control period (total 8 months), combined-type oral contraceptive agents (OCAs) (50 micrograms mestranol and 1 mg norethindrone for 21 days each month) were administered to each monkey for 4 months. Serum copper and ceruloplasmin were significantly elevated during OCA treatment. There were no significant changes in plasma or leukocyte AA values during OCA use; however, urinary AA excretion decreased significantly. During the last month of the control period and the 3rd month of OCA treatment, 50 muCi of 1-14C-L-ascorbic acid were injected intravenously into each monkey. Urinary excretion of radioactivity, measured for 1 month, indicated a significantly faster AA turnover rate during the period of OCA use. These results suggest that women using OCAs may have an increased dietary requirement for AA.

Animals↗