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PubMed2001

Ascorbic acid levels in human tears after photorefractive keratectomy, transepithelial photorefractive keratectomy, and laser in situ keratomileusis.

PURPOSE: To investigate the level of ascorbic acid in human tear fluid after photorefractive keratectomy (PRK), transepithelial PRK, and laser in situ keratomileusis (LASIK). SETTING: Departments of Ophthalmology and Biochemistry, School of Medicine, Gazi University, Ankara, Turkey. METHODS: Twenty patients (7 women and 13 men) were included in this study. Traditional PRK with epithelial scraping by a blunt spatula followed by surface ablation (7 eyes), transepithelial PRK (7 eyes), or LASIK (6 eyes) was performed. Tears were collected preoperatively and 1 and 5 days postoperatively. Ascorbic acid levels were measured using 2-4 dinitrophenylhydrazine. RESULTS: Ascorbic acid levels in the tear fluid were decreased significantly 1 day after PRK, transepithelial PRK, and LASIK (P <.05). On the fifth day, the ascorbic acid levels were significantly lower than preoperatively in all groups. CONCLUSION: After PRK, transepithelial PRK, and LASIK, the ascorbic acid levels of the tear fluid decreased significantly. Because ascorbic acid is the major scavenger of superoxide radicals in tears, topical ascorbic acid therapy may help eliminate the harmful effect of free radicals from excimer laser surgery.

Adult↗
PubMed2003

Effects of dietary supplemental L-carnitine and ascorbic acid on performance, carcass composition and plasma L-carnitine concentration of broiler chicks reared under different temperature.

The present study was initiated to determine whether dietary supplemental L-carnitine and ascorbic acid affect growth performance, carcass yield and composition, abdominal fat and plasma L-carnitine concentration of broiler chicks reared under normal and high temperature. During the experiment, two temperature regimes were employed in two experimental rooms, which were identical but different in environmental temperature. The regimes were thermoneutral (20-22 degrees C for 24 h) or recycling hot (34-36 degrees C for 8 h and 20-22 degrees C for 16 h). One-day-old broiler chicks (ROSS) were used in the experiment. A 2 x 2 x 2 factorial arrangement was employed with two levels (0 and 50 mg/kg) of supplemental L-carnitine and two levels (0 or 500 mg/kg) of supplemental ascorbic acid in drinking water under thermoneutral or high temperature regimes. Body weight gain was affected by high temperature. However, body weight gain was significantly improved in animals receiving supplemental L-carnitine, ascorbic acid or L-carnitine + ascorbic acid compared to animals receiving unsupplemented diet under high temperature. On the other hand, supplemental L-carnitine or L-carnitine + ascorbic acid reduced body weight gain under thermoneutral condition. Supplemental ascorbic acid significantly improved feed conversion efficiency, the improvement was relatively greater under high temperature. The L-carnitine content in the plasma was higher in the groups receiving supplemental L-carnitine and ascorbic acid under high temperature, while broilers fed supplemental L-carnitine and ascorbic acid had a decreased level of plasma L-carnitine concentration under normal temperature. It is concluded that dietary supplemental L-carnitine or L-carnitine + ascorbic acid may have positive effects on body weight gain, carcass weight under high temperature conditions.

Adipose Tissue↗
PubMed2004

Ascorbic acid does not increase the oxidative stress induced by dietary iron in C3H mice.

Iron is a potent prooxidant that can induce lipid peroxidation. Ascorbic acid, a potent antioxidant, has prooxidant effects in the presence of iron in vitro. We investigated whether ascorbic acid and iron co-supplementation in ascorbic acid-sufficient mice increases hepatic oxidative stress. C3H/He mice were fed diets supplemented with iron to 100 mg/kg diet or 300 mg/kg diet with or without ascorbic acid (15 g/kg diet) for 3 wk. Liver iron concentration, malondialdehyde (MDA), glutathione (GSH), glutathione S-transferase (GST), glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT) were measured. High dietary iron increased liver iron concentrations slightly (P < 0.05), whereas it dramatically increased hepatic MDA (P < 0.0001). Ascorbic acid increased MDA but only in mice fed the low-iron diet (P < 0.05). The high-iron diet reduced GPx (P < 0.0001), CAT (P < 0.0005), SOD (P < 0.05), and GST (P < 0.005) activities regardless of ascorbic acid supplementation. In contrast, ascorbic acid reduced GPx (P < 0.0001) and CAT (P < 0.05) activities only in mice fed the low-iron diet. In conclusion, ascorbic acid supplementation can have prooxidant effects in the liver. However, ascorbic acid does not further increase the oxidative stress induced by increased dietary iron.

Animals↗
PubMed1984

Ascorbic acid content and accumulation by alveolar macrophages from cigarette smokers and nonsmokers.

The lung is at risk for injury from inhaled oxidants, including components of cigarette smoke; therefore, maintaining a chemical antioxidant defense would be advantageous. The potential for ascorbic acid to assume this protective role was investigated by comparing the total ascorbate content of alveolar macrophages obtained from human smokers and nonsmokers, from hamsters that were exposed to cigarette smoke for 4 to 6 weeks, and from a control group of unexposed hamsters. The abilities of alveolar macrophages from these four sources to accumulate 14C-labeled ascorbic acid and dehydroascorbate were also compared. The total ascorbate content in hamster macrophages was 19.5 +/- 1.7 and 44.3 +/- 2.8 nmol/10(7) cells for nonsmokers and smokers, (n = 5) and 73.8 +/- 13.1 nmol/10(7) cells (n = 13, p less than 0.1) for nonsmokers and smokers, respectively. In both humans and hamsters, the rates of accumulation of ascorbic acid and dehydroascorbate were significantly greater (p less than 0.05) for alveolar macrophages from smokers compared with nonsmokers of the same species. After internalization, greater than or equal to 70% of the dehydroascorbate was reduced to ascorbic acid by alveolar macrophages from nonsmokers and smokers of both species. An aqueous extract of cigarette smoke oxidized significantly more ascorbic acid to dehydroascorbate in vitro than a comparable volume of phosphate-buffered saline solution without smoke. The increased content of total ascorbate in alveolar macrophages from smokers and their enhanced ability to accumulate ascorbic acid and dehydroascorbate in vitro may reflect protective utilization of ascorbic acid under conditions of increased oxidant stress, compared with nonsmokers. In addition, alveolar macrophages may internalize dehydroascorbate that has been generated by oxidants in the alveolar space and reduce it to ascorbic acid so it can be reused as an antioxidant.

Adult↗
PubMed1998

17beta-estradiol inhibition of ascorbic acid accumulation in human intestinal Caco-2 cells.

We investigated the effect of estrogen on the accumulation of ascorbic acid by human intestinal Caco-2 cells. 17beta-estradiol, synthetic estrogen diethylstilbestrol, and partial agonist tamoxifen were found to inhibit ascorbic acid accumulation in a dose-dependent fashion. The inhibitory effect of estrogens can be observed at as short as 5 min of incubation. An additive effect was observed when they were used in combination. Similar to dietary flavonoids, inhibition was also observed in two other intestinal cell lines, HT-29 and IEC-6. These chemicals affected both Na+ -dependent and Na+ -independent(K+ substituting Na+) accumulation of ascorbic acid and did not affect the efflux of accumulated ascorbic acid. Kinetic analysis of diethylstilbestrol showed a non-competitive inhibition with an apparent Ki of 23 microM. The hormone-ascorbic acid interaction in the intestinal cell could help to explain the known reduction in blood ascorbic acid level among oral contraceptive users and female guinea pigs given contraceptive hormones.

Ascorbic Acid↗
PubMed1979

L-ascorbic acid: effects on aortic glycosaminoglycan 35S incorporation in rabbit-induced atherogenesis.

The effects of L-ascorbic acid on 35S-incorporation into thoracic aorta glycosaminoglycans and upon aorta cholesterol levels were determined in hypercholesterolemic rabbits. No significant difference was observed in serum free or esterified cholesterol levels between animals receiving L-ascorbic acid supplementation or saline while maintained on a cholesterol diet (0.5%). A 15-fold higher serum cholesterol was observed in animals on the cholesterol diet to those animals which received a normal rabbit (Purina) diet. L-Ascorbic acid increased sulfated glycosaminoglycans concentrations in hypercholesterolemic rabbits which paralleled lower tissue free and esterified cholesterol levels. The 35S-specific activity of glycosaminoglycans in hypercholesterolemic animals receiving saline was much greater than in those animals receiving L-ascorbic acid. This suggests that L-ascorbic acid plays a role in the maintenance of adequate levels of aortic sulfated glycosaminoglycans. This then is a suggested biochemical mechanism of L-ascorbic acids interaction in the atherogenic process.

Animals↗
PubMed1998

Effect of antioxidants (digoxin, quercetin, and ascorbic acid) on catalytic properties of horseradish peroxidase.

Antioxidants (digoxin, quercetin, and ascorbic acid) inhibited the oxidation of o-dianisidine catalyzed by horseradish peroxidase. Digoxin bound with the enzyme-substrate complex which included a stable semioxidized product of o-dianisidine and inhibited horseradish peroxidase by the anticompetitive pattern, while the enzyme inhibition by quercetin followed the mixed pattern. The oxidation of ascorbic acid and o-dianisidine with their combined presence in the reaction mixture was differentiated. o-Dianisidine was oxidized after the oxidation of 90-100% of ascorbic acid was completed. The rate of peroxidase oxidation of ascorbic acid in the presence of o-dianisidine was more than two orders higher than the rate of its individual oxidation and 1.5-2.0 times higher than the rate of o-dianisidine oxidation. Feasible inhibition mechanisms of peroxidase oxidation of o-dianisidine are discussed.

Antioxidants↗
PubMed1980

Effect of dietary ascorbic acid on the susceptibility of steelhead trout (Salmo gairdneri) to nitrite toxicity.

Four diets, each containing different levels of ascorbic acid were fed to duplicate groups of steelhead trout (Salmo gairdneri) in two four-week periods. Tolerance to nitrites increased when the concentration of ascorbic acid was high. Flow-through bioassays in fingerlings showed that when the temperature increased the percent of methemoglobin in their blood also increased. The tolerance to nitrite toxicity was less in large fish than in those smaller fed the same concentration of ascorbic acid. Possibly ascorbic acid acts in the reduction of methemoglobin to hemoglobin, and also it has a protective effect against stress in the fish. A "safe" level of 200 mg/kg of ascorbic acid in practical diets was reached.

Animal Feed↗
PubMed1977

Augmentative effect of ascorbic acid upon induction of human ovulation in clomiphene-ineffective anovulatory women.

The effect of the administration of 1-ascorbic acid, either alone or combined with clomiphene, upon induction of human ovulation was investigated in clomiphene-inffective anovulatory women. Oral administration of daily 400 mg of ascorbic acid induced ovulation in two out of five habitually anovulatory cycles and in one out of eight first-grade amenorrhea cases, and was ineffective in all six second-grade hypothalamic amenorrhea cases. Combined administration of ascorbic acid with 5 days of clomiphene induced ovulation in five out of five habitually anovulatory cycles, in 10 out of 17 first-grade hypothalamic amenorrhea cases, and in two out of nine second-grade hypothalamic amenorrhea cases. Pregnancy was established in eight out of 18 sterile, habitually-anovulatory or first-grade amenorrheic women with the combined ascorbic acid-clomiphene therapy, and in one out of five sterile, habitually anovulatory women with ascorbic acid therapy alone. Since administration of ascorbic acid induced no changed in blood FSH, LH, and amount of cervical mucus, and it is well established that LH decreases dose-dependency of the ascorbic acid content in the rat ovaries, the possible site of action of ascorbic acid seems to be at the ovarian level.

Administration, Oral↗
PubMed2006

Synthesis, structural studies, and cytostatic evaluation of 5,6-di-O-modified L-ascorbic acid derivatives.

The 5,6-di-O-tosylated derivative of l-ascorbic acid was synthesized by selective protection and deprotection of 2,3- and 5,6-dihydroxy functional groups involving 5,6-ditosylation in the final step, while the novel 6-acetoxy, 6-hydroxy, and 6-chloro derivatives of 4,5-didehydro-l-ascorbic acid were obtained by reaction of ditosylated compound with nucleophilic reagents. The analysis of 3JH-4-H-5 homonuclear coupling constants shows that all l-ascorbic acid derivatives except for epoxy and 4,5-didehydro compounds exist in high population as gauche conformers across C-4-C-5 bonds, while 3JC-3-H-5 heteronuclear coupling constants in 4,5-didehydro derivatives indicate cis geometry along C-4-C-5 double bond. The X-ray crystal structure analysis of 2,3-di-O-benzyl-5,6-epoxy- and 5,6-isopropylidene-l-ascorbic acid shows that the oxygen atoms attached at positions 2 and 3 of the lactone ring are disposed in a synperiplanar fashion. Besides that, the dioxolane ring adopts half-chair conformation. The molecules of epoxy derivative are joined into infinite chains by one weak hydrogen bond of C-H...O type. Two O-H...O, and C-H...O hydrogen bonds link the molecules of 5,6-di-O-isopropylidene compound into two-dimensional network. 6-Chloro derivative of 2,3-di-O-benzyl-l-ascorbic acid showed the best cytostatic effects against all tested malignant tumor cells (IC50: approximately 18 microM).

Antineoplastic Agents↗
PubMed1999

Treatment of progressive pigmented purpura with oral bioflavonoids and ascorbic acid: an open pilot study in 3 patients.

BACKGROUND: Bioflavonoids and ascorbic acid have been shown to increase capillary resistance and to mediate potent antioxidative radical scavenging activities. OBJECTIVE: We evaluated the clinical effect of oral bioflavonoids and ascorbic acid in patients with chronic progressive pigmented purpura (PPP). METHODS: In an open pilot study, oral rutoside (50 mg twice a day) and ascorbic acid (500 mg twice a day) were administered to 3 patients with chronic PPP. RESULTS: At the end of the 4-week treatment period, complete clearance of the skin lesions was achieved in all 3 patients. No adverse reactions were noted. All patients remained free of lesions at the end of 3 months after treatment. CONCLUSION: Our results suggest a beneficial effect of bioflavonoids in combination with ascorbic acid on PPP. Because the disease is mostly resistant to other treatment modalities, placebo-controlled studies are necessary to determine the usefulness of this therapy in PPP.

Administration, Oral↗
PubMed1989

Acetylcholine receptor alpha-subunit mRNA is increased by ascorbic acid in cloned L5 muscle cells: Northern blot analysis and in situ hybridization.

Ascorbic acid is the major factor in brain extract responsible for increasing the average acetylcholine receptor (AChR) site density on the cloned muscle cell line L5. In the present study, we show that this effect of ascorbic acid requires mRNA synthesis, and that the mRNA level for the AChR alpha-subunit is increased to about the same level as are the surface receptors. We have found no increase in the mRNA levels of the beta-, gamma-, and delta-subunits, or in the mRNAs of other muscle-specific proteins, such as that of light chain myosin 2, alpha-actin, and creatine kinase. By in situ hybridization, we further show that the increase in alpha-mRNA in response to ascorbic acid is exclusively in myotubes and is located near clusters of nuclei. mRNA levels for the alpha-subunit in mononucleated cells are very low and do not significantly increase in response to ascorbic acid. The mononucleated cells are thus excluded as a possible source for the increase in alpha-subunit mRNA detected by Northern blot analysis. Our results indicate that there is a very specific action of ascorbic acid on the regulation of AChR alpha-mRNA in the L5 muscle cells, and that the expression of surface receptors in these cells is limited by the amount of AChR alpha-subunit mRNA.

Animals↗
PubMed1988

[Ascorbic acid and hydroxyproline levels in the serum and granulation tissue of rats with aseptic and infected wounds].

Hydroxyproline and ascorbic acid were measured in wound tissues and ascorbic acid was determined in the blood sera of 230 mature male Wistar rats with aseptic and infected surface wounds on days 1-10 (daily), 12, and 15. The principal morphologic characteristics of the granulation tissue were assessed by semiquantitative methods. An infected wound is characterized by increased hydroxyproline levels in the granulation tissue and elevated ascorbic acid concentration in the blood serum. The granulation tissue ascorbic acid level augments during the first nine days in case of an aseptic wound and during twelve days in case of an infected wound. Morphologic and biochemical correlations are indicative of a relationship between the ascorbic acid level on the one hand and granulation tissue vascularization and fibroblast proliferation on the other.

Animals↗
PubMed2004

Augmentation of wound healing by ascorbic acid treatment in mice exposed to gamma-radiation.

PURPOSE: Because of the crucial practical importance of acute radiation exposure associated with combined injuries, the study was undertaken to investigate the effect of various doses of ascorbic acid on the survival and healing of wounds in mice exposed to whole-body gamma-radiation. MATERIALS AND METHODS: Animals were given double-distilled water or different doses of ascorbic acid by intraperitoneal injection before exposure to 0 or 10 Gy whole-body gamma-radiation to evaluate the effect of ascorbic acid on radiation-induced mortality. The animals were monitored daily for the symptoms of radiation sickness and mortality. In a separate experiment, animals were administered with either double-distilled water or different doses of ascorbic acid before exposure to 0 or 6 Gy whole-body gamma-radiation to investigate the effect of ascorbic acid on the irradiated wound. A full-thickness skin wound was created on the dorsum of the irradiated mice and the progression of wound contraction was monitored by capturing video images of the wound at various post-irradiation periods. RESULT: Treatment of mice with various doses of ascorbic acid elevated survival of mice and a highest number of survivors (67 and 33% for 10 and 30 days post-irradiation) was observed for 250 mg kg(-1) (p<0.002 and<0.02 for 10- and 30-day survival, respectively). Ascorbic acid treatment caused a dose-dependent elevation in the wound contraction and highest contraction was observed for 250 mg kg(-1). The wound contraction was significantly greater at 3 (p<0.005), 6 (<0.05) and 9 (<0.05) days post-irradiation with 250 mg kg(-1) ascorbic acid. The complete healing of the wound was effected by day 22.8 post-irradiation in the ascorbic acid-treated irradiation group. CONCLUSION: Administration of ascorbic acid protected mice against radiation-induced sickness, mortality and improved healing of wounds after exposure to whole-body gamma-radiation. Additional studies will be directed toward analysing the role of successive administration of ascorbic acid to protect non-target tissues during radiotherapy and in initiating and supporting the cascade of tissue repair processes in radiotherapy delayed wounds.

Animals↗
PubMed2000

Potentiation of ethanol-induced loss of the righting reflex by ascorbic acid in mice: interaction with dopamine antagonists.

The present investigation was carried out to determine the effect of ascorbic acid on ethanol-induced loss of the righting reflex (LORR) and the interactions between ascorbic acid and dopamine receptor antagonists in affecting this action of ethanol in mice. To test the effect of each drug on ethanol-induced LORR, ascorbic acid (31.25, 62.5, 125, 250, 500, 1000 mg/kg intraperitoneally [IP]) and dopamine receptor antagonists (haloperidol 0.5, 1.0 mg/kg; L-sulpiride 20, 40, 80 mg/kg; clozapine 0.625, 1.25, 2.5 mg/kg; SCH 23390 0.5, 1.0, 2.0 mg/kg subcutaneously [SC]) were administered, respectively, 30 min before ethanol (4.0 g/kg IP) administration. Ascorbic acid, at the dose of 1000 mg/kg, significantly potentiated ethanol-induced LORR in mice. Dopamine D(2) antagonists haloperidol (0.5, 1.0 mg/kg SC), and L-sulpiride (80 mg/kg SC) also significantly prolonged the duration of LORR induced by ethanol. Clozapine and SCH 23390, at the doses used, did not affect ethanol-induced LORR. In the interaction study, the synergistic effect of ascorbic acid (1000 mg/kg IP) on ethanol-induced LORR was significantly enhanced by dopamine D(2) antagonists haloperidol, L-sulpiride, and clozapine, and the highest dose of dopamine D(1) antagonist SCH 23390. These results suggest that ascorbic acid may potentiate ethanol-induced LORR partially via a mechanism mainly linked to blockade of dopamine D(2) receptors.

Animals↗
PubMed2003

Vitamin C (ascorbic acid) induced hydroxyl radical formation in copper contaminated household drinking water: role of bicarbonate concentration.

We have previously shown that Vitamin C (ascorbic acid) can trigger hydroxyl radical formation in copper contaminated household drinking water. We report here that the capacity of ascorbic acid to catalyze hydroxyl radical generation in the drinking water samples is strongly dependent on the bicarbonate concentration (buffer capacity and pH) of the samples. We found that at least 50 mg/l bicarbonate was required in the water samples to maintain the pH over 5.0 after ascorbic acid addition. At this pH, that is higher than the pKa1 4.25 of ascorbic acid, a hydroxyl radical generating redox cycling reaction involving the mono-anion of vitamin C and copper could take place. The ascorbic acid induced hydroxyl radical generating reaction could easily be mimicked in Milli-Q water by supplementing the water with copper and bicarbonate. Our results demonstrate that ascorbic acid can induce a pH dependent hydroxyl radical generating reaction in copper contaminated household tap water that is buffered with bicarbonate. The impact of consuming ascorbic acid together with copper and bicarbonate containing drinking water on human health is discussed.

Anions↗
PubMed1991

Comparison of the anti-scorbutic activity of L-ascorbic acid and Ester C in the non-ascorbate synthesizing Osteogenic Disorder Shionogi (ODS) rat.

The Osteogenic Disorder Shionogi (ODS) rat, Clea Inc., Tokyo, Japan lacks the ability to synthesize L-ascorbic acid (AA). As with man, monkey and the guinea pig, this rat lacks L-gulonolactone oxidase necessary for the synthesis of AA from glucose. This study shows this animal to be an alternative to the guinea pig in AA studies. The anti-scorbutic potency of Ester C (EC), a calcium ascorbate and calcium threonate mixture, was compared with an AA dose of equal ascorbate activity equivalents (AAE) for anti-scorbutic activity in the ODS rat. The minimal anti-scorbutic dose of EC was determined to be 0.44 mg/kg/day (AAE), while an AA dose of 0.51 mg/kg/day (AAE) was not anti-scorbutic in a 24 day study. At 24 days EC rats gained 125% of initial body weight (BW) and the AA rats only 45% BW. Scorbutic signs at 24 days were scored on a 0 (min) to 3 (max) scale. The EC/AA ratio scores were: hemorrhage 0/1.4, behavior change 0/2.0, piloerection 0/2.2, mobility 0.4/2.2, dysbasia 0.6/2.8 and ataxia 0.4/1.0. Pearson's correlation coefficient for BW versus AAE was r = .34 for the AA group and r = .90 for the EC group. The morbidity index for EC was 0/5 and for the AA group 2/5. The AAE dose of AA which was 16% higher/day than the EC AAE dose was not anti-scorbutic, while the EC dose was anti-scorbutic. EC rats had 3.5X greater weight gain, a sensitive indicator of scurvy, than the AA rats. EC rats had 3-4 times less, if any, scorbutic signs than AA rats. The results clearly show that, based on ascorbate activity equivalents, EC has more available ascorbate activity/potency than AA. The mechanism of this increased potency is believed to be due to the facilitated transport of AAE into the cell by the threonate (a normal in vivo metabolite of AA) present in the EC product. In addition, previous studies have shown EC (AAE) to be higher in plasma and excreted less rapidly than the AAE derived from AA administered orally.

Animals↗