Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ASCORBIC ACID”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,693 records · Page 94Linked to original sources
PubMed1981

Increased ascorbic acid content in chronic lymphocytic leukemia B lymphocytes.

Human lymphocyte extracts analyzed by high-performance liquid chromatography reveal a major UV-absorbing peak that was shown to be ascorbic acid by spectral, chemical, and enzymatic criteria. Because this peak appeared very prominent in the elution profile of chronic lymphocytic leukemia (CLL) lymphocyte extracts, we measured the ascorbic acid content in lymphocytes from the blood of normal subjects and untreated patients with chronic lymphocytic leukemia. A significantly higher concentration of 111 +/- 15.3 nmol per 10(8) cells (mean +/- SEM) was found in CLL lymphocytes than in normal blood lymphocytes, which contained 42.2 +/- 3.3 nmol per 10(8) cells. Selective enrichment with B and T cells showed that this difference was limited to the chronic lymphocytic leukemia B cell, which had a 5- to 15-fold higher content of ascorbic acid than normal B cells had. In contrast, the ascorbic acid level was similar in normal and CLL T cells. The very high ascorbic acid content provides the chronic lymphocytic leukemia B cell with a reducing substance that could react with oxidants or free radicals.

Ascorbic Acid↗
PubMed2001

A randomized controlled trial of high dose ascorbic acid for reduction of blood pressure, cortisol, and subjective responses to psychological stress.

RATIONALE: Physiological responses to stress are considered disruptive to health. High-dose ascorbic acid has reduced indices of stress in laboratory animals. METHODS: We conducted a randomized double-blind, placebo-controlled 14-day trial of sustained-release ascorbic acid (60 healthy young adults; 3 x1000 mg/day Cetebe) and placebo (60 healthy young adults) for reduction of blood pressure, cortisol, and subjective response to acute psychological stress (Trier Social Stress Test, TSST, consisting of public speaking and mental arithmetic). Six subjects from each group were excluded. RESULTS: Compared to the placebo group, the ascorbic acid group had less systolic blood pressure (an increase of 23 versus 31 mmHg), diastolic blood pressure, and subjective stress responses to the TSST; and also had faster salivary cortisol recovery (but not smaller overall cortisol response). Cortisol response to 1 microg ACTH, and reported side-effects during the trial did not differ between groups. Plasma ascorbic acid level at the end of the trial but not pre-trial was associated with reduced stress reactivity of systolic blood pressure, diastolic blood pressure, and subjective stress, and with greater salivary cortisol recovery. CONCLUSIONS: Treatment with high-dose sustained-release ascorbic acid palliates blood pressure, cortisol, and subjective response to acute psychological stress. These effects are not attributable to modification of adrenal responsiveness.

Adult↗
PubMed1984

The effect of ascorbic acid on the seasonal variations in serum cholesterol levels.

One gram of ascorbic acid (Vitamin C) administered randomly to a group of healthy young people (aged 29 +/- 5 years) produced a significant mean fall in serum cholesterol of 16 per cent within two months. A similar supplement to a group of healthy older people (aged 58 +/- 3 years) produced a significant mean fall in serum cholesterol of 14 per cent but required six to 12 months' administration. Serial observations on a mixed age group of healthy people (aged 38 +/- 12 years) over one calendar year revealed a seasonal fluctuation in serum cholesterol, the lowest levels being in summer (June 5.5 +/- 0.7 mmols/l) and the highest levels in winter (January 6.4 +/- 0.8 mmols/l), a significant rise of 16 per cent. These changes showed an inverse relationship with the leucocyte and serum ascorbic acid levels which also revealed a seasonal fluctuation, the months April/September being higher than the months October/March. The administration of 1g of ascorbic acid per day throughout the year abolished the winter rise in serum cholesterol levels. These results are discussed in the light of the relationship between cholesterol and vascular disease and the observations by Sir Richard Doll that lowering the cholesterol level, whether achieved by drugs or diet, results in a reduction in morbidity from myocardial infarction.

Adult↗
PubMed1993

Determination of plasma ascorbic acid by high-performance liquid chromatography with ultraviolet and electrochemical detection.

A convenient and reliable reversed-phase liquid chromatographic method for the routine determination of ascorbic acid with ultraviolet detection is described. This system avoids the use of modifier and ion-pairing reagent. The mobile phase consists of 20 mM ammonium dihydrogenphosphate with 0.015% metaphosphoric acid. This method enables the detection of plasma ascorbic acid at a concentration of 120 ng/ml within 5 min. The recovery and reproducibility were above 95%. A comparative study was also performed using ultraviolet and electrochemical detectors. Excellent agreement was observed between the two detection modes, with a correlation coefficient of 0.99. In addition, the storage conditions and stability of ascorbic acid in plasma and whole blood were investigated. The results showed that ascorbic acid was more stable in whole blood when stored below 4 degrees C.

Ascorbic Acid↗
PubMed1997

The role of microsomal beta-glucuronidase in ascorbic acid biosynthesis stimulated by xenobiotics in rats.

We (Horio et al., 1993) have reported that the stimulation of the expression of the UDPglucuronosyltransferase (UDPGT) gene played a key role in the ascorbic acid biosynthesis induced by xenobiotics, such as 3-methylcholanthrene (3MC) and phenobarbital (PB). beta-Glucuronidase catalyzes the hydrolysis of glucuronide formed by UDPGT. The role of microsomal beta-glucuronidase in ascorbic acid biosynthesis induced by xenobiotics was investigated using homozygous and heterozygous EHBRs (Eisai hyperbilirubinuria rats) which are deficient in microsomal beta-glucuronidase. Homozygous EHBRs, heterozygous EHBRs, and Sprague Dawley (SD) rats were injected intraperitoneally once with 3MC (20 mg/kg body weight), or once a day for 2 d with PB (100 mg/day kg body weight). In these three strains of rats, the hepatic level of xenobiotics-inducible UDPGT mRNA was elevated similarly by the treatment with xenobiotics. The increases of the hepatic concentration of ascorbic acid and the urinary excretion of ascorbic acid by the treatment with 3MC or PB were markedly suppressed in both EHBRs compared with those in the control SD rats. These results indicate that the microsomal beta-glucuronidase has an important role in the hepatic ascorbic acid biosynthesis induced by xenobiotics.

Animals↗
PubMed1994

A long-lasting vitamin C derivative, ascorbic acid 2-phosphate, increases myogenin gene expression and promotes differentiation in L6 muscle cells.

Hormones and growth factors are important regulators of myogenic cell differentiation, but little is known about the effect of vitamins on muscle differentiation and development. We recently showed that L-ascorbic acid 2-phosphate, a stable form of vitamin C, increased the expression of muscle-specific glucose and ion transporters. We now show the effect of L-ascorbic acid 2-phosphate on the kinetics of myogenin expression at both the mRNA and protein levels during differentiation of L6 muscle cells. At the fully differentiated stage, control and L-ascorbic acid 2-phosphate treated cultures showed the same degree of cell fusion, but L-ascorbic acid 2-phosphate treated myotubes had a larger diameter than control myotubes. During L6 cell differentiation, the amount of both myogenin mRNA and protein reached a maximal level on day 4 before full myotube formation and then declined. L-ascorbic acid 2-phosphate treated cells expressed a higher amount of myogenin at both the mRNA and protein levels on day 4 compared to untreated cultures. Ethyl-3,4-dihydroxybenzoate, an inhibitor of collagen synthesis, prevented expression of myogenin mRNA and protein in both the control and L-ascorbic acid 2-phosphate treated cells. These results demonstrate that vitamin C can promote muscle differentiation likely through the increase of myogenin expression in myogenic cells, which may in turn regulate muscle differentiation in vivo.

Animals↗
PubMed1987

Aortic ascorbic acid, trace elements, and superoxide dismutase activity in human aneurysmal and occlusive disease.

Altered trace elements and ascorbic acid metabolism have been implicated in the pathogenesis of atherosclerotic cardiovascular disease. However, their role in the disease process, or the effect of atherosclerosis on their tissue levels within plaque, is poorly understood. The present study analyzes the concentrations of Fe, Cu, Zn, and Mn, and ascorbic acid and superoxide dismutase (SOD) activity in tissue samples from 29 patients with abdominal aortic aneurysms (AAA) and 14 patients with atherosclerotic occlusive disease (AOD). It was observed that the Fe and Mn concentrations in AAA and AOD tissue were higher than the levels in nondiseased control aorta, whereas Cu and Zn levels in AAA and AOD tissue were similar to the levels in controls. The Zn:Cu ratio was significantly lower in the AAA tissue in comparison to both AOD and control tissue. In addition, AAA and AOD tissue had low ascorbic acid levels and low Cu,Zn-SOD activity with Cu,Zn-SOD:Mn-SOD ratios of 0.27 and 0.19, respectively, compared to a ratio of 3.20 in control aorta. These data indicate that aorta affected by aneurysms and occlusive disease have altered trace element and ascorbic acid concentrations, as well as low Cu,Zn-SOD activity. Although these observations do not directly support the hypothesis that AAA is associated with aortic Cu deficiency they do suggest a role for oxygen radicals or increased lipid peroxidation in occlusive and aneurysmal disease of the aorta.

Adult↗
PubMed2002

Analytical potential of the reaction between p-phenylenediamines and peroxodisulfate for kinetic spectrophotometric determination of traces of ascorbic acid.

The analytical potential of the redox reactions between N, N-dimethyl- or N, N, N', N'-tetramethyl- p-phenylenediamine (DMPPD or TMPPD, respectively) and peroxodisulfate in acidic media for kinetic spectrophotometric determination of trace amounts of ascorbic acid (AA) has been investigated. The goal was to explore reaction conditions ensuring an excess or a deficit of S(2)O(8)(2-), and to identify some kinetic features of the global process for the purpose of calibration. Because the induction period of the overall reaction increases significantly in the presence of micromolar amounts of AA, the most suitable calibration graphs are generated by plots of induction period against the analyte concentration. The best sensitivity was achieved for oxidation of DMPPD with a deficit of S(2)O(8)(2-). The calibration line obtained has an RSD of 2.6% for 4 x 10(-6) mol L(-1) AA (n=3) and the detection limit is 4 x 10(-8) mol L(-1) (7 micro g L(-1)), a value comparable with the best mentioned by the literature. No systematic study of interferents was performed. Instead, the effect of buffer reagents (phosphate, phthalate, citrate) and dissolved oxygen on the results is discussed. Experiments were performed under closely controlled conditions. This is the first report of ascorbic acid analysis in which "contamination" by environmental oxygen was prevented by rinsing all vessels and saturating all solutions with argon, an approach which enables determination of the actual ascorbic acid content. Because of the effort involved, however, the method might not be suitable for routine analysis. Analysis of a commercially available vitamin C pellet gave good results when a "special" calibration graph, obtained in the presence of all other constituents of the sample except AA, was employed. The AA was "removed" from the pellet by oxidation with environmental air. Although it seems rather elaborate, this procedure did not require prior preparation of the sample nor extraction and/or concentration of ascorbic acid from it.

Journal Article↗
PubMed2000

Supplemental oxygen does not modulate responses to acetylcholine or ascorbic acid in the forearm of patients with congestive heart failure.

Despite providing symptomatic relief in patients with congestive heart failure (CHF), supplemental oxygen (O(2)) has been demonstrated to increase total peripheral resistance. The present study investigated the possibility that O(2) inhalation reduces nitric oxide (NO) bioavailability, using endothelium-dependent (acetylcholine) and -independent (phentolamine) vasodilators, and the antioxidant ascorbic acid. Ten patients (nine male and one female) with primary left ventricular failure participated in the study. Forearm venous occlusion plethysmography was used to study blood flow responses to acetylcholine and the alpha-adrenergic antagonist phentolamine during inhalation of either room air or 100% O(2), with and without the simultaneous infusion of ascorbic acid. Neither O(2) inhalation (3.9+/-0.4 compared with 3.8+/-0.3 ml.min(-1).100 ml(-1)) nor ascorbic acid infusion (5.2+/-0.4 compared with 5.5+/-0.4 ml.min(-1).100 ml(-1)) affected resting forearm blood flow. The percentage increase from basal blood flow after acetylcholine infusion was not altered by either O(2) inhalation or ascorbic acid infusion (room air, 140+/-55%; O(2), 118+/-46%; ascorbic acid, 147+/-39%; ascorbic acid+O(2), 109+/-31%). O(2) inhalation did, however, reduce the dilation induced by phentolamine (room air, 131+/-24%; O(2), 80+/-14%; P<0.05). These data indicate that oxygen inhalation does not increase forearm vascular resistance. Secondly, preservation of reactivity to acetylcholine during O(2) inhalation suggests that degradation of NO by O(2)-derived free radicals is not enhanced. Attenuation of phentolamine-induced vasodilation during O(2) inhalation, however, implies increased adrenergic activity, which may possibly exacerbate the detrimental effects of elevated sympathetic activity in CHF.

Acetylcholine↗
PubMed1984

The alpha-amidation of alpha-melanocyte stimulating hormone in intermediate pituitary requires ascorbic acid.

Rat intermediate pituitary cells in primary culture display a time-dependent loss of the ability to produce COOH-terminally alpha-amidated alpha MSH (Glembotski, C.C., Eipper, B.A., and Mains, R.E. (1983) J. Biol. Chem. 258, 7299-7304). Instead of des-, mono-, and diacetyl-adrenocorticotropic hormone(ACTH) (1-13)NH2, the cells produce des-, mono-, and diacetyl-ACTH(1-14)OH. Since the pituitary secretory granule-associated alpha-amidation enzyme requires copper and ascorbic acid for optimal activity (Eipper, B.A., Mains, R.E., and Glembotski, C. C. (1983) Proc. Natl. Acad. Sci. U.S.A. 80, 5144-5148), these cofactors were added to cultures of intermediate pituitary cells in an attempt to reverse the loss of peptide alpha-amidation ability. When the cultures were supplemented with up to 100 microM cooper (II) there was very little change in the ability to alpha-amidate alpha-melanotropin. Ascorbic acid at concentrations of up to 500 microM resulted in a dramatic increase in the ability of the cells to form the alpha-amidated peptide. Various combinations of ascorbic acid and copper additions indicated that a relatively short exposure (hours) to ascorbic acid produced the maximal response. Ascorbic acid displayed a dose-dependent effect on the alpha-amidation ability with a half-optimal concentration of about 25 microM. Pulse-chase labeling experiments demonstrated the ascorbic acid-dependent conversion of labeled ACTH(1-14)OH-related peptides to ACTH(1-13)NH2-related peptides. These results correlate with the ascorbic acid requirement of the pituitary alpha-amidation enzyme and demonstrate that the direct precursors to ACTH(1-13)NH2-related peptides are ACTH(1-14)OH-related peptides. Combined with our previous data, the present studies support the notion that a wide range of neuro- and endocrine peptides become alpha-amidated in a similar ascorbic acid-dependent manner.

Adrenocorticotropic Hormone↗
PubMed1995

Altered ascorbic acid status in the mucosa from inflammatory bowel disease patients.

Attempts to establish the presence of oxidant stress and tissue damage in inflammatory bowel disease (IBD) have relied on determining the capacity of peripheral blood inflammatory cells to produce reactive oxygen species (ROS) and other indirect indices. These approaches have failed to address whether or not there are adequate chemical antioxidant defences to prevent oxidative injury in the inflamed mucosa. In this investigation we have determined the mucosal concentrations of reduced and total ascorbic acid and the redox status in paired non-inflamed and inflamed mucosa using colonic biopsies from IBD patients. In inflamed mucosa from Crohn's disease (CD) patients, reduced and total ascorbic acid content decreased by 35% (p = 0.014 and p = 0.009, respectively). In ulcerative colitis (UC) patients, mucosal total ascorbic acid content decreased by 73% (p = 0.069) and reduced ascorbic acid by 41% (p = 0.014). The proportion of total ascorbic acid present in its reduced form in histologically normal mucosa from CD patients was unusually low at approximately 30%. In the paired-inflamed mucosa from CD patients, the redox ratio was also approximately 30% despite the loss of 35% of total ascorbate. In UC patients, the ascorbate redox ratio in the non-inflamed mucosa was 23% which increased to 51% in paired inflamed mucosa. This increase reflected the loss (73%) of total ascorbate. Reduction of dehydroascorbic acid by GSH/NADPH dependent dehydroascorbic acid reductase decreased significantly (p = 0.046) in inflamed mucosa from UC patients, suggesting that the capacity of the inflamed mucosa to maintain the concentration of reduced ascorbic acid is also diminished. HPLC analysis of mucosal preparations for diketogulonic acid, the decomposition product of dehydroascorbic acid, did not account for the loss of total ascorbate in the inflamed mucosa suggesting that ascorbate equivalents underwent further decomposition reactions or were excreted to the colonic lumen. We conclude that the normal luminal environment is strongly oxidising in character and that oxidant stress derived from inflammatory cells contributes to the loss of 35-73% total and reduced ascorbate. In absolute terms, the overall loss of this antioxidant buffering capacity would decrease the capacity of the inflamed mucosa to prevent oxidative tissue damage and hinder recovery of the inflamed mucosa.

2,3-Diketogulonic Acid↗
PubMedDate not supplied

Noneffect of oral urinary copper ascorbic acid on reduction glucose test.

References and texts in the fields of diabetes and clinical chemistry commonly report that ascorbic acid when given orally or parenterally gives a false-positive reaction to the copper reduction glucose test (Clinitest). This impression is based on a study in which ascorbic acid (250 mg./dl.) was added to urine in vitro, with a resultant positive-test reading in the absence of glucose. Ascorbic acid is a reducing agent, and theoretically it could interfere with the copper reduction method of glucose detection. In the current study 10 nondiabetic men were ingesting 4 and 6 gm. ascorbic acid per day. A total of 360 glucose detection tests with the copper reduction method were undertaken. In no instance was there a positive reaction to the glucose test.

Administration, Oral↗
PubMed2004

Ascorbic acid reduced mutagenicity at the HPRT locus in CHO cells against thermal neutron radiation.

We investigated the biological effects of the long-lived radicals induced following neutron irradiation. It has been reported that radiation-induced long-lived radicals were scavenged by post-irradiation treatment of ascorbic acid (Koyama, 1998). We studied the effects of ascorbic acid acting as a long-lived radical scavenger on cell killing and mutagenicity in Chinese hamster ovary cells against thermal neutrons produced at the Kyoto University Research reactor. Ascorbic acid was added to cells 30 min after neutron irradiation and removed 150 min after irradiation. The biological end point of cell survival was measured by colony formation assay. The mutagenicity was measured by the mutant frequency in the HPRT locus. The post-irradiation treatment of ascorbic acid did not alter the cell killing effect of neutron radiation. However, the mutagenicity was decreased, especially when the cells were irradiated with boron. Our results suggested that ascorbic acid scavenged long-lived radicals effectively and caused apparent protective effects against mutagenicity of boron neutron capture therapy.

Animals↗
PubMed1984

The effects of ascorbic acid and butylated hydroxyanisole in the chemoprevention of 1,2-dimethylhydrazine-induced large bowel neoplasms.

Human large bowel neoplasia seems to be caused by environmental carcinogens. The experimental carcinogen, 1,2-dimethylhydrazine (DMH), must be oxidized in the body to have effect. The antioxidants, butylated hydroxyanisole (BHA) and ascorbic acid, were tested for efficacy in prevention of experimental large bowel neoplasia. Carcinogenesis was induced in female CF-1 mice by administering DMH, 20 mg/kg, sq for 24 weekly doses. Test animals received varying doses of ascorbic acid, BHA, or both agents together. Animals were sacrificed when moribund or at 35 weeks. All colons were totally embedded and analyzed histologically. Ascorbic acid demonstrated no effects on incidence or density of large bowel tumors. Ascorbic acid did increase the ratio of adenomas to adenocarcinomas. BHA decreased the incidence and density of large bowel tumors. The lowest incidence was obtained in the group receiving both agents combined. It is concluded that BHA is effective in the chemoprevention of DMH-induced large bowel neoplasms. Ascorbic acid demonstrates only modest effect. The greatest effect on tumor incidence is seen when ascorbic acid and BHA are administered together.

1,2-Dimethylhydrazine↗
PubMed1998

Inhibitory effects of ascorbic acid on dopamine uptake by rat striatal synaptosomes: relationship to lipid peroxidation and oxidation of protein sulfhydryl groups.

Ascorbic acid is frequently added in the incubation medium to prevent oxidation of dopamine (DA) during uptake assays. However, a preliminary study showed that the presence of ascorbic acid induced a decrease of DA uptake after prolonged incubation. The purpose of this study was to determine the mechanism underlying ascorbic acid-induced alterations of DA uptake in rat striatal synaptosomes. In this context, the effects of physiological concentrations of ascorbic acid (100-500 microM) on DA uptake and Na+/K+ ATPase activity (which is essential for DA transporter function) were assessed in synaptosomes before and after incubation at 37 degrees C. The capacity of synaptosomes to take up DA was significantly decreased after incubation owing to a reduction in DA transporters (but with no modification of their affinity for DA). This partial inhibition was associated with a decrease of Na+/K+ ATPase activity, a production of thiobarbituric acid reactive substances (TBARS) and malonaldehyde (MDA), and a loss of sulfhydryl group content. Addition of Trolox C to the medium prevented the reduction of DA uptake, the inhibition of Na+/K+ ATPase activity, the decrease in sulfhydryl group content and the production of TBARS and MDA. These results suggest that ascorbic acid in the presence of contaminant ferrous ions induced a decrease in functional DA transporters, probably through a lipid peroxidation process involving oxidation of sulfhydryl groups and at least in part through a decrease of Na+/K+ ATPase activity.

Animals↗
PubMed1969

Ascorbic acid and copper in linoleate oxidation. 3. Catalysts in combination.

In promoting oxidation of 0.02 m potassium linoleate in a buffered (pH 7.0) aqueous dispersion at 37 degrees C, ascorbic acid at low concentrations (1.8 x 10(-6) and 1.8 x 10(-5) m) in combination with copper (1.3 x 10(-7) to 1.3 x 10(-3) m) had greater catalytic activity than the additive activity of the two catalysts individually. Possible explanations for the enhanced catalysis include reduction of copper by ascorbic acid to the cuprous form, increased concentration of semidehydroascorbic acid radical, and formation of a metal-ascorbic acid-oxygen complex. Some combinations of ascorbic acid (1.8 x 10(-4) and 1.8 x 10(-3) m) and copper (1.3 x 10(-6) and 1.3 x 10(-3) m) inhibited the formation of conjugated dienes but not the oxidation of ascorbic acid, and caused rapid loss of part of the conjugated dienes that were already present. It is suggested that free-radical inhibitors formed by the combination of catalysts inhibit initiation of lipid oxidation but not copper-catalyzed oxidation of ascorbic acid. Effects of the inhibitory combinations on changes in UV absorption by conjugated dienes, and absorbance in the TBA test, indicate the presence of at least two conjugated dienes that differ in stability.

Alkenes↗
PubMed2005

[Determination of ascorbic acid by indirect fluorimetry].

Experiments indicated that cerium(IV) ion which could not emit fluorescence was deoxidized by ascorbic acid to cerium(III) ion which could emit its characteristic fluorescence in water solution, while sodium hexametaphosphate added could greatly enhance the fluorescence intensity of the system. From this, an indirect sensitive method for determining ascorbic acid was developed. The fluorescence intensity of the system was measured in a 1 cm quartz cell with the excitation and emission wavelengths of 303 and 340 nm, respectively. The results showed that the fluorescence intensity of the system presented a linear relationship with the concentration of ascorbic acid in the range of 1.0 x 10(-7)-8.0 x 10(-6) mol x L(-1), the correlation coefficient r was 0.9997, and the detection limit (S/N = 3) was 1.6 x 10(-8) mol x L(-1). The presented method was used to determine ascorbic acid sample and vitamin C tablet, and the results were satisfactory.

Ascorbic Acid↗
PubMed1989

In vivo antimutagenic effect of ascorbic acid against mutagenicity of the common antiamebic drug diiodohydroxyquinoline.

We have previously shown that the common antiamebic drug diiodohydroxyquinoline (DIHQ) exhibits mutagenic activity in the in vivo micronucleus test in Swiss albino mice. Results of experiments undertaken to study the influence of ascorbic acid (vitamin C) on the mutagenicity of DIHQ in this model system showed that ascorbic acid acts as an antimutagen against DIHQ. The effective antimutagenic doses of ascorbic acid themselves do not show any genotoxic effects in this in vivo system. It will be necessary, however, to elucidate the mechanism of action of ascorbic acid as well as its effects on the therapeutic properties of DIHQ before a practical use of ascorbic acid is contemplated for this purpose.

Administration, Oral↗