Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “AMINOBENZOIC 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 757 records · Page 42Linked to original sources
PubMed1976

An oral test of pancreatic chymotrypsin activity using N-acetyl-L-tyrosyl-p-amino-benzoic acid in rats.

After a single dose of up to 50 mg/kg body weight (optimal amount for the test) of p-aminobenzoic acid or the corresponding amount of synthetic chymotrypsin substrate N-acetyl-L-tyrosyl-p-aminobenzoic acid, the urinary excretion of p-aminobenzoic acid in rats increases approximately linearly during 24 h. Higher doses do not cause any further significant increase in the amount of urine excreted p-aminobenzoic acid. Compared with a 24 h collecting period, 82% of p-aminobenzoic acid and 77% of p-aminobenzoic acid from N-acetyl-L-tyrosyl-p-aminobenzoic acid were excreted in the urine during the first 6 h after oral application of these substances. Therefore it is sufficient for practical purposes to determine p-aminobenzoic acid in 6 h urine samples. Stimulation of pancreatic secretion by application of 2.5 U of pancreozymin and 2.5 U of secretin failed to bring about significant increase in the cleaved p-aminobenzoic acid in the urine.

4-Aminobenzoic Acid↗
PubMed1962

Niacin requirement for sporulation of Physarum polycephalum.

Daniel, John W. (University of Wisconsin, Madison, Wis.) and Harold P. Rusch. Niacin requirement for sporulation of Physarum polycephalum. J. Bacteriol. 83:1244-1250. 1962.-The myxomycete Physarum polycephalum undergoes sexual sporulation if exposed to light after 4 days of incubation in the dark on a salts medium containing niacin, niacinamide, or tryptophan. None of these compounds is required for growth. Quinic acid, shikimic acid, intermediates of the kynurenine pathway, diphosphopyridine nucleotide (DPN), and triphosphopyridine nucleotide (TPN) replace niacin but a number of other tryptophan metabolites do not. Analogues of niacin inhibit sporulation when added at the beginning but not at the end of dark incubation with niacin. Folic acid, p-aminobenzoic acid, and p-aminobenzenesulfonamide inhibit sporulation if added at any time during the incubation or illumination periods. Reduced di- or triphosphopyridine nucleotide, but not DPN or TPN, reverse the p-aminobenzoic acid inhibition but do not replace the light requirement or shorten the dark incubation period. Gluconate and 2-ketogluconate also replace niacin. Glucose, pyruvate, malate, and oxalacetate inhibit the niacin-induced sporulation. Iodoacetate and fluoride do not counteract the glucose effect or inhibit sporulation.

4-Aminobenzoic Acid↗
PubMed1981

Organic acid proton donors decrease intestinal secretion caused by enterotoxins.

The effects of several weak acids on the secretory actions of cholera toxin and the heat-stable enterotoxin of Escherichia coli (ST) have been examined in ligated jejunal loops in weanling pigs. Ascorbic and acetic acids had no effect, but L-lactic acid reduced the net fluid secretion caused by cholera toxin. Glutaric acid and p-aminobenzoic acid blocked net fluid secretion caused by cholera toxin or by ST. Antisecretory effects were pH dependent for p-aminobenzoic acid in this study and for nicotinic acid in a previous report (6). At a pH of 5.0, p-aminobenzoic acid treatment increased lumen-to-blood sodium flux and decreased the blood-to-lumen sodium flux caused by cholera toxin. These weak acid effects were more marked on fluid fluxes in enterotoxin-treated loops than in control loops and persisted for 20-30 min after acid removal from loops. These findings are discussed in terms of requirements for antisecretory activity and possible modes of action of antisecretory compounds.

Animals↗
PubMed1984

[The PABA test].

PABA test has proved to be an easy and reliable test for determination of exocrine pancreatic insufficiency. N-benzoyl-L-tyrosyl-p-aminobenzoic acid or 4-(N-acetyl-L-tyrosyl) aminobenzoic acid are split by action of chymotrypsin in the small intestine. N.O-diacetyl-L-tyrosyl-p-aminobenzoic acid is converted easy in vivo in 4(N-acetyl-L-tyrosyl) aminobenzoic acid. The amount of 4-aminobenzoic acid (PABA) in urine collected for 6-10 hours is used as an index of chymotrypsin production. The concentration of PABA (and aromatic amines) is estimated in urine by the Bratton and Marshall method. p-dimethylamino cinnamaldehyde is less useful for the determination of urinary PABA. 60 min are necessary as time for acid hydrolysis of conjugated PABA metabolites. False abnormal test results are found for instance in patients with inflammatory bowel diseases, small bowel resection, impaired liver function, anorexia nervosa, lambliasis or renal insufficiency. The PABA test appears in consideration of these restrictions to be an useful simple method in the assessment of exocrine pancreatic function.

4-Aminobenzoic Acid↗
PubMed1998

Penicillium expansum growth and production of patulin in the presence of benzoic acid and its derivatives.

This study was conducted in order to evaluate the influence of benzoic acid and its derivatives: o-nitrobenzoic acid, o- and p-aminobenzoic acids, o-hydroxybenzoic acid, acetylsalicylic acid, cinnamic acid and aldehyde, methyl and ethyl esters of benzoic acid, methyl ester of p-hydroxybenzoic acid and ethyl ester of p-aminobenzoic acid on the growth and the ability to produce patulin by Penicillium expansum. The growth of the mycelium and its ability to produce patulin in the liquid enriched Czapek medium, and the dynamics of its linear growth and sporulation, on the Sabouraud medium with addition of the above mentioned compounds were evaluated. Benzoic acid and most of its derivatives, within the studied range of concentrations, limited the growth of the microfungus, while methyl ester of benzoic acid and o-aminobenzoic acid stimulated its growth.

Benzoates↗
PubMed1996

Indirect examination of exocrine pancreatic function in vivo by determination of chymotrypsin activity in animal intestine using a synthetic substrate.

Using the substrate N-acetyl-L-tyrosyl-p-aminobenzoic acid, we determined chymotrypsin activity in the small intestine of calf, pig, and poultry. Orally administered N-acetyl-L-tyrosyl-p-aminobenzoic acid is enzymatically cleaved in vivo, and the released p-aminobenzoic acid is determined by HPLC. We found that the p-aminobenzoic acid concentration in plasma and urine was significantly influenced by the feeding of soya flour. After soybean flour feeding, the p-aminobenzoic acid concentration significantly increased in the plasma of calves and hens, in contrast to pigs, where the p-aminobenzoic acid concentration significantly decreased. This shows that the oral administration of N-acetyl-L-tyrosyl-p-aminobenzoic acid with subsequent determination of p-aminobenzoic acid is suitable for the estimation of exocrine pancreatic function and for determination of changes in intestinal proteolytic activity caused by antinutritive substances.

4-Aminobenzoic Acid↗
PubMed1976

Conditional virulence of a p-aminobenzoic acid-requiring mutant of Aspergillus fumigatus.

The induced auxotrophy for p-aminobenzoic acid (PABA) resulted in a complete loss of virulence of Aspergillus fumigatus for normal as well as cortisone-treated mice. The PABA-requiring mutant of A. fumigatus survived in vivo for 4 to 7 days without causing any infection. However, it showed conditional virulence in animals receiving PABA in very small quantities. Repeated inoculations of the viable spores of the avirulent mutant strain gave favorable results in building immunity against intravenous challenge of the virulent strain. The immunogenicity of the PABA-requiring mutant was comparable with that of a wild strain of the fungus in agar gel double-diffusion tests using clinical and hyperimmune sera and in skin tests on patients with allergic bronchopulmonary aspergillosis.

Aminobenzoates↗
PubMed1985

In vitro activities of and mechanisms of resistance to antifol antimalarial drugs.

Certain drugs that interfere with folate metabolism (sulfones, sulfonamides, and inhibitors of dihydrofolate reductase) play an important role in the chemotherapy and prophylaxis of malaria. The activities and mechanisms of action of these drugs are regarded as similar in most respects to their activities against procaryotic microorganisms. Believed incapable of utilizing intact exogenous folates, plasmodia have been regarded as dependent on de novo synthesis of required folate cofactors. The present investigation, conducted in pursuit of a method for testing the in vitro susceptibility of Plasmodium falciparum to antifol antimalarial drugs, produced evidence that earlier assumptions about the folate metabolism of this organism are not correct. Three of four isolates of P. falciparum were successfully maintained in a culture medium depleted of folic acid and p-aminobenzoic acid. The antimalarial activities of sulfonamides and dihydrofolate reductase inhibitors were, furthermore, variably antagonized by the presence of folic acid and p-aminobenzoic acid in the culture medium. Optimum conditions for assessment of antifol antimalarial activity in vitro therefore require precise control of these factors in the culture medium. Our results suggest that resistance to antifol antimalarial drugs involves a complex of factors related to both the de novo synthesis of active folate cofactors and the ability to utilize exogenous intact folates in various forms.

4-Aminobenzoic Acid↗
PubMed1983

Continuous cultivation and improved drug responsiveness of Plasmodium falciparum in p-aminobenzoic acid-deficient medium.

Long term cultivation of three culture lines of Plasmodium falciparum was achieved in Waymouth and RPMI media, both supplemented with 10% heat-inactivated human serum. Observations on parasite multiplication over a 6-mo period showed no difference in the rate of parasite population increase. Growth of asexual erythrocytic stages in Waymouth medium was as good as that in RPMI when measured by the rate of glucose utilization and extent of 3H-isoleucine and 3H-methionine incorporation. Responsiveness of the parasites to pyrimethamine and sulfadoxine was demonstrated to increase when tested in Waymouth medium because it contained no p-aminobenzoic acid to compete with the drugs.

4-Aminobenzoic Acid↗
PubMed1997

Euglena gracilis as an eukaryotic test organism for detecting mutagens and antimutagens.

The unicellular flagellate Euglena gracilis was used in order to assess the inhibition of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and N-methyl-N-nitrosourea (MNU) mutagenicities, which induce white mutants due to the irreversible loss of chloroplasts. All tested compounds, including o-aminobenzoic acid and p-aminobenzoic acid, salicylic acid, acetylsalicylic acid, sodium salicylate and p-aminosalicylic acid, were not mutagenic per se and inhibited MNNG mutagenicity by at least 50%. The last two compounds inhibited by at least 50% also MNU mutagenicity.

4-Aminobenzoic Acid↗
PubMed1991

Metabolism and elimination of benzocaine by rainbow trout, Oncorhynchus mykiss.

1. Branchial and urinary elimination of benzocaine residues was evaluated in adult rainbow trout, Oncorhynchus mykiss, given a single dorsal aortic dose of 14C-benzocaine hydrochloride. 2. Branchial elimination of benzocaine residues was rapid and accounted for 59.2% of the dose during the first 3 h after dosing. Renal elimination of radioactivity was considerably slower; the kidney excreted 2.7% dose within 3 h and 9.0% within 24 h. Gallbladder bile contained 2.0% dose 24 h after injection. 3. Of the radioactivity in radiochromatograms from water taken 3 min after injection, 87.3% was benzocaine and 12.7% was N-acetylated benzocaine. After 60 min, 32.7% was benzocaine and 67.3% was N-acetylated benzocaine. 4. Of the radioactivity in radiochromatograms from urine taken 1 h after dosing, 7.6% was para-aminobenzoic acid, 59.7% was N-acetylated para-aminobenzoic acid, 19.5% was benzocaine, and 8.0% was N-acetylated benzocaine. The proportion of the radioactivity in urine changed with time so that by 20 h, 1.0% was para-aminobenzoic acid and 96.6% was N-acetylated para-aminobenzoic acid. 5. Benzocaine and a more hydrophobic metabolite, N-acetylated benzocaine, were eliminated primarily through the gills; renal and biliary pathways were less significant elimination routes for benzocaine residues.

Animals↗
PubMed1994

2-Aminofluorene metabolism and DNA adduct formation by mononuclear leukocytes from rapid and slow acetylator mouse strains.

Following exposure of mice to the arylamine carcinogen 2-aminofluorene, DNA-carcinogen adducts can be found in the target tissues liver and bladder, and also in circulating leukocytes. Evidence is presented here that mouse mononuclear leukocytes (MNL) are capable of metabolizing 2-aminofluorene to DNA-binding metabolites which give rise to the adducts found in the MNL. Both lymphocytes and monocytes were able to acetylate arylamines during 18 h of culture. The degree of acetylation was determined by the N-acetyltransferase genotype of the mice as shown through use of acetylator congenic strains which differ only in the Nat-2 gene. Cultured MNL from rapid acetylator mice (C57BL/6J and A.B6-Natr) produced about twice as much N-acetylaminofluorene from 2-aminofluorene and 6- to 8-fold as much N-acetyl-p-aminobenzoic acid from p-aminobenzoic acid as cells from slow acetylator mice (B6.A-Nat(s) and A/J). Other differences in arylamine metabolism by MNL in culture were observed and shown to be due to genetic factors, currently unidentified, other than N-acetyltransferase. DNA adduct formation following incubation of MNL with the arylamine carcinogen 2-aminofluorene was related to both acetylation capacity and to other genetic metabolic factors in the mouse genome. MNL from rapid acetylator mice with the C57BL/6J background (B6) had 3-fold the DNA adduct levels of cells from the corresponding slow acetylator congenic (B6.A-Nat(s)). Similarly, MNL from rapid acetylator mice with the A/J background (A.B6-Natr) had twice the DNA adduct levels of those from their corresponding slow congenic (A). Adduct levels in MNL from C57BL/6J were nearly the same as those of MNL from A/J, again indicating the involvement of loci other than acetylation in DNA adduct formation. The finding of genetically dependent arylamine carcinogen metabolism and DNA adduct formation in cultured MNL suggests the possibility of using cultured MNL for assessing individual susceptibility to arylamine-induced DNA damage.

4-Aminobenzoic Acid↗
PubMed2005

Separation of 2-aminobenzoic acid-derivatized glycosaminoglycans and asparagine-linked glycans by capillary electrophoresis.

A capillary electrophoresis method was developed for the analysis of oligosaccharides combined with derivatization with 2-aminobenzoic acid. Glycosaminoglycan delta-disaccharides were effectively resolved on a fused-silica capillary tube using 150 mM borate, pH 8.5, as a running electrolyte solution. This analytical method was applied to the identification of glycosaminoglycan in combination with enzymatic digestion. The separation of N-glycans or glucose-oligomers was performed with a phosphate buffer containing polyethylene glycol or borate as an electrolyte solution. This method is expected to be useful in the determination of oligosaccharide structures in a glycoprotein.

Animals↗
PubMed1995

Effects of select medium supplements on in vitro development of Cryptosporidium parvum in HCT-8 cells.

Surface-sterilized oocysts of Cryptosporidium parvum were applied to subconfluent monolayers of human adenocarcinoma (HCT-8) cells grown on coverslips in six-well cluster plates. Parasite-infected cultures were then incubated in RPMI 1640 with 10% fetal bovine serum, 15 mM HEPES (N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid) buffer, and antibiotics at 37 degrees C in a 5% CO2-95% air incubator for 2 h to allow sporozoites to excyst and enter cells. After cultures were washed free of debris, fresh cell culture media containing select supplements were added and cultures were reincubated. Parasite growth was assessed 66 h later by counting the number of parasite developmental stages in 25 random x 100 oil fields by Nomarski interference-contrast microscopy. Four vitamin supplements, calcium pantothenate, L-ascorbic acid, folic acid, and 4-(para)-aminobenzoic acid, each resulted in a significant increase in parasite numbers in vitro. The addition of insulin and the sugars glucose, galactose, and maltose also had a positive effect on parasite growth, although the effect was less pronounced than with any of the vitamins. Using the above information, we developed a supplemental medium formulation consisting of RPMI 1640 with 10% fetal bovine serum, 15 mM HEPES, 50 mM glucose, and 35 micrograms of ascorbic acid, 1.0 micrograms of folic acid, 4.0 micrograms of 4-aminobenzoic acid, 2.0 micrograms of calcium pantothenate, 0.1 U of insulin, 100 U of penicillin G, 100 micrograms of streptomycin, and 0.25 microgram of amphotericin B (Fungizone) per ml (pH 7.4). The growth of c. parvum in this medium was found to be enhanced approximately 10-fold compared with that in control medium without additional glucose, insulin, or vitamins.

Animals↗
PubMedDate not supplied

Inhibitory actions of emodin on arylamine N-acetyltransferase activity in strains of Helicobacter pylori from peptic ulcer patients.

Arylamine N-acetyltransferase (NAT) activities with p-aminobenzoic acid and 2-aminofluorene were determined in Helicobacter pylori, a gram-negative rod bacteria collected from peptic ulcer patients. The NAT activity was determined using a acetyl CoA recycling assay and HPLC. Cytosols or suspensions of H. pylori with and without selected concentrations of emodin co-treatment showed different percentages of 2-aminofluorene and p-aminobenzoic acid acetylation. The data indicate that there were decreased NAT activity associated with increased emodin in H. pylori cytosols. As 400 microns of emodin can obviously inhibit NAT activity both in vitro and in vivo (inhibition rate 90% and 93% for 2-aminofluorene and p-aminobenzoic acid in vitro, and 90% and 92%, respectively, for both substrate in vivo). For in vitro examination, the apparent values of Km and Vmax were 3.12 +/- 0.38 mM and 15.20 +/- 3.16 nmol/min/mg protein for 2-aminofluorene, and 0.56 +/- 0.12 mM and 0.74 +/- 0.09 nmol/min mg protein for p-aminobenzoic acid. However, when emodin was added to the reaction mixtures, the values of apparent Km and Vmax were 2.40 +/- 0.32 mM and 10.62 +/- 0.04 nmol/min/mg protein for 2-aminofluorene, and 0.23 +/- 0.02 mM and 0.62 +/- 0.08 nmol/min/mg protein for p-aminobenzoic acid. For in vivo examination, the apparent Km and Vmax were 0.82 +/- 0.18 mM and 0.92 +/- 0.21 nmol/min/10 x 10(10) colony forming units (CFU) for 2-aminofluorene, and 0.78 +/- 0.14 mM and 0.52 +/- 0.06 nmol/min/ 10 x 10(10) (CFU) for p-aminobenzoic acid. However, when emodin was added to the reaction mixtures, the values of apparent Km and Vmax were 0.50 +/- 0.08 mM and 0.62 +/- 0.22 nmol/min/ 10 x 10(10) (CFU) for 2-aminofluorene, and 0.52 +/- 0.21 mM and 0.26 +/- 0.04 nmol/min/ 10 x 10(10) (CFU) for p-aminobenzoic acid. This report is the first finding of emodin inhibition of arylamine N-acetyltransferase activity in a strain of H. pylori.

4-Aminobenzoic Acid↗
PubMed1997

Kinetics of arylamine N-acetyltransferase in tissues from human breast cancer.

N-Acetyltransferase activity and Michaelis-Menten kinetic constants were determined in cancerous and non-cancerous breast tissues from 30 female patients with breast cancer. The results derived from tissue cytosol showed that 12 rapid, ten intermediate and eight slow acetylators based on p-aminobenzoic acid and 2-aminofluorene for substrates. The mean apparent Km values for the monomorphic substrate p-aminobenzoic acid and polymorphic substrate 2-aminofluorene were: 55.0 +/- 18.7, 114.0 +/- 30.0, and 137.0 +/- 37.2 microM; and 62.5 +/- 23.7, 166.0 +/- 67.0, and 239.0 +/- 76.6 microM for the slow, intermediate, and rapid enzymes, respectively. Compared to the enzymes from slow acetylators, the rapid acetylators exhibited mean apparent Vmax values eight- and ten-fold greater for p-aminobenzoic acid and 2-aminofluorene, respectively. A similar trend was obtained from the blood cytosols of cancerous patients and healthy volunteers. N-Acetyltransferase activity of breast cancerous and non-cancerous tissues were 1.5- and 2.2-fold different between rapid and slow acetylator with p-aminobenzoic acid and 2-aminofluorene as substrates, respectively. In breast cancerous tissues, 75% and 70% of the cytosolic N-acetyltransferase activity were inhibited under 2 mM of tamoxifen as substrates of 2-aminofluorene and p-aminobenzoic acid, respectively. Similar results were also found in non-cancerous tissues and blood samples from breast cancer patients and healthy volunteers. The effect of 1 mM tamoxifen on the N-acetyltransferase activity from breast cancerous tissues with positive estrogen receptor was 1.6-fold higher than that of negative estrogen receptor. This is the first demonstration to show that anti-estrogen drug can affect N-acetyltransferase activity in breast cancerous tissues. Therefore, this finding may provide a clue to the use of tamoxifen in prevention of human breast cancer.

4-Aminobenzoic Acid↗