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PubMedDate not supplied

N-Acetylation of drugs. A genetically controlled reciprocal relationship between drug N-acetylating enzymes of rabbit liver and peripheral blood cells.

The reciprocal relation between liver isoniazid N-acetyltransferase and blood p-aminobenzoic and N-acetyltransferase previously reported is confirmed and found to be expressed in erythrocytes and lymphocytes of genetically rapid and slow isoniazid-acetylator rabbits. Both erythrocytes and lymphocytes from slow acetylator rabbits contained 2.5-3.3 times as much p-aminobenzoic acid N-acetyltransferase activity as the same cells from rapid acetylator rabbits. Mechanisms which might account for the reciprocal association between liver and blood N-acetyltransferases are considered.

4-Aminobenzoic Acid↗
PubMed1981

Photocontact allergy to benzocaine.

A photodermatitis developed in two patients after the use of commercial sunscreens and a topical anesthetic lotion containing benzocaine. Photopatch testing indicated the presence of photocontact allergy to benzocaine. One patient had a positive photopatch test to a commercial glyceryl para-aminobenzoic acid (PABA) preparation that was heavily contaminated with benzocaine, but not to a benzocaine-free sample of glyceryl PABA. Benzocaine failed to produce phototoxic reactions in normal volunteers. Efforts to induce photocontact allergy in guinea pigs were unsuccessful.

4-Aminobenzoic Acid↗
PubMed2001

Vitamin C inhibited DNA adduct formation and arylamine N-acetyltransferase activity and gene expression in rat glial tumor cells.

Studies have been demonstrated that vitamin C (ascorbic acid) exhibit the protective role of vin in certain types of cancer. Rat glial tumor cells also have been shown have N-acetyltransferase activity. In this study, we reported the effects of vitamin C on arylamine N-acetyltransferase (NAT) activity and DNA adduct formation in rat glial tumor cell line (C6 glioma). The activity of NAT was measured by high performance liquid chromatography assaying for the amounts of acetylated 2-aminofluorene and p-aminobenzoic acid and nonacetylated 2-aminofluorene and p-amonibenzoic acid. Rat C6 glioma cells were used for examining NAT activity and gene expression and 2-aminofluorene-DNA adduct formation. The results demonstrated that NAT activity and 2-aminofluorene-DNA adduct formation in C6 glioma cells were inhibited and decreased by vitamin C in a dose-dependent manner. But vitamin C did not affect NAT gene expression in examined cells. The apparent kinetic parameters (apparent values of Km and Vmax) from C6 glioma cells were also determined with or without vitamin C cotreatment. The data also indicated that vitamin C decreased the apparent values of Km and Vmax from C6 glioma cells.

4-Aminobenzoic Acid↗
PubMed1994

Molecular genetics of Aspergillus pathogenicity.

Aspergillus fumigatus is the most frequent cause of Invasive Pulmonary Aspergillosis (IPA), a life-threatening disease of immunosuppressed patients. In addition to a number of general physiological attributes of this fungus, it has been suggested that extracellular elastase and toxins might facilitate its growth in lung tissue. We have investigated the roles of two extracellular proteins, an alkaline protease with elastase activity (AFAlp), and the ribotoxin restrictocin in murine models of IPA. Gene disruption was used to create stable null mutant strains of the fungus lacking one or other protein, and their virulence and histopathological features were compared with an isogenic parental strain in steroid-treated and neutropenic mice. We have been unable to demonstrate any significant differences between the three strains, which shows that, considered independently, these proteins are not important virulence determinants. We are also interested in identifying fungal-specific gene products involved in general metabolism and which are required for growth in the lung, because these could represent new targets for antifungal drugs. For this work a model of murine IPA involving Aspergillus nidulans was established, to take advantage of the many well characterised mutations affecting metabolic pathways. Pathogenicity tests with strains carrying one of two auxotrophic mutations, lysA2 and pabaA1, have shown while lysine biosynthesis is not essential for the fungus to cause pulmonary disease, biosynthesis of p-aminobenzoic acid is essential. We are now in the process of cloning the A. fumigatus pabaA homologue to determine its function and whether this gene is required for growth of the clinically important species in the lung.

4-Aminobenzoic Acid↗
PubMed1969

Growth of Ferrobacillus ferrooxidans on organic matter.

Following a brief adaptation period to glucose, Ferrobacillus ferrooxidans was grown on glucose, mannitol, several other sugars, and a few amino acids in the absence of an oxidizable iron source. Prolonged growth on an organic substrate free from iron rendered the organism obligately organotrophic. The growth rate of the bacterium was greater in heterotrophic culture; the doubling time was approximately 4.5 hr on glucose. The bacterium retained its acidophilic properties during adaptation and growth on glucose and would not grow in neutral or slightly alkaline media. Addition of p-aminobenzoic acid was necessary for abundant growth of the cells on glucose. Of the eight strains of Fe(++)-oxidizing bacteria studied, only two strains grew on glucose in a nondialyzed system. The results of manometric studies are discussed with regard to metabolic efficiency of organic matter in this organism.

Adaptation, Physiological↗
PubMed1988

Hepatic N-acetyltransferases: selective inactivation in vivo by a carcinogenic N-arylhydroxamic acid.

N-Hydroxy-2-acetamidofluorene (N-OH-AAF), a carcinogenic N-arylhydroxamic acid, is a selective and irreversible inhibitor of arylamine N-acetyltransferase (NAT) activity in vitro. The present study demonstrates that intraperitoneal administration of N-OH-AAF to hamsters caused an irreversible reduction of the hepatic transacetylase activity that catalyzes the transfer of the acetyl group from N-OH-AAF to 4-aminoazobenzene (AAB), but did not affect the acetyl coenzyme A (CoASAc) dependent NAT that is responsible for acetylation of p-aminobenzoic acid (PABA). A 40% loss of N-OH-AAF:AAB transacetylase activity occurred 4 hr after administration of 50 mg/kg of N-OH-AAF. To determine whether biotransformation of N-OH-AAF is a factor in determining its ability to inactivate N-OH-AAF:AAB transacetylase activity in vivo, the enzyme-inducing agent phenobarbital and the esterase/acylamidase inhibitor bis(p-nitrophenyl)phosphate (BNPP) were administered to the animals prior to the administration of N-OH-AAF. The loss of N-OH-AAF:AAB transacetylase activity was prevented by treatment of the animals with either phenobarbital or with BNPP. The ability of the esterase/acylamidase inhibitor, BNPP, to prevent the N-OH-AAF-mediated loss of transacetylase activity indicates that, in contrast to the inactivation process in vitro, esterase-catalyzed deacetylation of N-OH-AAF may be required for transacetylase inactivation in vivo. It is proposed that in vivo the endogenous acetyl donor, CoASAc, acetylates the enzyme and prevents the deacetylation of N-OH-AAF by NAT, thereby impeding the N-OH-AAF-mediated inactivation process, but facilitating enzyme inactivation by N-hydroxy-2-aminofluorene. The latter proposal was supported by the demonstration that CoASAc inhibited the in vitro inactivation of N-OH-AAF:AAB transacetylase activity by N-OH-AAF.

2-Acetylaminofluorene↗
PubMedDate not supplied

Metabolism of sulfanilamide and related drugs in isolated rat and rabbit liver cells.

Parenchymal and nonparenchymal cells were isolated from rat and rabbit liver by perfusion with collagenase. Pure parenchymal cells were obtained by centrifugation at low speed and nonparenchymal cells were purified by treatment with pronase. Suspensions of parenchymal cells from rat liver metabolized sulfamethazine, sulfanilamide, and p-aminobenzoic acid at rates of 39.0, 75.8, and 173.2 pmol/min/10(6) cells, respectively, but did not metabolize sulfadiazine. Rabbit liver parenchymal cells gave somewhat higher activities and also metabolized sulfadiazine. Nonparenchymal cells from both rat and rabbit liver failed to metabolize any of the compounds.

4-Aminobenzoic Acid↗
PubMed1994

Expression of monomorphic and polymorphic N-acetyltransferases in human colon.

The metabolism of sulfamethazine (SMZ) and p-aminobenzoic acid (PABA) by N-acetyltransferase (NAT) was measured in human colorectal cytosols from 12 slow and 11 rapid acetylators whose genotype was determined independently by a specific polymerase chain reaction. SMZ metabolism was significantly greater in the rapid than in the slow phenotype (192 +/- 22 versus 94 +/- 11 pmol N-acetylsulfamethazine/min/mg protein), while PABA metabolism was similar in both phenotypes (23.7 +/- 4.4 versus 23.0 +/- 3.9 nmol N-acetyl-p-aminobenzoic acid/min/mg protein). Both monomorphic and polymorphic NAT mRNAs were detected by the polymerase chain reaction in the colorectal mucosa of most samples. The finding that polymorphic NAT is expressed in a phenotype-dependent manner in colorectal mucosa indicates that this tissue has the capacity to participate in local bioactivation of dietary and environmental aryl- or heterocyclic amine carcinogens and may explain, in part, the phenotype-dependent occurrence of colorectal cancer.

4-Aminobenzoic Acid↗
PubMed1998

Separation of inorganic and organic anions by capillary zone electrophoresis with simultaneous indirect UV and conductivity detection.

The analysis of low-molecular-mass anionic compounds using capillary zone electrophoresis (CZE) with simultaneous direct conductivity and indirect UV detection is described. A number of carrier electrolyte compositions has been investigated with respect to the crucial parameters for their compatibility with both detection principles discussed in this paper (UV absorptivity and electrophoretic mobility of the buffer coion). Additionally, parameters including pH and buffer concentration affecting both peak symmetry and signal-to-noise ratio obtained for the analytes of interest had to be optimized. Best results could be achieved with a carrier electrolyte consisting of 4-aminobenzoic acid, bis(2-hydroxyethyl)imino-tris(hydroxymethyl)aminomethane (BIS-Tris) and a pH of 7.0 adjusted with LiOH. This running buffer was used for the analysis of low-molecular-mass anionic compounds in a sample of white wine.

4-Aminobenzoic Acid↗
PubMed1983

Effect of indomethacin on alteration of ATPase-positive Langerhans cell density and cutaneous sunburn reaction induced by ultraviolet-B radiation.

We have investigated the effect of ultraviolet-B (UVB) irradiation on the density of epidermal ATPase-positive Langerhans cells, and the modulation of this effect by indomethacin (IND). Depilated backs of albino guinea pigs were exposed to varying doses of UVB (10-550 mJ/cm2). Skin biopsies were taken serially. There was an UVB dose-dependent decrease in the density of dendritic epidermal Langerhans cells, as identified by their membrane ATPase activity. This was accompanied by thinning and shortening, or disappearance of dendritic processes. Such changes were followed by a gradual recovery of the cell density to preirradiation level by day 21. Despite the high doses of UVB given, the maximal decrease in the density of ATPase-positive cells was only 58%. Topical application of IND, a prostaglandin-synthetase inhibitor, after irradiation resulted in a decrease of the erythema; however, the decrease in the density of ATPase-positive cells was still observed. In contrast, guinea pigs that received IND topically prior to irradiation showed a decrease erythemal response, but failed to show any decrease in the density of ATPase-positive cells. Administration of IND orally for 3 days prior to UVB exposure did not prevent the decrease in the cell density. The protective effect of topical IND, applied prior to irradiation, may be explained by its in vitro absorbance at both the UVB and UVA ranges. Topical application of IND 20 min prior to exposure to UVB in 2 human subjects resulted in an increase in the minimal erythema dose, giving a sun protection factor of 1.6, which is comparable to that produced by an equimolar concentration of para-aminobenzoic acid solution. The sun-protective property of IND, together with its activity as a prostaglandin synthetase inhibitor, indicate that it potentially could be a useful sunscreen agent. Its clinical safety and efficacy, however, remain to be determined.

4-Aminobenzoic Acid↗
PubMed1991

Topical photoprotection for hereditary polymorphic light eruption of American Indians.

We evaluated the photoprotective efficacy of a broad-spectrum sunscreen containing a UVA screen (butyl methoxydibenzoylmethane) and a UVB screen (octyl dimethyl p-aminobenzoic acid) in patients with hereditary polymorphic light eruption. At least 18 of the 30 patients who enrolled in the study were sensitive to sunlight through window glass, an indication of UVA sensitivity. Of the 21 patients who completed the clinical trial, the physician's evaluation was that 18 (86%) obtained good to excellent results. Self-evaluation by the patients revealed that 16 (76%) noted more photoprotection than from previous treatments.

4-Aminobenzoic Acid↗
PubMed2004

Arylsulfonyl acridinyl derivatives acting on Plasmodium falciparum.

Several arylacridinyl sulfones have been synthesized and their antimalarial action was tested on Plasmodium falciparum. PABA (para-aminobenzoic acid) has no antagonistic effect with these compounds as opposed to the observed effect with dapsone and sulfonamides previously studied. A possible relationship between the ability of cleavage of the S-9C acridinic bond and activity is suggested.

4-Aminobenzoic Acid↗
PubMed1991

Inhibition of Plasmodium falciparum dihydropteroate synthetase and growth in vitro by sulfa drugs.

The Michaelis-Menten inhibitory constants (Kis) and the concentrations required for 50% inhibition of the Plasmodium falciparum dihydropteroate synthetase were determined for six sulfa drugs. These drugs inhibited the in vitro growth of P. falciparum (50% lethal concentration) at concentrations of 30 to 500 nM; these concentrations were 100 to 1,000 times lower than the concentrations required for 50% inhibition and Kis (6 to 500 microM). The uptake of p-aminobenzoic acid was not inhibited by the sulfa drugs. However, infected erythrocytes took up more labeled sulfamethoxazole than did uninfected erythrocytes. Thus, the concentration of sulfa drugs by malaria parasites may explain how sulfa drugs inhibit in vitro growth of parasites through the inhibition of dihydropteroate synthetase.

4-Aminobenzoic Acid↗
PubMed1991

Lack of pancreatic maldigestion in atopic dermatitis.

Twenty adult patients affected by atopic dermatitis (AD) were submitted to the p-aminobenzoic acid (PABA) test in order to evaluate the proteolytic pancreatic function. All but one showed a normal PABA test. These results seem to exclude a proteolytic maldigestion as a pathogenetic factor in AD.

4-Aminobenzoic Acid↗
PubMed1995

Identification of arylamine N-acetyltransferase activity in the bovine lens.

Arylamine N-acetyltransferase (NAT) activity was identified and partially characterized in the bovine lens. According to size-exclusion HPLC, the molecular mass of the arylamine NAT is approximately 30-kDa. Based upon substrate specificity analysis, it is best described as an arylamine NAT which has some ability to N-acetylate arylalkylamines. This arylamine NAT acetylates para-aminobenzoic acid thereby demonstrating a monomorphic pattern of N-acetylation. It demonstrates low sensitivity to methotrexate inhibition as indicated by the relatively high IC50 value (470 microM). NAT could be involved in lenticular detoxification of both endogenous amines and exogenous drugs.

4-Aminobenzoic Acid↗
PubMed1991

Expression of monomorphic arylamine N-acetyltransferase (NAT1) in human leukocytes.

The expression of arylamine N-acetyltransferase (NAT) in leukocytes was investigated using p-aminobenzoic acid (PABA) and sulfamethazine (SMZ), substrates which are preferentially acetylated by the monomorphic NAT1 and polymorphic NAT2 enzymes, respectively. Activity towards both substrates was detected in mononuclear leukocytes (MNL; preparation containing approximately 80% lymphocytes), monocytes and neutrophils. PABA and SMZ acetylation rates were highly correlated in each of the isolated cell types. The NAT in leukocytes displayed a much higher affinity and turnover rate for the acetylation of PABA than for SMZ. These kinetic characteristics suggest that the acetylating activity in human leukocytes is predominantly attributable to the monomorphic enzyme NAT1. Neutrophils showed evidence of biphasic kinetics for SMZ which would indicate the coexpression of NAT1 and low levels of the polymorphic enzyme, NAT2. NAT activity in MNL was not influenced by the acetylator phenotype of the individual. There was, however, a significant correlation between NAT activity in MNL and the in vivo acetylation (urinary metabolite ratio) of p-aminosalicylic acid, which is monomorphically acetylated in humans. The expression of NAT1 in leukocytes and the virtuall absence of NAT2 may have important toxicological implications. The in vitro/in vivo correlation suggests that leukocytes may be a useful marker of systemic NAT1 activity.

4-Aminobenzoic Acid↗
PubMed1997

Diagnosis of chronic pancreatitis using noninvasive tests of exocrine pancreatic function--comparison to duodenal intubation tests.

The diagnosis of chronic pancreatitis usually is based on imaging studies, pancreatic function tests, and the presence of characteristic clinical features. In Japan, diagnostic criteria for chronic pancreatitis were established in 1983 and revised in 1995. Under the new criteria, the secretin test (a duodenal intubation test) and the combination of noninvasive tests, N-benzoyl-L-tyrosyl-p-aminobenzoic acid (BT-PABA) and fecal chymotrypsin (FCT), have been recommended for evaluating exocrine pancreatic function in patients with chronic pancreatitis. In the present study, the diagnostic value of these two noninvasive tests was compared to the secretin test. Although noninvasive tests are less sensitive and specific for determining exocrine pancreatic impairment than the secretin test, greater reliability for diagnosing chronic pancreatitis can be obtained by performing the BT-PABA and fecal chymotrypsin tests simultaneously. Combining BT-PABA and FCT is easy and useful and should be performed at least twice to obtain reliable results.

4-Aminobenzoic Acid↗
PubMed1995

Kinetic characterization of 4-amino 4-deoxychorismate synthase from Escherichia coli.

The metabolic fate of p-aminobenzoic acid (PABA) in Escherichia coli is its incorporation into the vitamin folic acid. PABA is derived from the aromatic branch point precursor chorismate in two steps. Aminodeoxychorismate (ADC) synthase converts chorismate and glutamine to ADC and glutamate and is composed of two subunits, PabA and PabB. ADC lyase removes pyruvate from ADC, aromatizes the ring, and generates PABA. While there is much interest in the mechanism of chorismate aminations, there has been little work done on the ADC synthase reaction. We report that PabA requires a preincubation with dithiothreitol for maximal activity as measured by its ability to support the glutamine-dependent amination of chorismate by PabB. PabB glutamine enhances the protective effect of PabA. Incubation with fresh dithiothreitol reverses the inactivation of PabB. We conclude that both PabA and PabB have cysteine residues which are essential for catalytic function and/or for subunit interaction. Using conditions established for maximal activity of the proteins, we measured the Km values for the glutamine-dependent and ammonia-dependent aminations of chorismate, catalyzed by PabB alone and by the ADC synthase complex. Kinetic studies with substrates and the inhibitor 6-diazo-5-oxo-L-norleucine were consistent with an ordered bi-bi mechanism in which chorismate binds first. No inhibition of ADC synthase activity was observed when p-aminobenzoate, sulfanilamide, sulfathiazole, and several compounds requiring folate for their biosynthesis were used.

4-Aminobenzoic Acid↗