Disease relevance of Potaba

• The bentiromide test using plasma p-aminobenzoic acid for diagnosing pancreatic insufficiency in young children. The effect of two different doses and a liquid meal [1].
• Bentiromide test for assessing pancreatic dysfunction using analysis of para-aminobenzoic acid in plasma and urine. Studies in cystic fibrosis and Shwachman's syndrome [2].
• In Escherichia coli, PABA is made from chorismate in two steps [3].
• Fungi, actinomycetes, and Plasmodium spp. also synthesize PABA but have proteins comprising fused domains homologous to PabA and PabB [3].
• Serum PABA test in chronic pancreatitis [4].

Psychiatry related information on Potaba

• We have prepared mouse monoclonal antibodies against idiotypic (Id) determinants on chicken antibodies to N-acetylglucosamine (NAGA) and p-aminobenzoic acid (PABA) made by inbred line EL 6(3) birds [5].
• Because Alzheimer's disease (AD) is a medical problem characterized by progressive loss of memory and cognition that is associated with a deficient cholinergic system, this work aims to evaluate some p-aminobenzoic acid (PABA) derivatives as acetylcholinesterase inhibitors in vitro, in continuation with our last studies [6].

High impact information on Potaba

• High-dose bentiromide with a liquid meal produced a delayed increase in plasma p-aminobenzoic acid in the control subjects probably caused by retarded gastric emptying [1].
• Pancreatic function was estimated by measuring enzymatic activities in the duodenal contents after a test meal and by determination of urinary excretion of p-aminobenzoic acid (pancreatic function test) after oral ingestion of the chymotrypsin-labile peptide N-benzoyl-L-tyrosyl-p-aminobenzoic acid [7].
• These results demonstrate that engineering a moderate increase in pteridine production can significantly enhance the folate content in food plants and that boosting the PABA supply can produce further gains [8].
• The enzyme behaved as a monomer in size-exclusion chromatography and was not inhibited by physiological concentrations of PABA, its glucose ester, or folates [3].
• When the putative targeting peptide was fused to GFP and expressed in protoplasts, the fusion protein appeared only in chloroplasts, indicating that PABA synthesis is plastidial [3].

Chemical compound and disease context of Potaba

• Metabolism of procainamide and p-aminobenzoic acid in patients with chronic liver disease [9].
• In Escherichia coli, this step is catalyzed by the PabC protein, a beta-lyase that converts 4-amino-4-deoxychorismate (ADC)--the reaction product of the PabA and PabB enzymes--to PABA and pyruvate [10].
• These results indicate that the N-acetyltransferase polymorphism is expressed in mouse colon when 2-aminofluorene or p-aminobenzoic acid is used as substrate and therefore the mouse may be a model for study of the effect of acetylator phenotype on development of colorectal cancer in humans [11].
• When administered i.p. simultaneously with 7.5 mg/kg DDP, PABA (100 mg/kg) significantly reduced plasma urea nitrogen (PUN) and plasma creatinine levels as well as DDP-induced weight loss [12].
• Chorismate aminations: partial purification of Escherichia coli PABA synthase and mechanistic comparison with anthranilate synthase [13].

Biological context of Potaba

• Isolation involved random mutagenesis of a cloned line of P. falciparum and subsequent selection of PABA-dependent parasites [14].
• When the NAT1 genotype was compared with the NAT1 phenotype in bladder and colon tissue samples (p-aminobenzoic acid activity), we observed a approximately 2-fold higher NAT1 enzyme activity in samples from individuals who inherited a variant polyadenylation signal (NAT1*10 allele) [15].
• Kinetics of the oxidation of p-aminobenzoic acid catalyzed by horseradish peroxidase compounds I and II [16].
• We have investigated the effects of carcinogenic doses of UVB-irradiation, psoralen plus UVA light (PUVA), PABA containing sunscreen preparations, and topically applied corticosteroids on both Langerhans cell densities and immunologic responsiveness to contact sensitizers applied to the treated site [17].
• Sex differences were apparent in this activity in C57BL/6J mouse kidney, with males exhibiting approximately 2.5-fold higher activity for aminofluorene and approximately 3-fold higher activity for p-aminobenzoic acid than did females [18].

Anatomical context of Potaba

• One gram N-benzoyl-L-tyrosyl PABA was orally administered to 24 controls, 15 patients with chronic exocrine pancreatic disease, 13 patients after an attack of acute pancreatitis, two patients with gluten-sensitive enteropathy, and 10 patients with biliary tract disease, peptic ulcer, or other pathology of the gastrointestinal tract [19].
• Using 25 microM p-aminobenzoic acid as substrate, maximal inhibition of NAT activity was 32.0 +/- 2.1% with liver cytosol and 5.8 +/- 0.16% with duodenal cytosol, whereas no inhibition of lung NAT activity was observed [20].
• We have used mouse embryo fibroblasts (MEFs) null for GSTpi (GSTpi(-/-)) to show that the absence of GSTpi results in a decreased sensitivity to PABA/NO [21].
• PABA also induced down-regulation of NAT1 activity in several human cell lines grown at confluence [22].
• In contrast, activated neutrophils metabolized PABA/PAS to the 3-chloro metabolite even in the presence of 1% serum [23].

Associations of Potaba with other chemical compounds

• In support of this selectivity, IL4I1 is inhibited by aromatic competitors (benzoic acid and para-aminobenzoic acid), but not by nonaromatic LAAO inhibitors [24].
• The pH dependence of the second order rate constants for the reaction of p-aminobenzoic acid with free Compounds I and II is similar to results obtained for the comparable reactions of ferrocyanide, suggesting similar proton-transfer mechanisms for both reducing substrates [16].
• The spectra of radicals formed upon the addition of .OH radicals to the 3 position of substrates for p-hydroxybenzoate hydroxylase (4-hydroxybenzoic acid, 2,4-dihydroxybenzoic acid, and 4-aminobenzoic acid) have been determined using pulse radiolysis combined with the results from high performance liquid chromatography measurements [25].
• The intronless coding regions of Nat-1 and Nat-2 showed different substrate specificities; isoniazid was a preferred substrate for NAT-1, whereas p-aminobenzoic acid was preferred for NAT-2(99asn) and NAT-2(99ile) [26].
• Biotransformation of para-aminobenzoic acid and salicylic acid by PMN [27].

Gene context of Potaba

• Moreover, the DNA adduct levels in these tissues correlated with their NAT1-dependent PABA activities (r = 0.52; P < 0.01) but not with their OAT activities [28].
• In slow acetylators who have decreased levels of hepatic NAT2, the AFMU/1X ratio was significantly correlated with PABA acetylation in MNL (r = 0.8; p = 0.0002) [29].
• A disruption of pabC was constructed and transferred to the chromosome, and the pabC mutant strain required PABA for growth [30].
• However, expression analysis using chromosomal pabA-lacZ translational fusions indicated that P1 expressed PabA at least 50-fold more efficiently than P2. pabA-dependent growth rate analysis indicates that P1 is essential and P2 is dispensable for PABA metabolism [31].
• The use of stronger promoters to drive FOL1 expression led to increased sulfamethoxazole resistance when para-aminobenzoic acid (pABA) levels were elevated [32].

Analytical, diagnostic and therapeutic context of Potaba

• The 295- to 320-nm wave band appeared to be responsible for this immunosuppressive effect of sunlight because suppression was prevented by filtration of the radiation through Mylar and by application of a sunscreen containing para-aminobenzoic acid [33].
• We found evidence to the contrary in a prospective study of 70 patients who were evaluated by endoscopic retrograde cholangiopancreatography and sequential measurements of stool fat, percent urinary PABA excretion, and serum trypsin during a follow-up time period of 1-4 yr [34].
• Further, in rat experiments urinary excretions of PABA were measured for six hours after oral administration of 15 mg PABA-UDCA disulphate [35].
• METHODS: Each patient underwent 1) ERCP, 2) the Bentiromide PABA, 3) 72-hour fecal fat test, 4) oral glucose tolerance test (OGTT) and 5) fat meal (LIPOMUL)--stimulated pancreatic polypeptide release (PP) [36].
• Semiquantitative reverse transcriptase polymerase chain reaction of mRNA isolated from treated and untreated cells revealed no effect of PABA on NAT1 mRNA levels [22].

References