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PubMed1992

A new method for sequence analysis of glycosaminoglycans from heavily substituted proteoglycans reveals non-random positioning of 4- and 6-O-sulphated N-acetylgalactosamine in aggrecan-derived chondroitin sulphate.

We have developed a new procedure for the sequence analysis of glycosaminoglycans, which is particularly suitable for the analysis of chains from heavily substituted proteoglycans. The procedure has been applied to various aggrecan-derived chondroitin sulphates. The glycans are released from the core protein by alkaline scission of the xylose-serine bond, subjected to reductive amination using p-aminobenzoic acid and finally radioiodinated at an acidic pH. Sequence analysis is performed by using various enzymic degradations, partial or complete, followed by high-resolution polyacrylamide gel electrophoresis, blotting and autoradiography to identify segments extending from the labelled reducing end to the point of cleavage. By using chondroitin C lyase to identify the location of 6-O-sulphated hexosamines, we find that chondroitin sulphate from tracheal cartilage has its 6-O-sulphated repeats concentrated to the extreme non-reducing terminal portion of the chain. In chondroitin sulphates derived from intervertebral discs (nucleus pulposus), the 6-O-sulphated repeats have a biphasic distribution; they occur mostly near the linkage region (i.e. the reducing end), but also in the non-reducing portion of the chain. Chondroitin sulphate from nasal cartilage, which is mostly 4-O-sulphated, displays considerable heterogeneity in the linkage region. Three or possibly more charge variants are observed.

4-Aminobenzoic Acid↗
PubMed1990

Postprandial exocrine pancreatic function during long-term treatment with the somatostatin analogue SMS 201-995 in acromegalic patients.

Long-term treatment with the somatostatin analogue SMS 201-995 (SMS) might impair exocrine pancreatic function, secretion of cholecystokinin (CCK) and pancreatic polypeptide (PP), and pancreatic size. In five acromegalics on chronic treatment with SMS, we investigated postprandial 6-h urinary excretion of p-aminobenzoic acid (PABA) and p-aminosalicylic acid (PAS) after s.c. injection of 100 micrograms SMS or placebo and after ingestion of 2 mmol nBT-PABA and 2 mmol PAS. In the acromegalics, urinary PABA/PAS ratio (reflecting exocrine pancreatic function) after SMS was similar to that after placebo (P greater than 0.10) and higher than in healthy volunteers (n = 8, P = 0.05). The initial inhibition of plasma CCK secretion by SMS was cancelled during the 3rd h after the meal, whereas PP release remained completely abolished. Pancreatic size as measured by ultrasonography, was not reduced in seven acromegalics compared with 14 healthy volunteers. It is concluded that despite a blunted release of the trophic hormone CCK, long-term treatment with SMS 201-995 neither induces an abnormally small pancreas nor deterioration of postprandial exocrine pancreatic function in patients with acromegaly.

4-Aminobenzoic Acid↗
PubMed1996

Folate synthesized by bacteria in the human upper small intestine is assimilated by the host.

BACKGROUND & AIMS: Some intestinal flora are known to synthesize folate. The aim of this study was to determine whether folate synthesized by small intestinal flora is assimilated by the human host. METHODS: Subjects with atrophic gastritis and healthy volunteers were studied before and after omeprazole administration. A double-lumen perfusion tube was placed in the duodenum. 3H-labeled P-aminobenzoic acid, a precursor substrate for bacterial folate synthesis, was perfused. Downstream intestinal aspirates and a 48-hour urine collection were obtained. RESULTS: Atrophic gastritis and omeprazole administration were associated with increases in duodenal pH and in small intestinal flora. Bacterially synthesized folates were isolated from the intestinal aspirates. Tritiated 5-methyltetrahydrofolate, a major metabolite of folate, was isolated from the urine of omeprazole-treated subjects in greater quantities than from drug-free subjects (P<0.01); the quantity of tritiated 5-methyltetrahydrofolate in the urine of the subjects with atrophic gastritis was similarly elevated. CONCLUSIONS: (1) Mild bacterial overgrowth caused by atrophic gastritis and administration of omeprazole are associated with de novo folate synthesis in the lumen of the small intestine; (2) the human host absorbs and uses some of these folates; and (3) the contribution to folate nutriture from this source remains unclear.

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PubMed2000

Do we eat less fat, or just report so?

OBJECTIVE: To examine secular trends in diet reporting error. METHODS: Dietary information was obtained from 228 Danish men and women in 1987-88, and from 122 men and women in 1993-94. RESULTS: Bias in dietary reporting of energy and protein intake was assessed by comparing reported intake with intake data, estimated from 24 h nitrogen output, validated by administering P-aminobenzoic acid, and estimated 24 h energy expenditure. Total energy was under-reported more than energy from protein at both surveys, suggesting that energy from other nutrients, like fat and/or carbohydrate, must have been under-reported too. There was a greater under-reporting for energy than for protein in 1993-94 (29%) than in 1987-88 (15%). Obesity was positively associated with under-reporting, both in 1987-88 and in 1993-94. CONCLUSION: The higher macro-nutrient specific error in 1993-94 compared to 1987-88 may reflect a trend to increasingly omitting fat and/or carbohydrate-rich foods in dietary reporting. This may be a consequence of increased awareness of diet intake, which, in turn, may be related to intensified public health campaigns to reduce intake of fat and/or simple carbohydrate. These results may have consequences for our understanding of the apparent decline in dietary fat and associated health benefits.

4-Aminobenzoic Acid↗
PubMedDate not supplied

[Time course of interferon status of patients with herpetic keratitis during treatment with actipol, a new inteferon inducer].

Interferon (IFN) status was evaluated in 20 patients with various forms of herpetic keratitis over the course of treatment with actipol (0.07% para-aminobenzoic acid). Actipol was injected subconjunctivally parabulbarly in combination with instillations into the conjunctival sac or only instilled, depending on the disease severity. The following parameters were evaluated: 1) total content of various IFN types in circulating blood and 2) leukocyte capacity to produce IFN in vitro in patient's whole blood cells. IFN-alpha was induced with Newcastle disease virus and IFN-beta with staphylococcal enterotoxin. Before treatment IFN-producing capacity of blood cells in vitro was decreased in 60% patients and was normal or increased in 40%. Plasma concentrations of IFN were moderately increased in 45% patients. All IFN parameters in patients with initially disordered IFN status normalized during actipol therapy and after clinical cure and did not change in the patients with initially normal IFN values. Hence, local actipol therapy in patients with various forms of ophthalmic herpes modifies IFN status.

4-Aminobenzoic Acid↗
PubMed1990

High capacity of human skin for N-acetylation of arylamines.

Human skin showed high activity of cytosolic N-acetylation for two typical arylamine substrates, p-aminobenzoic acid (PABA) and 2-aminofluorene (AF). Their specific activities (per milligram protein basis) were comparable with those of hamster skin, which is known to have high acetylating capacities for several arylamines. In hamster skin, two other types of acetylation, N-hydroxy-4-acetylaminobiphenyl-dependent N-acetylation of AF (N,N'-acetyltransfer) and acetyl CoA-dependent O-acetylation of 2-hydroxyamino-6-methyl-pyrido[1,2-a:3',2'-d]imidazole (O-acetylation) also occurred, but no appreciable activity was observed in human skin for these two reactions. These results suggest that arylamines including prohaptens and carcinogens may be modified metabolically through N-acetylation at the first contact site, human skin. In addition, a good correlation was observed for N-acetylations of PABA and AF in human skin, implying that these N-acetylations may be catalyzed by the same or a closely related enzyme in human skin.

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PubMed1998

Oral absorption tests: absorption site of each substrate.

Three oral absorption tests have been used in patients with short bowel syndrome (SBS) to evaluate the absorption site of each substrate. In this study, three absorption tests were applied: the oral pancreatic function test using N-benzoyl-L-tyrosyl-p-aminobenzoic acid (NBT-PABA), the D-xylose tolerance test, and the oral fat tolerance test. Examinations were performed in eight patients with either a duodenostomy or a jejunostomy located less than 60 cm from the ligament of Treitz, and in a patient with an end ileostomy. Forty-six healthy volunteers participated as controls for the oral fat tolerance test. PABA and D-xylose concentrations were measured in urine. The serum triacylglycerol concentration was determined at 0, 1, 2, and 3 h after ingestion. All eight patients with SBS demonstrated pathologic absorption on each test. We conclude that small bowel integrity is critical for evaluation of the NBT-PABA test. We also determined that the duodenum and proximal jejunum do not play an important role in the absorption of D-xylose and triacylglycerol. We could also evaluate limitations and advantages of the other kinds of oral absorption tests and nutrients through patients with SBS.

4-Aminobenzoic Acid↗
PubMed1997

Cytosolic arylamine N-acetyltransferase (NAT) deficiency in the dog and other canids due to an absence of NAT genes.

The purpose of this study was to determine the molecular basis in the dog for an unusual and absolute deficiency in the activity of cytosolic N-acetyltransferase (NAT), an enzyme important for the metabolism of arylamine and hydrazine compounds. NAT activity towards two NAT substrates, p-aminobenzoic acid and sulfamethazine, was undetectable in dog liver cytosol, despite substrate concentrations ranging from 10 microM to 4 mM and a wide range of incubation times. Similarly, no protein immunoreactive to NAT antibody was evident on western blot analysis of canine liver cytosol. Southern blot analysis of genomic DNA from a total of twenty-five purebred and mixed bred dogs, and eight wild canids, probed with a full-length human NAT2 cDNA, suggested an absence of NAT sequences in all canids. Polymerase chain reaction amplification of genomic DNA using degenerate primers designed to mammalian NAT1 and NAT2 consensus sequences generated products of the expected size in human, mouse, rabbit, and cat DNA, but no NAT products in any dog or wild canids. These results support the conclusion that cytosolic NAT deficiency in the domestic dog is due to a complete absence of NAT genes, and that this defect is shared by other canids.

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PubMed1984

Exocrine pancreatic function in diabetic children.

Exocrine pancreatic function was evaluated in 19 diabetic children on the basis of a pancreozymin-secretin test, a p-aminobenzoic acid (PABA) test, and a determination of fasting plasma trypsin and elastase-1 levels. In the pancreozymin-secretin test, the diabetics exhibited lower mean values in all the parameters measured, significant differences being seen in the volume of duodenal fluid and the output of bicarbonate and amylase. Compared to the controls, the diabetics also had lower levels in the PABA test and in the trypsin and elastase-1 measurements. No significant correlation was seen between exocrine pancreatic dysfunction and the duration of diabetes. However, the duration of diabetes in children who showed extremely low levels (below the mean +/- 2 SD for the control subjects) in the PABA test and low plasma trypsin and elastase-1 values was more than 1 year. This study revealed that diabetic children had reduced exocrine pancreatic function, some in an early stage of the disease. Therefore, the reduction may be due to a functional disturbance rather than to an anatomical loss of exocrine pancreatic tissue.

4-Aminobenzoic Acid↗
PubMed1990

The effect of short-term application of PABA on photocarcinogenesis.

Photocarcinogenesis was induced in 90 lightly-pigmented hairless mice using a Philips Tl 40 W/12 light source which emits mainly UVB (290-320 nm). During one-third of the induction period (weeks 16-26) a group of 30 mice were protected by topical para-aminobenzoic acid (PABA) and then irradiated again without protection up to week 30 and observed for a further 10 weeks. The application of PABA resulted in a significant delay (p less than 0.05) in tumour induction and discontinuation of PABA caused an abrupt decline in the number of tumour-free animals. At the end of the study there was a significant difference in the yield of carcinomas for the PABA group, 20, compared with 78 for non-protected mice (p less than 0.05). There was also a statistically significant difference (p less than 0.05) between the weight of dorsal skin in non-protected mice compared with the PABA-protected group, the latter showing no difference from a control group of non-irradiated mice. The proportion of benign tumours in the PABA group was significantly (p less than 0.05) higher than in the non-protected group, suggesting an inhibition of the photo-carcinogenic process.

4-Aminobenzoic Acid↗
PubMed1977

Bioproduction of rubratoxin in a glucose-mineral salts broth with nutritional supplements and metabolic inhibitors.

A sterile glucose-salts broth fortified with various metabolic inhibitors and nutritional supplements was inoculated with conidia of Penicillium rubrum P3290, and incubated quiescently at 28 degrees C for 14 days. Potassium sulfite and sodium metabisulfite at all test concentrations caused moderate reduction in rubratoxin formation; at high concentrations (greater than or equal to 2.7 X 10(-2)M) accumulation of fungal tissue was also retarded. Production of rubratoxin and cell mass was inhibited by p-aminobenzoic acid; syntheses of toxin were completely blocked by 7.5 X 10(-2)M of the vitamin. Effects of sodium fluoride on P. rubrum cultures grown on inorganic nitrogen sources varied from inhibition of mold growth and (or) rubratoxin A production to reduction in formation of rubratoxin B. With organic nitrogen sources, fluoride caused a 30 and 60% reduction in synthesis of rubratoxins A and B, respectively. Sodium acetate at all test concentrations enhanced formation of rubratoxin; mold growth was enhanced when acetate concentration was larger than or equal to 6.0 X 10(-2)M. A moderate reduction in mold growth was caused by lower acetate concentrations (1.2 X 10(-2)M or 2.4 X 10(-2)M). Sodium arsenite and iodoacetate at test concentrations blocked mold growth and toxin formation; sodium azide and 2,4-dinitrophenol caused a marked reduction in mold growth but inhibited toxin formation completely. However, sodium azide permitted slight growth and toxin formation when mold cultures were incubated for 28 days.

4-Aminobenzoic Acid↗
PubMed2001

Kinetics of acetyl coenzyme A: arylamine N-acetyltransferase from human cumulus cells.

PURPOSE: N-acetyltransferase (NAT) activity is involved in the detoxification of exogenous amines. We aimed to evaluate the kinetics of acetyl coenzyme A (AcCoA): arylamine NAT for human cumulus cells. METHODS: Thirty infertile women who were undergoing controlled ovarian hyperstimulation (COH) and oocyte retrievals were recruited. Human cumulus cells were obtained during oocyte retrievals. Using 2-aminofluorene (2-AF) and p-aminobenzoic acid (PABA) as substrates, NAT activity and Michaelis-Menten kinetics constants of all samples were determined by using high-pressure liquid chromatography. RESULTS: There were 6 rapid, 10 intermediate, and 14 slow acetylators. 2-AF-NAT and PABA-NAT activities were 0.97 +/- 0.74 and 0.89 +/- 0.77 nmol/min/mg protein, respectively. Km/Vmax of rapid and slow acetylators for 2-AF were (161 +/- 55)/(15.6 +/- 2.9) and (27.8 +/- 11.4)/(2.6 +/- 0.9), respectively. Km/Vmax of rapid and slow acetylators for PABA were (104 +/- 36)/(13.2 +/- 2.8) versus (20.0 +/- 10)/(2.0 +/- 0.7), respectively. Compared to slow acetylators, the rapid acetylators exhibited higher Km/Vmax values for 2-AF (5.8-/6-fold) and PABA (6-/6.6-fold), respectively. CONCLUSION: Human cumulus could acetylate arylamine carcinogen (2-AF) and noncarcinogen drug (PABA). Higher percentage of rapid acetylators established in the cumulus during COH. It provides a model for monitoring the effects of pollution or carcinogenesis upon the oocyte during COH and oocyte retrievals.

4-Aminobenzoic Acid↗
PubMed1989

Exocrine pancreatic function in Sjögren's syndrome.

Pancreatic function testing was carried out in 19 patients with Sjögren's syndrome (SS) (nine primary type, ten secondary) by the N-benzoyl-tyrosil-p-aminobenzoic acid (PABA) test, serum immunoreactive trypsin (IRT) levels, and stool fat measurements to evaluate the incidence and type of exocrine pancreatic alterations in this disease. Exocrine pancreatic impairment was found to be present in 63% of the patients. Three types of secretory patterns were observed: (1) normal PABA test results and normal IRT levels (37% [7/19] of the patients); (2) normal PABA test results and elevated IRT levels (42% [8/19]; and (3) low PABA test results and elevated IRT levels (21% [4/19]), including two patients with steatorrhea. Functional pancreatic impairment tended to be more severe in patients with longer disease duration and it was related to the degree of alteration of salivary flow but not to labial salivary gland histologic changes or the type of SS. Inasmuch as hypertrypsinemia was the common marker of pancreatic dysfunction in all patients, we suggest a periodic measurement of serum IRT levels in the follow-up of patients with SS to detect early stages of pancreatic involvement.

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PubMedDate not supplied

[The new interferon inducer Aktipol in the treatment of herpetic keratitis].

Previous experiments demonstrated the efficiency of 0.007% para-aminobenzoic acid (PABA) in the treatment of dendriform herpetic keratitis in rabbits and showed the interferonogenic activity of local administration of PABA in this concentration in ocular tissues. A new drug Aktipol based on 0.007% PABA was developed for the treatment of viral diseases of the eyes. The drug was used in the treatment of patients with surface herpetic keratitis. It was instilled into the conjunctival sac (2 drops 8-10 times a day) or instillations were combined with subconjunctival, parabulbar injections 1-3 times a week, depending on the disease severity and course. Clinical studies demonstrated that Aktipol is effective in the treatment of surface forms of herpetic keratitis (118 patients). Cure was attained in 89.8% patients in 11.3 +/- 0.6 days. Aktipol is superior to IDU (cure in 70.6% patients) and is comparable to that of acyclovir (87.7%). Aktipol accelerates ulcer healing, resorption of infiltration, and cure by 4-5 days in comparison with IDU and is comparable to acyclovir. Aktipol is better tolerated than antiviral IDU agents and acyclovir ointment.

4-Aminobenzoic Acid↗
PubMed1985

Monocyclic pteridine analogues. Inhibition of Escherichia coli dihydropteroate synthase by 6-amino-5-nitrosoisocytosines.

A variety of 5,6-disubstituted isocytosine derivatives were evaluated in vitro as inhibitors of dihydropteroate synthase from Escherichia coli. A number of 6-(alkylamino)-5-nitrosoisocytosines have in vitro potency equivalent with or superior to that of therapeutically effective sulfonamide inhibitors of the synthase. The sulfonamide drugs are known to compete for the p-aminobenzoic acid binding site of the synthase, and kinetic analysis of inhibition of the synthase by 6-(methylamino)-5-nitrosoisocytosine (16; I50 = 1.6 microM) and by the 6-(3-phenoxypropyl) amino analogue (33; I50 = 3.7 microM) indicated that the nitrosoisocytosine inhibitors compete with the pteridine substrate for the enzyme. Structure-activity studies demonstrated that the enzyme surface has a low tolerance for steric bulk in the region surrounding the isocytosine 6-amino function. However, this steric intolerance may be counterbalanced to a significant degree by positive allosteric interactions achieved by certain analogues that have a 6-(omega-phenylalkyl)amino substituent. For example, 6-[(7-phenylheptyl)amino]-5-nitrosoisocytosine (28) is as effective an inhibitor (I50 = 1.4 microM) as the 6-methylamino compound 16. Although several members of the 5-nitroso series were potent synthase inhibitors, none of the nitrosoisocytosines exhibited significant antibacterial activity. This observation may reflect poor transport of these compounds through the bacterial cell wall or, alternatively, may result from a rapid metabolic inactivation process.

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PubMedDate not supplied

Kinetics of acetyl CoA: arylamine N-acetyltransferase from rapid and slow acetylator human liver.

Michaelis-Menten kinetic constants for sulfamethazine (SMZ) and p-aminobenzoic acid (PABA) metabolism were determined in 2 very rapid, 8 intermediate, and 10 slow acetylator human livers. The mean apparent KM values for the monomorphic substrate PABA were 70 +/- 20, 180 +/- 50, and 310 +/- 30 microM for the slow, intermediate, and very rapid enzymes, respectively, whereas the polymorphic substrate SMZ exhibited little interphenotypic KM variation. Compared to the slow enzymes, the rapid acetylators exhibited mean apparent Vmax values 15- and 20-fold greater for PABA and SMZ, respectively. Furthermore, under in vitro conditions where enzyme saturation was achieved, PABA showed polymorphic acetylation characteristics, in contrast to events in vivo, where monomorphic acetylation patterns were observed. As the acetyl coenzyme A concentration in the reaction mixture was increased, the KM and Vmax for PABA increased, in accordance with "ping-pong" kinetic principles. As occurs with polymorphic substrates, a binary ping-pong mechanism appears to govern N-acetylation of monomorphic substrates in human liver, as evidenced by initial velocity patterns and limiting values for the KM and Vmax for PABA.

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PubMed1982

[Value of various therapeutic procedures in penile induration].

Etiology, pathogenesis and optimal therapy of Peyronie's disease are, 240 years after its first description, still unclear. Diagnosis includes palpation, measurement and exact drawing of the mostly dorsally and laterally located penile induration, photography of erectile deviation, cavernosography and ultrasound as follow-up controls. Pathogenesis of fibrotic stimulation is related to direct local causes such as vascular lesions, microtrauma and hemorrhage and to indirect induction of plasma exudation via autoimmune mechanisms by toxins, infections and vasoactive substances. Symptomatology in 116 of our own patients included the obligatory penile scar, erectile deviation in 75%, pain during erection in 33% and difficult or impossible intercourse in 40%. Radiotherapy in 113 patients led to healing or marked improvement in 44% of cases. In 41% the disease came to a standstill and in 15% of cases symptoms became worse. An analysis of the world literature shows surprisingly a 75% improvement by vitamin E therapy and almost a 60% amelioration by p-aminobenzoic acid and corticoid injections. Favorable results of radiotherapy vary in the literature between 50 and 70%. Reports on these successful treatments include unclear and optimistic criteria in small series and the possible spontaneous standstill or regression of the disease. Indications of operation are erectile pain, impossible invagination and a high degree of penile deviation. Surgical techniques are: (1) Excision of smaller fibrotic segments followed by longitudinal suture of the corpora cavernosa; (2) symmetric and cylindrical resection of both cavernous bodies followed by a watertight reanastomosis after mobilization of the corpus spongiosum; (3) after excision of larger plaques the defect may be covered by autologous material (danger: scar formation, aneurysmatic protrusion, impotence), and (4) hydraulic or semirigid penile prostheses are an ultima ratio. Since there was a 85% improvement or standstill of the disease and little side reactions in 113 of our patients following radiotherapy we recommend it particularly in the early inflammatory phase. An operation might be indicated for patients who do not benefit from this treatment and who show above-mentioned symptoms.

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PubMedDate not supplied

Identification and kinetic characterization of acetylator genotype-dependent and -independent arylamine carcinogen N-acetyltransferases in hamster bladder cytosol.

Recent studies from our laboratory have shown relatively high levels of polymorphic N-acetyltransferase (NAT)(EC 2.3.1.5) activity toward carcinogenic arylamines in urinary bladder cytosol of humans and in the inbred hamster model of the N-acetylation polymorphism. The expression of this polymorphism is of interest because of the higher incidence of bladder cancer among human slow acetylators with documented exposures to arylamine bladder carcinogens. In this study, arylamine NAT activity was partially purified and characterized in inbred hamster urinary bladder cytosols of defined acetylator genotype. Acetylator gene-dose response relationships were observed for the N-acetylation of p-aminobenzoic acid, p-aminosalicyclic acid, and the arylamine carcinogens 2-aminofluorene, 4-aminobiphenyl, and beta-naphthylamine in hamster bladder cytosol. Partial purification of hamster bladder cytosol by anion-exchange fast protein liquid chromatography yielded two NAT isozymes that catalyzed the N-acetylation of each of the arylamine substrates. The catalytic activity of the first isozyme was acetylator genotype-dependent (polymorphic), whereas the second isozyme appeared to be acetylator genotype-independent (monomorphic). Catalytic activities between homozygous rapid, heterozygous, and homozygous slow acetylator genotypes were compared with respect to both initial rates and apparent maximum velocities. Comparison of homozygous rapid and slow acetylator bladder cytosol showed that the apparent Vmax for 2-aminofluorene NAT activity was significantly higher in rapid than slow acetylators (6-fold in cytosol, 50-fold in the polymorphic NAT isozyme). These results suggest a key role for a polymorphic NAT isozyme, regulated by the acetylator genotype and expressed in urinary bladder cytosol, in the initiation of bladder cancer via arylamine carcinogens.

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