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PubMed1982

Characterization of rat cecum cellulolytic bacteria.

Cellulose-degrading bacteria previously isolated from the ceca of rats have been characterized and identified. The most commonly isolated type was rods identified as Bacteroides succinogenes. These bacteria fermented only cellulose (e.g., pebble-milled Whatman no. 1 filter paper), cellobiose, and in 43 of 47 strains, glucose, with succinic and acetic acids as the major products. The only organic growth factors found to be required by selected strains were p-aminobenzoic acid, cyanocobalamine, thiamine, and a straight-chain and a branched-chain volatile fatty acid. These vitamin requirements differ from those of rumen strains of B. succinogenes, indicating the rat strains may form a distinct subgroup within the species. The mole percent guanine plus cytosine was 45%, a value lower than those (48 to 51%) found for three rumen strains of B. succinogenes included in this study. Cellulolytic cocci were isolated less frequently than the rods and were identified as Rumminococcus flavefaciens. Most strains fermented only cellulose and cellobiose, and their major fermentation products were also succinic and acetic acids. Their required growth factors were not identified but were supplied by rumen fluid.

Animals↗
PubMedDate not supplied

Enhanced cytogenetic and antineoplastic effects by the combined action of two esteric steroidal derivatives of nitrogen mustards.

The authors studied the effect of two modified steroids containing different proportions (%) of alkylating agents alone or in combination on sister chromatid exchange (SCE) rates and on human lymphocyte proliferation kinetics. The antitumor activity of these compounds was tested on leukemia P388- and leukemia L1210-bearing mice. The two chemicals in mixtures enhance SCE induction and antitumor activity in a synergistic manner. The homo-aza-steroidal ester of p-bis(2-chloroethyl)aminophenyl acetic acid was found to be more effective than the homo-aza-steroidal ester of o-bis(2-chloroethyl)aminobenzoic acid in causing cytogenetic damage and antineoplastic activity. A correlation was observed between the magnitude of the SCE response and the depression of the cell proliferation index. The order of the antitumor effectiveness of the five different treatments tested coincided with the order of the cytogenetic effects they induced.

Animals↗
PubMedDate not supplied

Main metabolites of 1-(2-chloroethyl)-3-[1'-(5'-p-nitrobenzoyl-2',3'-isopropylidene)-alpha, beta-D-ribofuranosyl]-1-nitrosourea and 1-(2-chloroethyl)-3-(2',3', 4'-tri-O-acetyl-alpha, beta-D-ribopyranosyl)-1-nitrosourea in rats.

The metabolism of two glycosylnitrosoureas, 1-(2-chloroethyl)-3-[1'-(5'-p-nitrobenzoyl-2',3'-isopropylidene)-alpha, beta-D-ribofuranosyl]-1-nitrosourea (RFCNU) and 1-(2-chloroethyl)-3-(2',3',4'-tri-O-acetyl-alpha, beta-D-ribopyranosyl)-1-nitrosourea (RPCNU), has been investigated in the rat. With the label on the carboxyl moiety of RFCNU, we have shown that hydrolysis of the 4-nitrobenzoyl ester occurred to a large extent in vivo; 4-nitrobenzoic acid and its glucuronide were the major urinary metabolites. Two other minor metabolites and their glucuronides were identified as 4-aminobenzoic acid and 4-acetamidobenzoic acid. With the label on the chloroethyl moieties of RFCNU and RPCNU, we have shown that chloroethanol was a major degradation product of this alkylating part of the molecule. The concentration of chloroethanol in plasma vs. time has been determined. In urine, four metabolites derived from alkylated glutathione, namely thiodiacetic acid and its sulfoxide, N-acetylcarboxymethylcysteine, and N-acetylhydroxyethylcysteine, have been identified.

Animals↗
PubMed1971

Inhibition of Pseudomonas aeruginosa by hyperbaric oxygen. I. Sulfonamide activity enhancement and reversal.

To elucidate an explanation for in vitro sulfonamide enhancement by high-pressure oxygen (HPO) and the reported absence of enhancement with in vivo therapy, Pseudomonas aeruginosa cultures were exposed to selected antifolate antimicrobials in the presence of 1.87 atm absolute of O(2) and compared with non-HPO treated controls. Under these conditions, HPO alone retarded growth. Trimethoprim, a non-sulfonamide which inhibits dihydrofolate reductase, was not bactericidal, nor did HPO enhance existent bacteriostatic activity. The sulfonamide, sulfisozazole, was not bactericidal, but HPO enhanced bacteriostatic activity twofold; bacteriostasis was mitigated in HPO-treated and control cultures by p-aminobenzoate but not by a mixture of compounds involved in folate-mediated "1-C" biosynthesis. Mafenide, a unique sulfonamide, at high concentrations with HPO, was synergistically bactericidal; non-HPO-treated cultures were bacteriostatically inhibited. Bacteriostatic activity of lower mafenide concentrations was also enhanced at least twofold by HPO. These inhibitory effects of mafenide, acting with or without HPO, were mitigated by the above mixture, but not by p-aminobenzoate. This may explain the lack of in vivo HPO-mafenide enhancement in burn-wound sepsis where exudates would contain such a mixture. Lastly, HPO itself was largely bactericidal at 2.87 atm absolute of O(2). This was reversed to various degrees by the above mixture, or its components, or by folic, folinic, or p-aminobenzoic acids. These in vitro interactions suggest HPO per se may act at the same site as some sulfonamides to inhibit folate synthesis (not primarily at the dihydrofolate reductase level), or coenzyme functions of folate, or both.

Aminobenzoates↗
PubMed2000

Purification and characterization of sea squirt alpha-N-acetylgalactosaminidase.

Sea squirt alpha-N-acetylgalactosaminidase was purified to homogeneity. Its molecular weight was estimated to be approximately 160,000 by gel filtration and 40,000 by SDS-polyacrylamide gel electrophoresis (SDS-PAGE) under reducing condition. The chromatographic and electrophoretic behaviors indicated that the enzyme was composed of four subunits. The optimum pH of the enzyme reaction was about 4.0 at 37 degrees C, while the enzyme was stable in the range of pH 5.0 to 6.0 during 4 h preincubation at 37 degrees C. Although the enzyme (0.1 unit) was stable at 0 degrees C for 30 min in the presence of 7.5 mM metal ions (Al3+, Ba2+, Ca2+, K+, Mn2+, Pb2+, Sr2+, and Zn2+), almost 40% of the enzyme activity was lost in the presence of Cu2+, Hg2+, monoiodoacetic acid, and EDTA. The enzyme hydrolyzed aryl N-acetyl-alpha-D-galactosaminide as well as GalNAcalpha1(-->4GalNAcalpha1-->)n 4GalNAc-p-aminobenzoic acid ethyl ester (ABEE) (n = 1-4), but GalNAcalpha1-->4GalNAc-ABEE only scarcely. Furthermore, an allergenic pentasaccharitol ABEE derivative, GalNAcalpha1-->2Fucalpha1-->3(GalNAcbeta1-->4) GlcNAcbeta1-->2(3-acetoamido-3-deoxy)L-threose-ABEE, the minimum structural unit for the sea squirt allergenicity was hydrolyzed to 95 mol% for 72 h incubation with the enzyme. The enzyme could be utilized as a powerful tool for the structural analyses of the carbohydrate epitopes of the sea squirt allergen molecules.

Journal Article↗
PubMed1992

Folylpolyglutamate analogs can inhibit casein kinase II from Xenopus laevis.

Polyglutamate analogs of folate and related compounds were tested as inhibitors of casein kinase II (CK II) obtained from Xenopus laevis. The inhibitory capacity of the pteroyl, 4-amino-10-methyl pteroyl (the methotrexate aromatic moiety), and p-aminobenzoil derivatives increased as the number of gamma-glutamates attached went from 2 to 7. The nature of the aromatic head, group was also important since hexa-gamma-glutamatic acid had no inhibitory activity while the folylhexaglutamate derivatives were strong inhibitors with relative potency of methotrexate greater than pteroyl greater than p-aminobenzoic acid. The inhibition of CK II by methotrexate gamma-pentaglutamate was competitive with casein and showed an apparent K(i) of 90 microM.

Animals↗
PubMed1987

High-performance liquid chromatographic assay for thyrotropin releasing hormone and benzyl alcohol in injectable formulation.

A stability-indicating, high-performance liquid chromatographic method is presented for the determination of thyrotropin releasing hormone (TRH) and benzyl alcohol in a multidose injectable formulation. Separation is achieved on a microparticulate octadecylsilica column, with pH 2.2 ion-pair reagent (octanesulfonic acid, sodium salt) solution/methanol/acetonitrile/triethylamine (92:4:4:0.01), at a flow rate of 1.5 ml/min and a detection wavelength of 215 nm. p-Aminobenzoic acid is used as an internal standard. The relative standard deviations of the method are +/- 0.6% for TRH and +/- 0.7% for benzyl alcohol. Recoveries from standard additions to placebos ranged from 99.0 to 101.3 and 99.7 to 101.8% for TRH and benzyl alcohol, respectively.

Benzyl Alcohols↗
PubMed1970

Detoxications in peripatus. Sulphate, phosphate and histidine conjugations.

Phenols were detoxified in the Onycophoran Peripatoides novaezealandiae by conjugation with sulphuric acid and phosphoric acid, but no evidence for a glycoside detoxication could be found. [(14)C]Benzoic acid was metabolized in 24h to N(2)-benzoyl-l-histidine, which was identified by electrophoresis, chromatography and dilution analysis. Similar conjugates were formed with p-aminobenzoic acid and p-nitrobenzoic acid. In longer-duration experiments further unidentified metabolites were formed, two of which appeared to result from the further metabolism of the histidine conjugate.

Aminobenzoates↗
PubMed1995

Cerulein-induced changes in plasma amino acid concentrations are not a valid test for pancreatic insufficiency.

OBJECTIVES: There is controversy about the cholecystokinin (CCK)-induced decrease of plasma amino acids for the diagnosis of pancreatic insufficiency in that it is unclear whether the conflicting results are due to different degrees of stimulation by CCK. We have therefore evaluated the amino acid consumption test by examining the dose-response relation among increasing doses of cerulein and plasma amino acids compared with the release of pancreatic polypeptide in six healthy volunteers and six patients with severe pancreatic insufficiency proven by a pathological para-aminobenzoic acid test. METHODS: Stepwise increasing doses of cerulein (10-80 pmol/kg/h) were given i.v., each for 60 min with a secretin background (1 CU/kg/h). In the volunteer group, an additional experiment with infusion of placebo (saline 0.9%) was performed. RESULTS: CCK-induced amino acid changes were small in volunteers (maximum decrease: 8.4 +/- 0.9%; mean +/- SEM), tended to be more pronounced in patients (maximum decrease: 13.8 +/- 2.8%; NS), and did not permit a distinction among volunteers and patients. There was no dose-response relationship between CCK and plasma amino acids in either group. In contrast, pancreatic polypeptide levels increased markedly and dose-dependently in volunteers and patients and tended to be lower in patients with pancreatic insufficiency. CONCLUSIONS: The decrease of plasma amino acid levels in response to cerulein does not reflect pancreatic function and does not permit the diagnosis of pancreatic insufficiency.

Adult↗
PubMed1966

Microbial growth on C1 compounds. The role of folat in the metabolism of Pseudomonas AM1.

1. The growth of Pseudomonas AM1 is much more sensitive to inhibition by sulphanilamide when methanol, rather than succinate, acts as the sole carbon and energy source; a sulphanilamide concentration of 1mm, which causes almost complete inhibition of growth on methanol, has little effect in a succinate medium. 2. Similar results have been obtained with sulphadiazine and sulphathiazole. Sulphanilic acid has little effect. 3. A similar differential sensitivity to sulphanilamide is shown by Protaminobacter ruber and Pseudomonas extorquens when grown on methanol media as compared with succinate. 4. Sulphanilamide inhibited the growth of Pseudomonas oxalaticus on formate, oxalate and succinate media to about the same extent. 5. Inhibition of growth of Pseudomonas AM1 by sulphanilamide is accompanied by an accumulation of glycine in the cells. 6. Inhibition of growth by sulphanilamide can be reversed by p-aminobenzoic acid. 7. Microbiological assays of the folate content of Pseudomonas AM1 have been performed after growth on both methanol and succinate, and the results are discussed in terms of differences in metabolism.

Aminobenzoates↗
PubMed1989

Hardness of restorative resins: effect of camphorquinone, amine, and inhibitor.

The influence of the content of camphorquinone (CQ), amine (DABE), and inhibitor (MHQ) on the Wallace indentation hardness of light-curing polymers was investigated. The hardness was measured on disc-shaped specimens made from 50 bisphenol-A-glycidyl-dimethacrylate/triethyleneglycol-dimethacryla te-based monomers with various contents of CQ, DABE, and MHQ. When no MHQ had been added, the hardness number decreased with increasing content of CQ. This was also the case with increasing content of DABE, but to a lesser extent. In the presence of MHQ, the contents of CQ and DABE did not influence the hardness number significantly.

4-Aminobenzoic Acid↗
PubMed2000

Determination of blood folate using acid extraction and internally standardized gas chromatography-mass spectrometry detection.

Whole blood folate level is a superior indicator of folate nutritional status than serum/plasma level. Problems with and lack of confidence in results of current whole blood folate assays have limited its popularity for assessing folate nutritional status. Here, an acid extraction GCMS detection method that measures total folate whole blood is presented. Folates are released from the matrix of whole blood and cleaved to para-aminobenzoic acid (pABA) by acid hydrolysis in the presence of [(13)C(6)]pABA as internal standard (IS). The hydrolysate is passed over a C18 resin to remove heme. The pABA isotopomers are ethyl esterified, isolated on C18 resin, and trifluoroacetylated. Following normal-phase HPLC separation, the isotopomers are silylated to their tBDMS derivatives. The abundance of these derivatives are measured at m/z 324 for [(13)C(6)]pABA as IS and m/z 318 for pABA from whole blood folate. Our method uses readily available chemicals and our results agree well with those using Lactobacillus casei, the current gold standard reference assay. The presence of folate analogs (methotrexate) or antibacterials (sulfonamines) does not affect our method. This feature makes it useful in monitoring folate status of patients undergoing chemotherapy. Before using our method, pABA supplements must be discontinued for a few days.

Acids↗
PubMed1999

Chromogenic and fluorogenic glycosylated and acetylglycosylated peptides as substrates for serine, thiol and aspartyl proteases.

We synthesized short chromogenic peptidyl-Arg-p-nitroanilides containing either (Galbeta)Ser or (Glcalpha,beta)Tyr at P2 or P3 sites as well as O-acetylated sugar moieties and studied their hydrolysis by bovine trypsin, papain, human tissue kallikrein and rat tonin. For comparison, the susceptibility to these enzymes of Acetyl-X-Arg-pNa and Acetyl-X-Phe-Arg-pNa series, in which X was Ala, Phe, Gln and Asn were examined. We also synthesized internally quenched fluorescent peptides with the amino acid sequence Phe8-His-Leu-Val-Ile-His-Asn14 of human angiotensinogen, in which [GlcNAcbeta]Asn was introduced before Phe8 and/or after His13 and ortho-aminobenzoic acid (Abz) and N-[2-, 4-dinitrophenyl]-ethylenediamine (EDDnp) were attached at N- and C-terminal ends as a donor/receptor fluorescent pair. These peptides were examined as substrates for human renin, human cathepsin D and porcine pepsin. The chromogenic substrates with hydrophilic sugar moiety increased their susceptibility to trypsin, tissue kallikrein and rat tonin. For papain, the effect of sugar depends on its position in the substrate, namely, at P3 it is unfavorable, in contrast to the P2 position that resulted in increasing affinity, as demonstrated by the higher inhibitory activity of Ac-(Gal3)Ser-Arg-pNa in comparison to Ac-Ser-Arg-pNa, and by the hydrolysis of Ac-(Glcalpha,beta)Tyr-Arg-pNa. On the other hand, the acetylation of sugar hydroxyl groups improved hydrolysis of the susceptible peptides to all enzymes, except tonin. The P'4 glycosylated peptide [Abz-F-H-L-V-I-H-(GIcNAcbeta)N-E-EDDnp], that corresponds to one of the natural glycosylation sites of angiotensinogen, was shown to be the only glycosylated substrate susceptible to human renin, and was hydrolysed with lower K(m) and higher k(cat) values than the same peptide without the sugar moiety. Human cathepsin D and porcine pepsin are more tolerant to substrate glycosylation, hydrolysing both the P'4 and P4 glycosylated substrates.

Angiotensinogen↗
PubMed2000

Additive effects of a two-amino-acid insertion and a single-amino-acid substitution in dihydropteroate synthase for the development of sulphonamide-resistant Neisseria meningitidis.

Sulphonamide resistance in some clinical isolates of Neisseria meningitidis is associated with an insertion in the chromosomal folP gene leading to the addition of two amino acids, serine and glycine, in the drug target enzyme dihydropteroate synthase (DHPS). Removal of the insertion resulted in a markedly higher Km for the substrate p-aminobenzoic acid and a markedly lower Km for 2-amino-4-hydroxy-6-(hydroxymethyl)-7,8-dihydropteridine pyrophosphate. In the same isolates an additional important difference, compared to wild-type enzymes, was found at amino acid position 68, which is a proline in most DHPS enzymes, but is serine in one and leucine in another clinical isolate of sulphonamide-resistant N. meningitidis. The alteration at position 68 was found to affect mainly the level of sulphonamide resistance and had only a minor effect on the Km for the substrates. Introduction of the serine-glycine dipeptide at position 194 and a proline to serine substitution at position 68 in DHPS from normal, susceptible N. meningitidis failed to produce a functional sulphonamide-resistant enzyme. The conclusion of this study is that it is not possible to change a normal chromosomally encoded DHPS of N. meningitidis to a sulphonamide-resistant one simply by an insertion of serine and glycine as seen in clinical isolates. It is likely that the resistance gene found in clinical isolates has evolved in another bacterial species where a combination of other amino acid changes may have contributed to produce a functionally resistant enzyme. This new resistance gene may have then been introduced into N. meningitidis by natural transformation.

Amino Acid Substitution↗
PubMed1975

Mutant enrichment in the colonial alga, Eudorina elegans.

An enrichment procedure has been developed that results in at least a 200 X increase in mutation frequency in the colonial alga, Eudorina elegans. A period of nitrogen starvation followed by treatment with 8-azaguanine results in the death of wild-type cells and the maintenance of mutants. N'-nitro-N-nitro-soguanidine-induced acetate, p-aminobenzoic acid and reduced nitrogen requiring mutants have been isolated by this procedure.

Acetates↗
PubMed1979

Studies on the 2,4-diamino-6-substituted quinazolines. III. The capacity of sulfadiazine to enhance the activities of WR-158,122 and WR-159,412 against infections with various drug-susceptible and drug-resistant strains of Plasmodium falciparum and Plasmodium vivax in owl monkeys.

Previous studies showed: 1) that the activities of the 2,4-diamino-6-substituted quinazolines. WR-158,122 and WR-159,412, against Plasmodium falciparum and Plasmodium vivax infections in owl monkeys, were seriously impaired when infecting strains were pyrimethamine-resistant; and 2) that primary treatment failure with either agent led frequently to emergence of parasites resistant to these derivatives. Taking advantage of the potencies of WR-158,122 and WR-159,412 as dihydrofolic acid reductase inhibitors, the current studies were aimed at determining whether the above liabilities could be reduced to manageable levels or eliminated by concomitant administration of a rho-aminobenzoic acid inhibitor such as sulfadiazine. Application of these combinations prevented emergence of parasites resistant to WR-158,122 or WR-159,412, but did not abolish the differences in effectiveness of either compound against infections with pyrimethamine-susceptible and pyrimethamine-resistant strains; however, activities against infections with either susceptible or resistant strains were enhanced markedly. With WR-158,122, this enhancement ranged from greater than 7-fold to 75-fold; with WR-159,412, it ranged from greater than 5-fold to 13-fold. Maximal increases in activity were attained with a remarkedly small dose of sulfadiazine, 5.0 mg per kg of body weight daily. With this augmentation of activity, acceptably small doses of WR-158,122 regularly cured infections with even the most highly pyrimethamine-resistant strain.

Animals↗
PubMed1993

A mechanism of inhibition of short-wavelength ultraviolet light-induced deamination of pyrimidine bases by ascorbic acid.

The relation of ascorbic acid to the ultraviolet light-induced deamination of cytosine (to uracil) and 5-methylcytosine (to thymine) was examined using gas chromatography-mass spectrometry. There was an inverse relation between the uracil content measured in solutions of cytosine after exposure to short wavelength (254 nm) ultraviolet light and the ascorbic acid concentration of the solution indicating inhibition of deamination of cytosine by ascorbic acid. Ascorbic acid also inhibited ultraviolet light-induced deamination of 5-methylcytosine. The ascorbic acid was only partially consumed during the exposure suggesting that protection from deamination was not due entirely to the antioxidant properties of ascorbic acid. Mercaptoethanol did not prevent ultraviolet light-induced deamination of either cytosine or 5-methylcytosine. However, near identical protection from ultraviolet light-induced deamination was provided by 4-aminobenzoic acid and ascorbic acid at equivalent ultraviolet light absorbing concentrations. This observation suggests that ascorbic acid prevents short wavelength ultraviolet light-induced deamination through absorbance of ultraviolet light rather than through antioxidant mechanisms.

5-Methylcytosine↗