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At least 19 recordsLinked to original sources
PubMed1984

Expanded solubility parameter approach. II: p-Hydroxybenzoic acid and methyl p-hydroxybenzoate in individual solvents.

The recently introduced four-parameter extended Hansen approach was used to study the solubility of p-hydroxybenzoic acid and methyl p-hydroxybenzoate in 32 and 35 individual solvents, respectively. The results are compared with those for benzoic acid in 40 solvents. Seventeen of the thirty-two or 53% of the calculated solubilities of p-hydroxybenzoic acid were within the established solubility criterion (i.e., less than 30% error from the experimental value). Twenty-two of thirty-six or 61% of the calculated solubility values for methyl p-hydroxybenzoate met the solubility criterion. Experimental excess free energies of solution for p-hydroxybenzoic acid and methyl p-hydroxybenzoate were plotted against theoretical values using the expanded four-parameter solubility regression equations. From such results, adjustments may be made in the partial solubility parameters to bring the calculated solubilities in line with experimental results. Multiple regression analyses were used to estimate the total solubility parameter and the four partial solubility parameters of the two benzoic acid derivatives. Satisfactory results were obtained for methyl p-hydroxybenzoate, but poor agreement was found for p-hydroxybenzoic acid for the total parameter when compared with the Fedors group contribution method. Both the multiple regression and group contribution methods may yield inaccurate solubility parameters for relatively polar solid solutes. Factor analysis was used to test the adequacy of three- and four-parameter approaches in the evaluation of drug solubility. A principal factor method without iteration and orthogonal factor rotation were used to compare the two expanded solubility parameter approaches.(ABSTRACT TRUNCATED AT 250 WORDS)

Chemical Phenomena↗
PubMed1994

Cloning and sequencing show that 4-hydroxybenzoate hydroxylase (PobA) is required for uptake of 4-hydroxybenzoate in Rhizobium leguminosarum.

Mutants of Rhizobium leguminosarum bv. viciae MNF300 and R. leguminosarum bv. trifolii WU95 unable to accumulate 4-hydroxybenzoate lack 4-hydroxybenzoate hydroxylase. The capacity of these mutants to take up and grow on 4-hydroxybenzoate was restored by a 2.0 kb EcoRI-PstI DNA fragment. This contained only one ORF which had over 60% DNA sequence similarity with the structural gene for 4-hydroxybenzoate hydroxylase (pobA) from Pseudomonas spp. and Acinetobacter. Reported effects of metabolic inhibitors and substrate analogues on the apparent uptake of 4-hydroxybenzoate have now been shown to be due to their direct effect on 4-hydroxybenzoate hydroxylase. We propose that uptake of 4-hydroxybenzoate is via a metabolic 'drag' mechanism dependent on the activity of the pobA gene product.

4-Hydroxybenzoate-3-Monooxygenase↗
PubMed1994

Catabolism of 4-hydroxybenzoate in Candida parapsilosis proceeds through initial oxidative decarboxylation by a FAD-dependent 4-hydroxybenzoate 1-hydroxylase.

The first two steps in the catabolism of 4-hydroxybenzoate by the ascomycetous yeast Candida parapsilosis CBS604 were investigated. In contrast to the well-known bacterial pathways and to what was previously assumed, metabolism of 4-hydroxybenzoate in C. parapsilosis proceeds through initial oxidative decarboxylation to give 1,4-dihydroxybenzene. This reaction is catalyzed by a NAD(P)H and FAD-dependent 4-hydroxybenzoate 1-hydroxylase. Further metabolism of 1,4-dihydroxybenzene to the ring-fission substrate 1,2,4-trihydroxybenzene is catalyzed by a NADPH-specific FAD-dependent aromatic hydroxylase acting on phenolic compounds. 19F-NMR experiments with cell extracts and 2-fluoro-4-hydroxybenzoate as the model compound confirm this metabolic pathway and exclude the alternative pathway proceeding through initial 3-hydroxylation followed by oxidative decarboxylation in the second step.

4-Hydroxybenzoate-3-Monooxygenase↗
PubMed1984

Simultaneous determination of methyl, ethyl, propyl, and butyl 4-hydroxybenzoates and 4-hydroxybenzoic acid in liquid antacid formulations by gas chromatography.

An isothermal chromatographic (GC) method employing an SE-30 column and flame-ionization detection has been developed for the simultaneous assay of methyl, ethyl, propyl, and butyl 4-hydroxybenzoates and 4-hydroxybenzoic acid in liquid antacid formulations. The method, which uses a silica column chromatographic cleanup step prior to GC, is specific for the compounds with respect to possible degradation products, impurities, and excipients.

Antacids↗
PubMed1997

19F NMR study on the regiospecificity of hydroxylation of tetrafluoro-4-hydroxybenzoate by wild-type and Y385F p-hydroxybenzoate hydroxylase: evidence for a consecutive oxygenolytic dehalogenation mechanism.

The regiospecificity of hydroxylation of tetrafluoro-4-hydroxybenzoate (F4-POHB) by p-hydroxybenzoate hydroxylase (PHBH) and its active site mutant Y385F was investigated by 19F NMR. Evidence is provided that the hydroxylation of F4-POHB is not restricted to the C3 center of the aromatic ring but rather involves sequential oxygenation and dehalogenation steps. The catalytic efficiency of PHBH and Y385F with F4-POHB was optimal near pH 6.5. Below pH 7.0, substantial substrate inhibition occurred. Dianionic F4-POHB was a competent effector, highly stimulating upon binding the rate of flavin reduction by NADPH. Hydroxylation of F4-POHB involved the formation of quinone intermediates as primary products of oxygenolytic defluorination. Ascorbate competed favorably with NADPH for the nonenzymatic reduction of these reactive intermediates and prevented the accumulation of nonspecific oxidation products. 19F NMR showed that the initial aromatic product 2,5,6-trifluoro-3,4-dihydroxybenzoate (F3-DOHB) was further converted to 5,6-difluoro-2,3,4-trihydroxybenzoate (5,6-F2-TOHB). This reaction was most efficient with Y385F. F3-DOHB was not bound in a unique regiospecific orientation as also 2,6-difluoro-3,4, 5-trihydroxybenzoate (2,6-F2-TOHB) was formed. The oxygenolytic dehalogenation of F3-DOHB by PHBH and Y385F is consistent with the electrophilic aromatic substitution mechanism proposed for this class of flavoenzymes. Nucleophilic attack of the carbon centers of F3-DOHB onto the distal oxygen of the electrophilic flavin C(4a)-hydroperoxide occurs when the carbon center has a relatively high HOMO density and is relatively close to the distal oxygen of the flavin C(4a)-hydroperoxide.

4-Hydroxybenzoate-3-Monooxygenase↗
PubMedDate not supplied

Interaction of 3-hydroxybenzoate with 3-hydroxybenzoate-6-hydroxylase.

The gradual quenching of the emission fluorescence of 3-HBA in the visible region upon titration with 3-HBA-6-hydroxylase and distinct changes in the near-UV circular dichroic spectrum of the enzyme in the presence of substrate suggest the formation of a stable enzyme-substrate complex. The binding of aromatic substrate 3-hydroxybenzoate to 3-hydroxybenzoate-6-hydroxylase occurs without gross changes in the backbone structure of the enzyme. The binding strength of the ES complex is partially reduced upon chemical modification of arginine, histidine, or tryptophan residues of enzyme, probably implicating their concerted action in the binding of substrate to enzyme. Partial inactivation of enzyme and diminished stability of the ES complex in response to treatment with 1 M urea could be ascribed to localized effects of the denaturant.

Amino Acids↗
PubMed1992

The anaerobic degradation of 3-chloro-4-hydroxybenzoate in freshwater sediment proceeds via either chlorophenol or hydroxybenzoate to phenol and subsequently to benzoate.

To study the anaerobic degradation of the chimera 3-chloro-4-hydroxybenzoate (3-Cl,4-OHB), anaerobic freshwater sediment samples from the vicinity of Athens, Ga., were adapted for the transformation of 4-hydroxybenzoate (4-OHB), 3-chlorobenzoate (3-CB), 2-chlorophenol (2-CP), and 2,4-dichlorophenol (2,4-DCP). In nonadapted samples, both 4-OHB (product of aryl dechlorination) and 2-CP (product of aryl decarboxylation) were observed as intermediates in the transformation of 3-Cl,4-OHB to phenol. The accumulated phenol was subsequently transformed to benzoate, an intermediate in the conversion to methane and CO2. In 4-OHB-adapted samples (i.e., samples adapted for aryl decarboxylation), 2-CP was the first intermediate which was subsequently dechlorinated to phenol. In 3-CB-adapted samples (i.e., samples adapted for meta-chlorobenzoate dehalogenation), 3-Cl,4-OHB was stoichiometrically dechlorinated to 4-OHB. In 2-CP-adapted samples (i.e., samples adapted for ortho-chlorophenol dehalogenation), 4-OHB was the first major intermediate. Furthermore, 3-CB was not dechlorinated in 2-CP-adapted sediment samples, suggesting the possibility that different 3-Cl,4-OHB dechlorinating systems were induced in the 2-CP- and 3-CB-adapted sediments. Adaptation of sediment samples for dechlorination of 2,4-DCP did not lead to adaptation for dechlorination of 3-Cl,4-OHB. However, 3-Cl,4-OHB was dechlorinated to 4-OHB in our stable, sediment-free 2,4-DCP-dechlorinating enrichment, isolated previously from the same environment.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Biological↗
PubMed1997

A New and Concise Synthesis of 3-Hydroxybenzo[c]phenanthrene and 12-Hydroxybenzo[g]chrysene, Useful Intermediates for the Synthesis of Fjord-Region Diol Epoxides of Benzo[c]phenanthrene and Benzo[g]chrysene.

A new strategy which involves a palladium-catalyzed cross-coupling reaction has been developed for the rapid synthesis of 3-hydroxybenzo[c]phenanthrene (5) and 12-hydroxybenzo[g]chrysene (6). These phenolic compounds are the key intermediates for the synthesis of highly carcinogenic fjord-region diol epoxide metabolites 3 and 4 of benzo[c]phenanthrene (1) and benzo[g]chrysene (2). The cross-coupling reaction of 2-bromo-5-methoxybenzaldehyde (9) with naphthalene-1-boronic acid (7) and phenanthrene-9-boronic acid (8) produced 2-(1-naphthyl)-5-methoxybenzaldehyde (10) and 2-(9-phenanthryl)-5-methoxybenzaldehyde (11), respectively, in quantitative yields. After reaction of these aldehydes with trimethylsulfonium iodide under phase-transfer conditions or with the Wittig reagent obtained from (methoxymethyl)triphenylphosphonium bromide and phenyllithium to generate an oxiranyl or methoxyethene side chain, the acid-catalyzed cyclization with methanesulfonic acid (or boron trifluoride) produced 3-methoxybenzo[c]phenanthrene (16) and 12-methoxybenzo[g]chrysene (17) in 61-64% yields. Finally, demethylation of these methoxy derivatives 16 and 17 with boron tribromide resulted in the formation of the hydroxy analogues 5 and 6, respectively. The availability of this short and high-yielding regiospecific method for the synthesis of phenols 5 and 6 should allow the preparative-scale synthesis of the fjord-region diol epoxides 3 and 4. These diol epoxides are required as starting compounds for the synthesis of site-specifically modified oligonucleotides which are critically needed to elucidate the mechanism of carcinogenesis at the molecular level.

Journal Article↗
PubMed1979

Carcinogenicity of 2-hydroxybenzo(a)pyrene and 6-hydroxybenzo(a)pyrene in newborn mice.

Benzo(a)pyrene (BP), 2-hydroxybenzo(a)pyrene (2-HOBP), and 6-hydroxybenzo(a)pyrene (6-HOBP) were tested for tumorigenicity by i.p. injection into newborn mice. The mice were treated sequentially with 200, 400, and 800 nmol of compound on the first, eighth and fifteenth day of life, and the animals were killed at 24 weeks of age. Treatment with 2-HOBP caused about 4-fold more pulmonary tumors than BP, while 6-HOBP had little or no tumorigenic activity. Newborn mice treated with 2-HOBP, BP, and 6-HOBP had a 98, 81, and 11% incidence of pulmonary adenomas with an average of 24, 6.4, and 0.11 adenomas per mouse, respectively. In the control group, 7.5% of the animals had pulmonary adenomas with an average of 0.08 adenoma per mouse. When 25, 50, or 100 nmol of BP or 2-HOBP was applied to mouse skin once every 2 weeks for 60 weeks, both compounds had about the same carcinogenic activity. These results demonstrate the importance of evaluating the carcinogenic potential of chemicals in more than one tumor system. BP and 2-HOBP were tested for mutagenicity towards two strains of Salmonella typhimurium and towards Chinese hamster V79 cells in the presence of hepatic microsomes from rats pretreated with Aroclor 1254. The products formed during the metabolism of 2-HOBP or BP by liver microsomes had significant mutagenic activity.

Adenoma↗
PubMed2000

HbaR, a 4-hydroxybenzoate sensor and FNR-CRP superfamily member, regulates anaerobic 4-hydroxybenzoate degradation by Rhodopseudomonas palustris.

Under anaerobic conditions, structurally diverse aromatic compounds are catabolized by bacteria to form benzoyl-coenzyme A (benzoyl-CoA), the starting compound for a central reductive pathway for aromatic ring degradation. The structural genes required for the conversion of 4-hydroxybenzoate (4-HBA) to benzoyl-CoA by Rhodopseudomonas palustris have been identified. Here we describe a regulatory gene, hbaR, that is part of the 4-HBA degradation gene cluster. An hbaR mutant that was constructed was unable to grow anaerobically on 4-HBA. However, the mutant retained the ability to grow aerobically on 4-HBA by an oxygen-requiring pathway distinct from the anaerobic route of 4-HBA degradation. The effect of the HbaR protein on expression of hbaA encoding 4-HBA-CoA ligase, the first enzyme for 4-HBA degradation, was investigated by using hbaA::'lacZ transcriptional fusions. HbaR was required for a 20-fold induction of beta-galactosidase activity that was observed with a chromosomal hbaA::'lacZ fusion when cells grown anaerobically on succinate were switched to anaerobic growth on succinate and 4-HBA. HbaR also activated expression from a plasmid-borne hbaA-'lacZ fusion when it was expressed in aerobically grown Pseudomonas aeruginosa cells, indicating that the activity of this regulator is not sensitive to oxygen. The deduced amino acid sequence of HbaR indicates that it is a member of the FNR-CRP superfamily of regulatory proteins. It is most closely related to transcriptional activators that are involved in regulating nitrate reduction. Previously, it has been shown that R. palustris has an FNR homologue, called AadR, that is also required for 4-HBA degradation. Our evidence indicates that AadR activates expression of hbaR in response to anaerobiosis and that HbaR, in turn, activates expression of 4-HBA degradation in response to 4-HBA as an effector molecule.

Aerobiosis↗
PubMed1990

Influence of D-galactosamine on the kinetics of metabolic processes for two intermediate metabolites, 9-hydroxybenzo(a)pyrene and 3-hydroxybenzo(a)pyrene, in 3T3 and RTG2 cells.

PAH metabolism is known to proceed in two successive steps, the first step resulting in the production of activated metabolites which are subsequently transformed by the different pathways involved in the second step. Microspectrofluorometry enables the study of the kinetics of these steps in living intact cells into which no imbalance has been artificially introduced. We used this technique to check the influence of pre-incubation with D-galactosamine on the kinetics of the detoxification step. 9- and 3-hydroxybenzo(a)pyrene (OH-B(a)P) were selected as fluorescent substrates because they are potential substrates for the different pathways of the second step. The physiological cell status was controlled at the level of the intrinsic cellular fluorescence. Pre-incubation with D-galactosamine results in a strong decrease of the experimental rate constants characteristic of the metabolism of 9- and 3-OH-B(a)P in both RTG2 and 3T3 cells. Moreover, such pre-incubation leads to a strong decrease of the transitory intracellular accumulation of 3-O-glucuronide when 3-OH-B(a)P is used as substrate for 3T3 cells. Nevertheless, it cannot be said that both phenols cannot be used as substrates by MFOs and STase, at least in rigorous experimental conditions.

Animals↗