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PubMed1980

Additional evidence for the involvement of the 3,4-diol 1,2-oxides in the metabolic activation of 7,12-dimethylbenz[a]anthracene in mouse skin.

The role of vicinal diol-epoxides in the metabolic activation of 7,12-dimethylbenz[a]anthracene to intermediates that react with nucleic acids was investigated using Sephadex LH-20 column chromatography and high pressure liquid chromatography. The results show that some of the hydrocarbon-DNA products formed in mouse skin treated in vivo with 7,12-dimethylbenz[a]anthracene arise from the reaction of DNA with 3,4-dihydro-3,4-dihydroxy-7,12-dimethylbenz[a]anthracene 1,2-oxides which, on the basis of this and other evidence, appears to be a biologically-active metabolite of 7,12-dimethylbenz[a]anthracene. However, since other nucleic acid-hydrocarbon adducts were also present that have not been identified as resulting from the reaction of the 3,4-diol 1,2-oxides with DNA, other mechanisms may also be involved in the metabolic activation of 7,12-dimethylbenz[a]anthracene in mouse skin.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1995

Benz[a]anthracene diols: predicted carcinogenicity and structure-estrogen receptor binding affinity relationships.

Benz[a]anthracenes are ubiquitous environmental carcinogens that exert estrogenic and antiestrogenic effects directly or via hydroxylated metabolites. In this paper, the structure-estrogen receptor binding relationships of four 3,9-benz[a]anthracene diols are described: unsubstituted, 7-methyl, 12-methyl, and 7,12-dimethyl. Compounds unsubstituted at the 12-position have flat molecular topology, whereas methyl substitution at the 12-position in the bay region induces twisting of the molecular framework. The oxygen-oxygen distances (11.94-11.98 A) are similar to diethylstilbestrol (12.1 A). The binding affinities range from 0.43% to 26% that of estradiol. Methyl substitution at the 7-position enhances affinity; 12-methyl substitution decreases it. These results are contrary to many estrogen receptor (ER) ligand systems, in which the compounds with the flatter molecular geometries typically have lower binding affinity. Molecular graphics were used to analyze the fit of the four compounds with a receptor excluded volume model for the ER. These studies suggest that these compounds bind to the ER in a manner in which the anthracene fragment acts as the steroid AB-ring mimic (i.e, the benz[a]anthracene 9-position corresponds to the estradiol 3-position). Molecular orbital (AM1) calculations were used to calculate the charges of selected atoms. The 7-methyl compound was found to have greater charge similarity to estradiol than the other three compounds. The high affinity of the 7-methyl compound is ascribed to its charge similarity to estradiol, hydrophobic interactions in the receptor region that would accommodate a substituent in the planar 6-position of a delta 6,7-steroid, and favorable dispersive interactions with the receptor secondary to its extended planar system. Molecular orbital calculations also suggest that some of the benz[a]anthracene monophenols and diphenols have sufficiently low ionization potentials to act as carcinogens by a radical cation process.

Benz(a)Anthracenes↗
PubMed2006

Operation of a two-phase partitioning bioreactor for the oxidation of anthracene by the enzyme manganese peroxidase.

A study was conducted to determine the potential of a two-phase partitioning bioreactor (TPPB) for the treatment of a poorly soluble compound, anthracene, by the enzyme manganese peroxidase (MnP) from the fungus Bjerkandera sp. BOS55. Silicone oil was used as the immiscible solvent, which contained anthracene at high concentrations. The optimization of the oxidation process was conducted taking into account the factors which may directly affect the MnP catalytic cycle (the concentration of H(2)O(2) and malonic acid) and those that affect the mass transfer of anthracene between the organic and the aqueous phase (solvent and agitation speed). The main objective was carried out in terms of improved efficiency, i.e., maximizing the anthracene oxidized per unit of enzyme used. The TPPB reached nearly complete oxidation of anthracene at a conversion rate of 1.8mgl(-1)h(-1) in 56h, which suggests the application of enzymatic TPPBs for the removal of poorly soluble compounds.

Anthracenes↗
PubMed1989

Continuous fluorescence microphotolysis of anthracene-labeled phospholipids in membranes. Theoretical approach of the simultaneous determination of their photodimerization and lateral diffusion rates.

Anthracene is a fluorescent and photoactivatable (dimerization) group which can be used for investigating the lateral distribution and dynamics of lipids in membranes. In fluorescence recovery after photobleaching or in microphotolysis experiments, and when using this fluorophore, the bleaching (or microphotolysis) step in the illuminated part of the membrane is in fact the sum of two antagonistic processes: fluorescence decay, which is due to dimerization of anthracene residues, and fluorescence recovery, which is due to a diffusion mediated exchange of bleached and unbleached particles between the illuminated and diffusion area in the membrane. Here, we propose a new mathematical algorithm that enables such a second-order reaction-diffusion process to be analyzed. After coupling a fluorescence recovery step to a microphotolysis step, this algorithm allows us to calculate the lateral diffusion coefficient D and the photodimerization constant K of anthracene-labeled lipids in membranes, two parameters which contribute to the understanding of the fluidity of the lipid phase in membranes. This algorithm also provides us with a complete description of the anthracene-labeled molecules distribution in the illuminated and diffusion area, at any time of the experiment. The fluorescence recovery after microphotolysis procedure we propose was tested with an anthracene-labeled phosphatidylcholine inserted in egg-phosphatidylcholine multilayers, in monolayers adsorbed onto alkylated glass surfaces and in the plasma membrane of Chinese hamster ovary cells. It is shown that this procedure can also be used to evaluate the important parameters of probe mobile fraction and to determine the relative size of the illuminated and diffusion areas. This will enable membranes to be explored in terms of microdomains and/or macrodomains.

Algorithms↗
PubMed2000

Gender-specific metabolism of benz[a]anthracene in hepatic microsomes from Long-Evans and Hooded Lister rats.

The cytochrome P450 isoforms responsible for the regio-selective metabolism of benz[a]anthracene (BA) are poorly defined but as with other polycyclic aromatic hydrocarbons (PAHs) may include members of the CYP2C sub-family. Since the expression of some of these is regulated in a gender-specific manner and may be altered by age, rat strain or by phenobarbital treatment, the effects of these variables on metabolism of BA to diols was investigated. These studies used hepatic, microsomal membranes from immature and adult Long-Evans rats and adult Hooded Lister rats. BA-diols were resolved by normal phase HPLC into three discrete peaks identified as benz[a]anthracene-5,6-diol (BA-5,6-diol), benz[a]anthracene-10, 11-diol (BA-10,11-diol) and a mixture of benz[a]anthracene-3,4- and -8,9-diols (BA-3,4-diol and BA-8,9-diol and termed Peak(3/8)). Significant gender-related differences were found in the rates of diol formation in adults of both the Long-Evans and Hooded Lister rat strains. Formation of BA-10,11-diol and to a lesser extent the components of Peak(3/8) were greater in the male compared to female animals by factors of at least 14 and two, respectively. An age-dependent effect is also observed in the Long-Evans rat since these differences are still apparent in prepubertal animals but to a lesser extent (gender ratio male:female BA-10,11-diol 9X; Peak(3/8) 1.4X). In contrast BA-5,6-diol was formed at similar rates by membranes from female and male rats whether mature (Long-Evans and Hooded Lister) or immature (Long-Evans). Phenobarbital treatment of the adult Long-Evans rats resulted in a moderate increase in the formation of each diol other than at the 10,11-position and the induction was not gender specific. The rate of formation of BA-10, 11-diol was decreased in phenobarbital-treated male rats suggesting modulation of a male specific isoform. Measurement of microsomal epoxide hydrolase revealed no gender or age differences and suggests that this enzyme is not rate limiting in BA-diol formation and thus is not responsible for the differences in BA-diol formation observed. The results suggest that CYP2C11 along with a male-specific isoenzyme not regulated by age are important in the formation of BA-10,11-diol and a component(s) of Peak(3/8) in males. CYPs 2B2 and/or 2C6 appear to be involved in formation of BA-5,6-diol in male and female. Identification of the CYPs involved in the regio-selective metabolism of BA may lead to an explanation of the lower carcinogenic potency of this PAH compared to dimethylbenz[a]anthracene and this study provides novel clues concerning the identities of the CYPs, which are important.

Age Factors↗
PubMed2000

High-performance liquid chromatographic method with fluorescence detection for the determination of 3-hydroxybenzo[a]pyrene and 3-hydroxybenz[a]anthracene in the urine of polycyclic aromatic hydrocarbon-exposed workers.

The described high-performance liquid chromatographic method with fluorescence detection (HPLC-FD) permits the simultaneous determination of 3-hydroxybenzo[a]pyrene and 3-hydroxybenz[a]anthracene as the most important metabolites of the carcinogenic polycyclic aromatic hydrocarbons (PAHs) benzo[a]pyrene and benz[a]anthracene in human urine. After enzymatic hydrolysis, to release the conjugated metabolites, the analytes are separated from the matrix by means of a liquid-solid extraction step which is followed by a coupled column HPLC procedure using an enriching precolumn consisting of silica modified with copper phthalocyanine. This special precolumn selectively adsorbs PAHs with at least three condensed rings and thus separates them from the urine matrix. The quantitative analysis was carried out using a switchable fluorescence detector. The detection limits were 6 ng/l urine (3-hydroxybenzo[a]pyrene) and 8 ng/l urine (3-hydroxybenz[a]anthracene). The relative standard deviations of the within-series imprecision ranged between 4.0% and 9.0%. The between-day imprecision was 7.7% (3-hydroxybenz[a]anthracene) and 12.9% (3-hydroxybenzo[a]pyrene). The recovery rates ranged between 102% and 124%. Using this analytical method we determined PAH metabolites in post shift urine samples from 19 workers engaged in the production of fire-proof materials. The urinary concentrations ranged from 3 to 198 ng 3-hydroxybenzo[a]pyrene per g creatinine and from 15 to 1871 ng 3-hydroxybenz[a]anthracene per g creatinine.

Adsorption↗
PubMed2003

Elucidation of the metabolic pathway of fluorene and cometabolic pathways of phenanthrene, fluoranthene, anthracene and dibenzothiophene by Sphingomonas sp. LB126.

The metabolic pathway of the PAH fluorene and the cometabolic pathway of the PAHs phenanthrene, fluoranthene, anthracene and dibenzothiophene in Sphingomonas sp. LB126 were examined. To our knowledge this is the first study on the cometabolic degradation of the three-ring PAHs phenanthrene, anthracene and the four-ring PAH fluoranthene by a fluorene-utilizing species. Metabolism of fluorene was shown to proceed via the 9-fluorenone pathway to form o-phthalic acid and protocatechuic acid. The cometabolic mono-hydroxylation found for phenanthrene, fluoranthene and anthracene shows similarity with the hydroxylation of fluorene. Several mono- and dihydroxy products and ring-cleavage products were identified for phenanthrene, fluoranthene and anthracene. It appeared that the cometabolism of those three compounds is a non-specific process, in contrast to the metabolism of fluorene. For dibenzothiophene the metabolites dibenzothiophene-5-oxide and dibenzothiophene-5,5-dioxide were identified; these compounds appeared to be the products of a dead-end pathway. Since apart from dibenzothiophene no metabolites were found in very high concentrations for any of the other substrates, complete degradation is suggested, even for the cometabolic degradation of phenanthrene, fluoranthene and anthracene.

Anthracenes↗
PubMed2001

Construction of peptide conjugates with peptide nucleic acids containing an anthracene probe and their interactions with DNA.

We designed and synthesized the peptide nucleic acid (PNA)-peptide conjugates having anthracene chromophores and investigated their interactions with calf thymus DNA, [d(AT)(10)](2), [d(GC)(10)](2), and [d(AT)(10)dA(6)](2). Considering the synthesis compatibility and expecting that a novel DNA analogue, PNA, can improve DNA binding properties of alpha-helix peptides, we attempted to attach thymine PNA oligomers at the C-terminus of a 14 amino acid alpha-helix peptide that contained a pair of artificial intercalators, anthracene, as a probe, and to examine their interactions with DNA using anthracene UV, fluorescence and circular dichroism properties. The results observed in this study showed that the designed peptide folded in an alpha-helix structure in the presence of calf thymus DNA, [d(AT)(10)](2), and [d(AT)(10)dA(6)](2) with the chromophores at the side-chain being fixed with a left-handed chiral-sense orientation. The alpha-helix and the anthracene signals were not observed for [d(GC)(10)](2). Incorporation of thymine PNA oligomers into the designed alpha-helix peptide increased the DNA binding ability to [d(AT)(10)dA(6)](2) with increasing the length of the PNA without changing the conformations of the peptide backbone and the anthracene side-chains.

Anthracenes↗
PubMed2006

Kinetic and product yield study of the heterogeneous gas-surface reaction of anthracene and ozone.

Little quantitative information exists regarding the products of the heterogeneous reaction of polycyclic aromatic hydrocarbons (PAHs) and ozone. We have, therefore, performed the first quantitative study investigating the kinetics and products of the heterogeneous gas-surface reaction of anthracene and ozone as a function of ozone concentration and relative humidity (RH). The reaction exhibited pseudo-first-order kinetics for anthracene loss under dry conditions (RH < 1%) and the pseudo-first-order rate coefficients displayed a Langmuir-Hinshelwood dependence on the gas-phase ozone concentration, which yielded the following fitting parameters: the equilibrium constant for ozone adsorption, K(O3) = (2.8 +/- 0.9) x 10(-15) cm3 and the maximum pseudo-first-order rate coefficient, k(I)max = (6.4 +/- 1.8) x 10(-3) s(-1). The kinetics were unchanged when experiments were performed at approximately 50% and 60% RH. In the product study, a nonlinear dependence, similar to a Langmuir adsorption plot, of the anthraquinone product yield as a function of ozone concentration was observed and resulted in the following fitting parameters: K(O3) = (3.4 +/- 1.5) x 10(-15) cm3 and the maximum anthraquinone yield, ANQmax % = 30 +/- 18%. Experiments performed under higher relative humidity conditions ( approximately 50% and 60% RH) revealed that the anthraquinone yield was unaffected by the presence of gas-phase water. It is noteworthy that both the anthracene loss kinetics and the anthraquinone yields have a similar dependence on the degree of ozone partitioning to the surface. This can be understood in terms of a mechanism whereby the rate-determining steps for anthracene loss and anthraquinone formation are both driven by the amounts of ozone adsorbed on the surface. Our results suggest that at atmospherically relevant ozone concentrations (100 ppb) the anthraquinone yield from the ozonolysis of anthracene under dry and high relative humidity conditions would be less than 1%.

Air↗
PubMed1967

The metabolism of 7- and 12-methylbenz[a]anthracene and their derivatives.

1. 7- and 12-Methylbenz[a]anthracene were converted by rat-liver homogenates into the corresponding hydroxymethyl derivatives, products that are probably the 8,9-dihydro-8,9-dihydroxy and the 5,6-dihydro-5,6-dihydroxy derivatives, and a number of phenolic products. 2. Both hydrocarbons were converted into glutathione conjugates; that from 7-methylbenz[a]anthracene was also formed, together with 5,6-dihydro-5,6-dihydroxy- and 5-hydroxy-benz[a]anthracene, from 5,6-epoxy-5,6-dihydro-7-methylbenz[a]anthracene. 3. 7- and 12-Hydroxymethyl-benz[a]anthracene were converted into products that are probably 8,9-dihydro-8,9-dihydroxy derivatives, and into phenols. 4. The preparation of a number of derivatives of the hydrocarbons is described. 5. The oxidation of the hydrocarbons with lead tetra-acetate was investigated.

Animals↗
PubMed1980

The metabolism of the 10,11-dihydrodiol of benz[a]-anthracene to a vicinal diol-epoxide that is not involved in metabolic activation.

Benz[a]anthracene-10,11-diol, a major metabolite of benz[a]anthracene, is metabolized by a rat-liver microsomal system to form anti-BA-10,11-diol 8, 9-oxide (t-10,r-11-dihydroxy-t-8,9-oxy-8,9,10,11 -tetrahydrobenz[a]anthracene) and, to a lesser extent, syn-BA-10,11-diol 8,9-oxide (t-10,r-11-dihydroxy-c-8,9-oxy-8,9,10,11-tetrahydrobenz[a] anthracene). However, when benz[a]anthracene is incubated with DNA in a rat-liver microsomal system, anti-BA-10,11-diol 8,9-oxide does not contribute to the covalent binding of this hydrocarbon to DNA.

Animals↗
PubMed1982

Anticarcinogenic and cocarcinogenic effects of benzo[e]pyrene and dibenz[a,c]anthracene on skin tumor initiation by polycyclic hydrocarbons.

In the present study, we have examined the effects of benzo[e]pyrene (B[e]P) and dibenz[a,c]anthracene (DB[a,c]A) on the skin tumor-initiating activities of methylated and non-methylated polycyclic aromatic hydrocarbons (PAH). B[e]P, when applied 5 min prior to initiation with seven different PAH skin carcinogens, effectively inhibited the tumor-initiating activities of 7,12-dimethylbenz[a]anthracene (DMBA) and dibenz[a,h]anthracene (DB[a,h]A) but had little or no effect on the tumor-initiating activities of 3-methyl-cholanthrene (MCA), 7-methylbenz[a]anthracene (7-MBA), 12-methylbenz[a]anthracene (12-MBA), and 5-methyl-chrysene (5-MeC). B[e]P potentiated the tumor-initiating activity of benzo[a]pyrene (B[a]P) by approximately 30%, DB[a,c]A, when applied 5 min prior to initiation, inhibited the tumor-initiating activities of DMBA, MCA, and DB[a,h]A but had little or no effect on the tumor-initiating activities of B[a]P, 7-MBA, 12-MBA, and 5-MeC. DB[a,c]A, when applied 12, 24, or 36 h prior to initiation with B[a]P, which allowed time for induction of epidermal monooxygenase enzymes, inhibited tumor initiation. The covalent binding of DMBA and B[a]P to epidermal DNA was examined under the influence of B[e]P. Doses of 20 and 200 nmol B[e]P given 5 min prior to 10 nmol [3H]DMBA reduced binding to 47 and 22%, respectively, of the control value. In contrast, doses of 200 or 2000 nmol B[e]P given 5 min prior to 200 nmol [3H]B[a]P had little or no effect on total binding. The data indicate that one cannot predict anti and cocarcinogenic effects of B[e]P and DB[a,c]A on the basis of a presence or absence of a methyl substituent. In addition, fundamental differences exist in the processing and metabolism of DMBA and B[a]P by mouse epidermal cells.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1988

Tumor-initiating activity of the bay-region dihydrodiols and diol-epoxides of dibenz[a,j]anthracene and cholanthrene on mouse skin.

The tumor-initiating activity of dibenz[a,j]anthracene, (+/-)dibenz[a,j]anthracene-trans-3,4-diol and (+/-)dibenz[a,j]-anthracene-anti-3,4-diol-1,2-epoxide in mouse skin was examined and compared to that of cholanthrene, (+/-) cholanthrene-trans-9,10-diol and (+/-)cholanthrene-anti-9,10-diol-7,8-epoxide. The tumor-initiating activity of these compounds dissolved in acetone or in tetrahydrofuran (THF) was also compared. In acetone, dibenz[a,j]anthracene was a weak tumor initiator with maximal tumor yields of 1.27 and 3.00 per mouse at 400 and 800 nmol doses, respectively. At the 400 nmol dose, the diol of this compound was slightly more active than the parent compound while the tumorigenic activity of the diol-epoxide was significantly higher. The diol-epoxide was almost three times more active than the parent compound as a tumor-initiator. Cholanthrene was a moderate tumor-initiator with maximal tumor yields of 6.90 and 8.86 tumors per mouse at 200 and 600 nmol doses, respectively, after 20 weeks of promotion. At comparable doses, (+/-)cholanthrene-trans-9,10-diol was approximately 50% as potent as cholanthrene as a tumor initiator whereas the diol-epoxide was only minimally active. Replacing the acetone with THF as solvent vehicle increased the tumor-initiating activity of cholanthrene-diol-epoxide; however, the parent compound still retained higher tumor-initiating activity than its bay-region diol-epoxide. The low tumorigenic activity of cholanthrene-diol-epoxide is thought to reflect the high chemical reactivity and low stability of this derivative, which may prevent it from penetrating to epidermal targets. In contrast, the bay-region diol-epoxide derivative of dibenz[a,j]anthracene appears to be stable enough to exert greater biologic activity when applied to mouse skin.

Animals↗
PubMed1988

Comparative tumor-initiating activity of methylene-bridged and bay-region methylated derivatives of benz[a]anthracene and chrysene.

Polycyclic aromatic hydrocarbons (PAHs) with a methylene-bridge spanning the bay region are often detected in higher concentrations in the environment than PAHs which have a bay-region methyl substituent. The tumor-initiating activity of methylene-bridged bay-region derivatives of chrysene and benz[a]anthracene was evaluated on the skin of female CD-1 mice. 4,5-Methylenechrysene elicited twice as many tumors as chrysene at each of the doses tested. At total initiation doses of 1.5, 0.5 and 0.15 mumol/mouse 4,5-methylenechrysene gave rise to 8.5, 6.8 and 1.1 tumors/animal respectively. There was a 100% incidence of tumor-bearing mice at the two higher doses and a 65% incidence at the lowest dose. This methylene-bridged hydrocarbon was less tumorigenic than 5-methylchrysene at each dose tested. Animals treated with 1,12-methylenebenz[a]anthracene developed 7.6, 4.9 and 1.6 tumors/animal at total initiating doses of 4.0, 2.0 and 0.5 mumol/mouse. The incidence of tumor-bearing mice was 90% at the higher doses and 75% at the lowest dose tested. 12-Methylbenz[a]anthracene was more tumorigenic than the methylene-bridged derivative at each dose. The keto-derivative of 1,12-methylenebenz[a]anthracene did not display significant (P greater than 0.05) tumor-initiating activity at these dose levels. Results from these bioassays indicate that methylene-bridged bay-region derivatives of chrysene and benz[a]anthracene contribute to the overall genotoxicity of environmentally occurring PAHs.

Animals↗
PubMed1994

K-region oxides and imines derived from alkylated benz[a]anthracene congeners: synthesis, stability in aqueous media and mutagenicity.

The K-region oxides and imines of benz[a]anthracene, 1-methylbenz[a]anthracene, 7-methylbenz[a]anthracene, 7-ethylbenz[a]anthracene and 7,12-dimethylbenz[a]anthracene were synthesized and characterized (melting point, 1H-NMR and electron impact mass spectra, elemental analysis, IR spectroscopy). All 10 compounds showed high mutagenic activity in Salmonella typhimurium (reversion of his- strains TA97, TA98, TA100 and TA104). The arene imines were more potent than the corresponding arene oxides. Alkyl substitutions strongly influenced the activities. Furthermore, all compounds were more active when exposure took place in the absence of inorganic ions than when KCl (125 mM) was present. The influence of the exposure medium was more pronounced with strain TA98 than with strain TA100. The half-lives of the test compounds were determined from mutagenicity experiments in which the compound was added to the exposure medium at varying times before the bacteria. In dilute sodium phosphate buffer (10 mM, pH 7.4), the half-lives of these chemicals (or their biological activity) varied from 0.5 to 110 min. Addition of KCl (150 mM) did not measurably affect the half-lives of some test compounds and appeared to slightly shorten those of others. Therefore, it is unlikely that the strong effect of KCl on mutagenicity and the dependence of this effect on the bacterial strain used can be explained by influences of KCl on the test compounds. Rather, it appears more likely than an effect of KCl on the bacteria may be an important factor. This study provides further examples of strong influences of unobtrusive media components on mutagenicity. It also demonstrates that small structural changes (alkyl substituents at diverse positions of the aromatic system) may play an important role in chemical reactivity and biological activity.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1997

Anthracene-9-carboxylic acid.

Anthracene-9-carboxylic acid, C15H10O2, was found to crystallize in the centrosymmetric space group P2(1)/n. The hydrogen bonding is of the cyclic-dimer type about a center of symmetry. The carboxyl O atoms are ordered, as is the carboxyl H atom. The anthracene core is almost planar and shows good agreement with the anthracene core of anthracene-1, 8-dicarboxylic acid. The carboxyl group plane makes a dihedral angle of 54.87 (6) degrees with the best-fit anthracene core plane.

Anthracenes↗
PubMed1997

Anthracene-1-carboxylic acid.

The title compound, C15H10O2, was found to crystallize in the centrosymmetric space group P2(1)/n. The hydrogen bonding is of the cyclic dimer type about a center of symmetry. The carboxyl O atoms are ordered as is the carboxyl H atom. The anthracene core, while less nearly planar, shows good agreement with the anthracene cores of anthracene-9-carboxylic acid and anthracene-1,6-dicarboxylic acid. The carboxyl group plane makes a dihedral angle of 12.4 (2) degrees with the best-fit anthracene core plane.

Anthracenes↗
PubMed1997

Evidence for the role of 2-hydroxychromene-2-carboxylate isomerase in the degradation of anthracene by Sphingomonas yanoikuyae B1.

Sphingomonas yanoikuyae B1 is extremely versatile in its catabolic ability. An insertional mutant strain, S. yamoikuyae EK504, which is unable to grow on naphthalene due to the loss of 2-hydroxychromene-2-carboxylate isomerase activity, was utilized to investigate the role of this enzyme in the degradation of anthracene by S. yanoikuyae B1. Although EK504 is unable to grow on anthracene, this strain could transform anthracene to some extent. A metabolite in the degradation of anthracene by EK504 was isolated by high-pressure liquid chromatography (HPLC) and was identified as 6,7-benzocoumarin by UV-visible, gas-chromatographic, HPLC/mass-spectrometric, and 1H nuclear magnetic resonance spectral techniques. The identification of 6,7-benzocoumarin provides direct chemical and genetic evidence for the involvement of nahD in the degradation of anthracene by S. yanoikuyae B1.

Anthracenes↗