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PubMed1996

The effect of fluoro substituents on reactivity of 7-methylbenz[a]anthracene diol epoxides.

The present study has examined potential mechanisms for the influence of F-substituents on the biologic activity of methylbenz[a]anthracenes. DNA adducts derived from reaction of the racemic bay-region anti-diol epoxides of 7-methylbenz[a]anthracene, and its 9- and 10- fluoro derivatives, with calf thymus DNA in vitro were partially characterized. All three hydrocarbon diol epoxides produced similar DNA adduct profiles upon reaction with calf thymus DNA in vitro that were composed of two deoxyganosine and two deoxyadenosine adducts (tentatively identified as trans addition products). The extent of covalent binding to calf thymus DNA, as estimated by 32P-postlabeling, was similar for all three diol epoxides. The reactivity of the unsubstituted and 10-F-substituted diol epoxide was further assessed by measuring overall pseudo-first-order rate constants for hydrolysis in water or 0.1 M Tris-HCl buffer, pH 7.0, and in the presence or absence of native or denatured DNA. The rate constant for hydrolysis of 7-methylbenz[a]anthracene diol epoxide in the absence of DNA was similar to that of 10-F-7-methylbenz[a]anthracene diol epoxide (t1/2 = 138 min vs 115 min in water, respectively, and 93 vs 83 min in 0.1 M Tris-HCl buffer, respectively). In addition, the presence of DNA accelerated hydrolysis rates to similar extents for both diol expoxides. The skin tumor-initiating activities of the 9- and 10-F-substituted 3,4-diols of 7-methyl-, 12-methyl-, and 7,12-dimethylbenz[a]anthracene were determined in SENCAR mice. The presence of F-substituents in the 9- or 10- position did not enhance or in some cases reduced the tumor-initiating activity of the 3,4-diols of these hydrocarbons. Collectively, these results, as well as previous results from our laboratory, suggest that the influence of a F-substituent at position 10 of the benz[a]anthracene nucleus is not due to increased or altered reactivity of the bay-region diol epoxide but rather likely on the initial formation of the 3,4-diol.

Animals↗

PubMed1977

Characterization of a photoproduct of 7,12-dimethylbenz[alpha]anthracene and its effects on chick-embryo cells in culture.

A common impurity of 7,12-dimethylbenz[alpha]anthracene was more effective than 7,12-dimethylbenz[alpha]anthracene in inducing morphological alterations, and in causing an increase in glucose uptake, DNA synthesis and cell number in chick-embryo fibroblasts. Gradual morphological transformation follows the increase in DNA synthesis after 2 days when either primary or secondary cultures are treated with 3 microgram of the compound/ml. The compound, isolated from 7,12-dimethylbenz[alpha]anthracene by alumina column chromatography, was characterized by t.l.c., mass spectroscopy, carbon-hydrogen analysis, u.v. and nuclear-magnetic-resonance spectroscopy and thermal decomposition. It was the photo-oxidation product of 7,12-dimethylbenz[alpha]anthracene, 7,12-epidioxy-7,12-dimethylbenz[alpha]anthracene. It is suggested that some of the biological effects observed after treatment of cultures with 7,12-dimethylbenz[alpha]anthracene may be due in part to the presence of the photo-oxidation product.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed1979

Identification of 7,12-dimethylbenz[a]anthracene metabolites that lead to mutagenesis in mammalian cells.

The mutagenicity of 7,12-dimethylbenz[a]-anthracene (DMBA) and 11 of its enzymatically derived metabolites was tested with Chinese hamster V79 cells for identification of mutagenic metabolites. The metabolites consisted of 7-hydroxymethyl-12-methylbenz[a]anthracene, 7-methyl-12-hydroxymethylbenz[a]anthracene, 7,12-dihydroxymethylbenz[a]anthracene, three trans-3,4-diols, two trans-5,6-diols, and three trans-8,9-diols, all of which derived from DMBA or from the hydroxymethyl derivatives. Mutations were characterized by resistance to ouabain and 6-thioguanine. None of the tested metabolites were mutagenic in V79 cells, which do not metabolize polycyclic aromatic hydrocarbons. Therefore, mutagenesis in the V79 cells was tested in the presence of golden hamster cells capable of metabolizing polycyclic aromatic hydrocarbons (cell-mediated assay). In this assay, DMBA, 7-hydroxymethyl-12-methylbenz[a]anthracene, 7-methyl-12-hydroxymethylbenz[a]anthracene, and their trans3,4-diols were mutagenic for both genetic markers, and the mutagenic response increased as a function of the hydrocarbon dose. All other metabolites were either inactive or showed up to a 4-fold higher mutation frequency than the untreated V79 cells for ouabain and 6-thioguanine resistance. The DMBA-trans-3,4-diol was the only metabolite that was more active than DMBA itself; at 0.05 muM it was 6-8 times more active than DMBA itself; at 0.05 muM it was 6-8 times more active than DMBA in inducing both ouabain and 6-thioguanine resistance. This diol was mutagenic at a dose as low as 0.01 muM. Mutagenesis by DMBA and the trans-3,4-diols was inhibited by 7,8-benzoflavone, an inhibitor of mixed-function oxidases. Analysis of DMBA metabolism in intact golden hamster cells indicated that DMBA-trans-3,4-diol is one of the major metabolites produced. Our results therefore suggest that DMBA-trans-3,4-diol may be metabolized to a diol-epoxide, presumably the trans-3,4-diol-1,2-epoxide, which may be a major reactive metabolite responsible for DMBA mutagenicity in mammalian cells.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed1981

Tumorigenicity of 7,12-dimethylbenz[a]anthracene, its hydroxymethylated derivatives and selected dihydrodiols in the newborn mouse.

The newborn mouse lung adenoma model has been shown to be a sensitive test for studying the tumorigenicity of bay region diol epoxides and their precursor dihydrodiols. When a total dose of 28 nmol of 7,12-dimethylbenz[a]anthracene (DMBA) or its derivatives was injected i.p. into the preweaning mice, it was found that the 3,4-dihydrodiols of both DMBA and 7-hydroxymethyl-12-methylbenz[a]anthracene caused 13.3 and 4.1 times more lung adenomas than DMBA, respectively. The mice treated with the 5,6- and 8,9-dihydrodiols of DMBA, 7-hydroxymethyl-12-methylbenz[a]anthracene and its 5,6- and 8,9- and 10,11-dihydrodiols, 7-methyl-12-hydroxymethylbenz[a]anthracene and 7,12-dihydroxymethylbenz[a]anthracene developed a level of lung adenomas/mouse less than 2-fold higher than that found in the DMSO-treated control group. Liver tumors also developed in some of the mice. The percentage of mice with liver tumors also indicated that the 3,4-dihydrodiols of both DMBA and 7-hydroxymethyl-12-methylbenz[a]anthracene were more tumorigenic than DMBA itself. These data indicate that the 3,4-dihydrodiols of both DMBA and its 7-hydroxymethyl derivative may be proximate carcinogenic metabolites of DMBA in the newborn mouse.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed1983

Dibenz[a,h]anthracene-induced subcutaneous tumors in mice. Strain sensitivity and the role of carcinogen metabolism.

Four inbred strains of mice (C3H/HeJ, C57BL/6J, AKR/J, and DBA/2J) were injected s.c. with 150 micrograms of dibenz[a,h]anthracene and followed for 9 months. Strains C3H/HeJ and C57BL/6J were most susceptible to dibenz[a,h]anthracene-induced carcinogenesis with 80% and 53% incidence of tumors, respectively. Strains AKR/J and DBA/2J were much less sensitive with only one tumor observed out of a total of 60 treated mice. Dibenz[a,h]anthracene was shown to induce hepatic aryl hydrocarbon hydroxylase activity in the two sensitive strains, C3H/HeJ and C57BL/6J, but not in the two resistant strains, AKR/J and DBA/2J. When 3-methylcholanthrene-treated liver microsomes from the four strains were studied for dibenz[a,h]anthracene metabolism in vitro, the two sensitive strains not only demonstrated a 3- to 4-fold greater overall rate of metabolism than the two resistant strains, but also showed a quantitative shift with a greater percentage of the total metabolites being the 3,4-diol of dibenz[a,h]anthracene. This diol is the presumed precursor to the apparent ultimate carcinogen, dibenz[a,h]anthracene 3,4-diol-1,2-epoxide.

Animals↗

PubMed1988

Comparative study of the lateral motion of extrinsic probes and anthracene-labelled constitutive phospholipids in the plasma membrane of Chinese hamster ovary cells.

9-(2-Anthryl)-nonanoic acid is a new photoactivatable fluorescent probe which has been designed for the study of the lateral diffusion and distribution of lipids in biological membranes by means of the anthracene photodimerization reaction. This anthracene fatty acid can be incorporated metabolically into the glycerophospholipids (phosphatidylcholine, phosphatidylethanolamine, phosphatidylserine, phosphatidylinositol) of Chinese hamster ovary (CHO) cells in culture. The diffusion coefficient of intrinsic lipids in the plasma membrane of these eukaryotic cells can thus be measured using the fluorescence recovery after a photobleaching technique, since illumination of the fluorescent anthracene groups yields non-fluorescent photodimers. For the sake of comparison, the extrinsic lipophilic probes 5-(N-hexadecanoyl)-aminofluorescein, 12-(9-anthroyloxy)-stearic acid, 9-(2-anthryl)-nonanoic acid and a synthetic anthracene-phosphatidylcholine were also used to label the plasma membrane of CHO cells. The diffusion coefficients for the extrinsic and intrinsic probes ranged over 1 - 2 x 10(-9) cm2/s. Small but significant differences were observed between the various probes reflecting differences they exhibit in size and polarity. All the extrinsic probes were free to diffuse, with a mobile fraction close to 100%. In contrast, a fractional recovery of only 75% was observed for the intrinsic anthracene-labelled phospholipids, suggesting that the anthracene fatty acid was metabolically incorporated into membrane lipid regions which were inaccessible to the extrinsic probes.

Affinity Labels↗

PubMed1990

Light-dependent cytotoxic reactions of anthracene.

Anthracene is a photodynamic compound in vitro. In the presence of oxygen, it is known to generate singlet oxygen and participate in Type II reactions. In aqueous solution, it also participates in Type I reactions, such as in the photoreduction of cytochrome c, which can be suppressed by superoxide dismutase. In argon, direct photoreduction of cytochrome c also takes place. Anthracene induces the photodynamic hemolysis of human erythrocytes and inactivates Escherichia coli cells photodynamically. By using a series of E. coli strains differing in DNA repair capabilities and catalase proficiency, sensitivity to inactivation by anthracene plus NUV was correlated with catalase deficiency rather than with particular repair deficiencies. The fact that carotenoid genes cloned and expressed in E. coli offered partial protection suggests that the membrane may be one possible target for inactivation by anthracene plus NUV. Anthracene plus NUV inactivated Haemophilus influenzae transforming DNA and led to nicking of supercoiled pBR322 DNA in vitro. In vivo, therefore, anthracene is a phototoxic molecule whose cytotoxicity could be the result of damage to more than one target.

Anthracenes↗

PubMed2003

Degradation of anthracene by Mycobacterium sp. strain LB501T proceeds via a novel pathway, through o-phthalic acid.

Mycobacterium sp. strain LB501T utilizes anthracene as a sole carbon and energy source. We analyzed cultures of the wild-type strain and of UV-generated mutants impaired in anthracene utilization for metabolites to determine the anthracene degradation pathway. Identification of metabolites by comparison with authentic standards and transient accumulation of o-phthalic acid by the wild-type strain during growth on anthracene suggest a pathway through o-phthalic acid and protocatechuic acid. As the only productive degradation pathway known so far for anthracene proceeds through 2,3-dihydroxynaphthalene and the naphthalene degradation pathway to form salicylate, this indicates the existence of a novel anthracene catabolic pathway in Mycobacterium sp. LB501T.

Anthracenes↗

PubMed1985

Stereoselectivity of microsomal epoxide hydrolase toward diol epoxides and tetrahydroepoxides derived from benz[a]anthracene.

We have examined the selectivity of rat liver microsomal epoxide hydrolase (EC 3.3.2.3) toward all of the possible positional isomers of benzo-ring diol epoxides and tetrahydroepoxides of benz[a]anthracene, as well as the 1,2-diol 3,4-epoxides of triphenylene. This set includes compounds with no bay region in the vicinity of the benzo-ring, a bay-region diol group, a bay-region epoxide group, and (for the triphenylene derivatives) both a bay-region diol and a bay-region epoxide. In all cases where both the tetrahydroepoxides and the corresponding diol epoxides were examined, there is a large retarding effect of hydroxyl substitution on the rate of the enzyme-catalyzed hydration. When the tetrahydroepoxides are fair or poor substrates (epoxide group in the 1,2-, 8,9-, or 10,11-position), the additional retardation introduced by adjacent hydroxyl groups causes the enzyme-catalyzed hydrolysis of the corresponding diol epoxides to be insignificantly slow or nonexistent. In contrast, a benz[a]anthracene derivative with an epoxide group in the 3,4-position, (-)-tetrahydrobenz[a]anthracene (3R,4S)-epoxide, has been identified as the best substrate known for epoxide hydrolase, with a Vmax at 37 degrees C and pH 8.4 of 6800 nmol/min/mg of protein, and the two diastereomeric (+/-)-benz[a]anthracene 1,2-diol 3,4-epoxides, unlike all the other diol epoxides examined to date, are moderately good substrates for epoxide hydrolase. This novel observation is accounted for by the fact that the very high reactivity of the tetrahydrobenz[a]anthracene 3,4-epoxide system towards epoxide hydrolase is large enough to overcome a kinetically unfavorable effect of hydroxyl substitution. The enantioselectivity and positional selectivity of the enzyme have been determined for the tetrahydro-1,2- and -3,4-epoxides of benz[a]anthracene as well as the 1,2-diol 3,4-epoxides. When the epoxide is located in the 3,4-position, the benzylic carbon is the preferred site of attack, whereas for the enantiomers of the bay-region tetrahydro-1,2-epoxides, the chemically less reactive non-benzylic carbon is preferred. The regio- and enantioselectivity of epoxide hydrolase are discussed in terms of a possible model for the hydrophobic binding site of this enzyme.

Animals↗

PubMed1993

Evidence for the involvement of a bis-diol-epoxide in the metabolic activation of dibenz[a,h]anthracene to DNA-binding species in mouse skin.

Dibenz[a,h]anthracene (DB[a,h]A) and its microsomal metabolites, trans-3,4-dihydro-3,4-dihydroxydibenz[a,h]anthracene (DBA-3,4-diol), trans,trans-3,4:8,9-tetrahydro-3,4:8,9-tetrahydroxydibenz[a,h]anth racene, trans,trans-3,4:10,11-tetrahydro-3,4:10,11-tetrahydroxydibenz[a,h] - anthracene (DBA-3,4,10,11-bis-diol) and trans,trans-3,4:12,13-tetrahydro-3,4:12,13- tetrahydroxydibenz[a,h]anthracene were each applied topically to mouse skin and the epidermal DNA isolated 24 h later. 32P-postlabeling analysis of each of the DNA samples was performed. DNA from mice treated with DB[a,h]A produced an adduct map on TLC consisting of one major and three minor adduct spots. A similar pattern of spots was produced by DBA-3,4-diol. No detectable DNA adducts were produced by trans,trans-3,4:12,13-tetrahydro-3,4:12,13-tetrahydroxy- dibenz[a,h]anthracene, although a single, minor adduct spot was produced by trans,trans-3,4:8,9-tetrahydro-3,4:8,9-tetrahydroxydibenz[a,h]- anthracene. However, DBA-3,4,10,11-bis-diol was found to produce a major single adduct that comigrated on thin layer chromatography with the major adduct produced by both DB[a,h]A and DBA-3,4-diol. In addition, this adduct was present at a level 10 times higher than the corresponding adduct produced by treatment with the parent hydrocarbon. Coelution of the major adducts formed from DB[a,h]A and DBA-3,4-diol with that formed from DBA-3,4,10,11-bis-diol was also demonstrated on reverse-phase high performance liquid chromatography. Thus, we propose that, in mouse skin, the major pathway of DB[a,h]A activation to DNA binding products is via a 3,4-diol to the 3,4,10,11-bis-diol and ultimately to a bis-diol-epoxide (potentially the 3,4,10,11-bis-dihydrodiol-1,2-oxide).

Animals↗

PubMed2006

Imaging by sensitized oxygenations of photochromic anthracene films: examination of effects that improve performance and reversibility.

The aliphatic anthracene compound 1 and the oligomeric anthracene 2 were synthesized. Thin films of 1 and 2 mixed with the sensitizers tetraphenylporphyrin (TPP) and methylene blue (MB) were irradiated with visible light in air. Upon formation of singlet oxygen, the anthracene units were converted quantitatively to the corresponding endoperoxides. Heating of the irradiated samples afforded the parent anthracenes with high yields. Here, we demonstrate that the kinetics and reversibility of this reaction strongly depend on the microenvironment of the anthracene groups in the two compounds. The photooxidation of thin films of 1 is accompanied by interesting changes in the morphology of the film and allows the first application of 1 as a nondestructive negative-tone photoresist for lithography and as an oxidizing ink. The morphology of 2 remained unchanged after photooxidation as a result of the stabilizing oligomer backbone. This stabilizing effect significantly improves the photochromic performance of 2. The reversibility of the photooxidation is very high (>90 %) for oligomeric films of 2 after several cycles of irradiation and heating. Decomposition of the anthracene and a loss of the activity of the sensitizer diminish slightly the performance of the monomeric species.

Journal Article↗

PubMed1997

The Effect of Ternary Complex Formation on the Partitioning of Pyrene and Anthracene in Aqueous Solutions Containing Sodium Dodecyl Sulfate and M-gamma-cyclodextrin

The partitioning behavior of pyrene and anthracene between n-decane and aqueous solutions containing a partially methylated gamma-cyclodextrin (M-gamma-CD) and sodium dodecyl sulfate (SDS) was studied by extraction experiments. At concentrations below the aqueous solubility of pyrene and anthracene both were found to form 1:1 complexes with M-gamma-CD. Formation constants were determined as 1843 M-1 for pyrene and 624 M-1 for anthracene. In micellar solutions of SDS pyrene was found to be better solubilized than anthracene. At constant concentrations of M-gamma-CD the dependence of the partition coefficients on increasing concentrations of SDS could be divided into three linear regions. At concentrations below a critical surfactant concentration (CSCSDS) the partition coefficients of both polyaromatic hydrocarbons as well as the fluorescence intensity of pyrene increased linearly with the addition of SDS. In the fluorescence spectra of anthracene the addition of SDS led to a shift of the maxima to higher wavelengths. These data suggest the formation of ternary complexes of M-gamma-CD with each of the polyaromatic hydrocarbons and SDS. The ternary complex with anthracene was found to be more stable than that of pyrene, which resulted in higher partition coefficients than seen with pyrene. Increasing the surfactant concentrations above the CSCSDS the partition coefficients remained constant until micelles were formed and another linear increase of the partition coefficients could be observed. CSCSDS and the critical micellization concentration (CMC) were found to increase linearly with cyclodextrin concentration. For CSCSDS a molar ratio of 3/1 was found for M-gamma-CD/SDS. Mixed micelles between SDS and gamma-CD are supposed to be formed above CSCSDS. Copyright 1997Academic Press

Journal Article↗

PubMed2000

Occupational exposure to polycyclic aromatic hydrocarbons in a fireproof stone producing plant: biological monitoring of 1-hydroxypyrene, 1-, 2-, 3- and 4-hydroxyphenanthrene, 3-hydroxybenz(a)anthracene and 3-hydroxybenzo(a)pyrene.

OBJECTIVES: Assessment of external and internal exposure to polycyclic aromatic hydrocarbons (PAH) in a fireproof stone producing plant. METHODS: Five personal and four stationary air measurements were performed to determine the concentrations of benz(a)anthracene, benzo(a)pyrene, benzo(b)fluoranthene, chrysene, dibenz(a,h)anthracene, fluoranthene, phenanthrene and pyrene, in air. To estimate internal exposure, we determined the urinary excretion of 1-hydroxypyrene, 1-, 2-, 3-, and 4-hydroxyphenanthrene, 3-hydroxybenz(a)anthracene and 3-hydroxybenzo(a)pyrene in 19 workers, using a sensitive and reliable high-performance liquid chromatographic method with fluorescence detection. RESULTS: During the production of fireproof stones, the German technical exposure limit (TRK) for benzo(a)pyrene of 2 microg/m3 was exceeded in two cases. The mean values of the sum of eight PAHs were 12.6 microg/m3 (stationary air measurement) and 22.2 microg/m3 (personal air measurement). Urinary 1-hydroxypyrene excretion predominated, with a median of 11.1 microg/g creatinine (creat.), followed by 3-hydroxyphenanthrene (median 2.2 microg/g creat.), 1-hydroxyphenanthrene (median 1.9 microg/g creat.) and 2-hydroxyphenanthrene (median 1.6 microg/g creat.). 4-Hydroxyphenanthrene (median 0.3 microg/g creat.) and 3-hydroxybenz(a)anthracene (median 0.17 microg/g creat.) were found in far lower concentrations, while 3-hydroxybenzo(a)pyrene was found only in very low concentrations (median 0.014 microg/g creat.). No correlations could be detected for a relationship between external and internal exposure. A significant correlation between urinary metabolite concentrations could be calculated only for 3-hydroxybenz(a)anthracene and 1-hydroxypyrene. CONCLUSIONS: In comparison with other industries, the internal PAH exposure at workplaces in a fireproof stone producing plant is high. This is probably caused by dermal PAH-absorption. Therefore, biological monitoring must be performed in the health surveillance of fireproof stone producing workers. The urinary PAH metabolites should be determined: 3-hydroxybenz(a)anthracene could probably be used as a biomarker representing the group of carcinogenic PAH.

Adult↗

PubMed2004

Photocatalytic oxygenation of anthracenes and olefins with dioxygen via selective radical coupling using 9-mesityl-10-methylacridinium ion as an effective electron-transfer photocatalyst.

Visible light irradiation of the absorption band of 9-mesityl-10-methylacridinium ion (Acr+-Mes) in an O2-saturated acetonitrile (MeCN) solution containing 9,10-dimethylanthracene results in formation of oxygenation product, i.e., dimethylepidioxyanthracene (Me2An-O2). Anthracene and 9-methylanthracene also undergo photocatalytic oxygenation with Acr+-Mes to afford the corresponding epidioxyanthracenes under the photoirradiation. In the case of anthracene, the further photoirradiation results in formation of anthraquinone as the final six-electron oxidation product, via 10-hydroxyanthrone, accompanied by generation of H2O2. When anthracene is replaced by olefins (tetraphenylethylene and tetramethylethylene), the photocatalytic oxygenation of olefins affords the corresponding dioxetane, in which the O-O bond is cleaved to yield the corresponding ketones. The photocatalytic oxygenation of anthracenes and olefins is initiated by photoexcitation of Acr+-Mes, which results in formation of the electron-transfer state: Acr*-Mes*+, followed by electron transfer from anthracenes and olefins to the Mes*+ moiety together with electron transfer from the Acr* moiety to O2. The resulting anthracene and olefin radical cations undergo the radical coupling reactions with O2*- to produce the epidioxyanthracene (An-O2) and dioxetane, respectively.

Journal Article↗

PubMed1996

Oxidation of Anthracene and Benzo[a]pyrene by Laccases from Trametes versicolor.

The in vitro oxidation of the two polycyclic aromatic hydrocarbons anthracene and benzo[a]pyrene, which have ionization potentials of <=7.45 eV, is catalyzed by laccases from Trametes versicolor. Crude laccase preparations were able to oxidize both anthracene and the potent carcinogen benzo[a]pyrene. Oxidation of benzo[a]pyrene was enhanced by the addition of the cooxidant 2,2(prm1)-azinobis(3-ethylbenzthiazoline-6-sulfonate) (ABTS), while an increased anthracene oxidizing ability was observed in the presence of the low-molecular-weight culture fluid ultrafiltrate. Two purified laccase isozymes from T. versicolor were found to have similar oxidative activities towards anthracene and benzo[a]pyrene. Oxidation of anthracene by the purified isozymes was enhanced in the presence of ABTS, while ABTS was essential for the oxidation of benzo[a]pyrene. In all cases anthraquinone was identified as the major end product of anthracene oxidation. These findings indicate that laccases may have a role in the oxidation of polycyclic aromatic hydrocarbons by white rot fungi.

Journal Article↗

PubMed2005

Synthesis and supramolecular properties of molecular clips with anthracene sidewalls.

Novel molecular clips with anthracene sidewalls (1 a-c) were synthesized; they form stable host-guest complexes with a variety of electron-deficient aromatic and quinoid molecules. According to single-crystal structure analyses of clip 1 c and 1,2,4,5-tetracyanobenzene (TCNB) complex 14@1 b, the clips' anthracene sidewalls have to be compressed substantially during the complex formation to provide attractive pi-pi interactions between the aromatic guest molecule and the two anthracene sidewalls in the complex. The compression and expansion of aromatic sidewalls are calculated by molecular mechanics to be low-energy processes, so the energy required for compression of the anthracene sidewalls during complex formation is apparently overcompensated by the gain in energy resulting from the attractive pi-pi interactions. The finding that complexes of the clips 1 a-c are more stable than those of the corresponding clips 2 a-c can be explained in terms of the larger van der Waals contact surfaces of the anthracene sidewalls in 1 a-c (relative to the naphthalene sidewalls in 2 a-c). Color changes resulting from charge-transfer (CT) bands are observed in complex formation by 1 a-c: from colorless to red or purple with TCNB (14), and from yellow to green with 2,4,7-trinitro-9-fluorenone TNF (17). Independently, the host 1 b and guest 14 fluoresce from their respective excited singlet states, whilst in the complex 14@1 b the charge-transfer state quenches the higher-energy singlet states of the two components, and as a result luminescence is only observed from this new CT state. To the best of our knowledge, complex 14@1 b is the first example of CT luminescence from a host-guest complex. The binding constant determined for the formation of the TCNB complex 14@1 b from a UV/Vis titration experiment (Ka = 12 400 m(-1)) agrees well with the value (K(a) = 12 800 m(-1)) obtained by 1H NMR titration.

Anthracenes↗

PubMed1977

The metabolic activation of 7-methylbenz(a)anthracene: the induction of malignant transformation and mutation in mammalian cells by non-K-region dihydrodiols.

Four different dihydrodiols derived from 7-methylbenz(a)anthracene have been tested, together with the parent hydrocarbon, for their ability to induce the in vitro malignant transformation of mouse M2 fibroblasts and mutations in V79 Chinese hamster cells. In the transformation tests withe the non-K-region dihydrodiols, the 3,4-diol was the most active dihydrodiol tested and the 8,9-diol was also more active than 7-methylbenz(a)anthracene itself; the 1,2-diol showed only slight activity. The K-region dihydrodiol, the 5,6-diol, which cannot be directly metabolized to a vicinal diol-epoxide, was inactive. These differences in biological activity were similar to those apparent in the results from the mutagenicity tests. The data support the general hypothesis that non-I-region dihydrodiols, which can be metabolized to vicinal diol-epoxides, are important in the metabolic activation of the carcinogenic polycyclic hydrocarbons and, when taken together with other results, indicate that 3,4-dihydro-3,4-dihydroxy-7-methylbenz(a)anthracene is most probably involved in the metabolic activation of 7-methylbenz(a)anthracene presumably following conversion into the related diol-epoxide, 3,4-dihydro-3,4-dihydroxy-7-methylbenz(a)anthracene 1,2,-oxide.

Animals↗

PubMed1980

The metabolic activation of benz[a]anthracene in hamster embryo cells: evidence that diol-epoxides react with guanosine, deoxyguanosine and adenosine in nucleic acids.

The principal nucleoside-hydrocarbon adducts present in hydrolysates of RNA and DNA isolated from hamster embryo cells treated with benz[a]anthracene (BA) were examined by chromatography on Sephadex LH 20 and by high pressure liquid chromatography (HPLC) on Spherisorb 5 ODS. The results extend the previous finding that a non-'bay-region' diol-epoxide, anti-BA-8,9-diol 10,11-oxide (r-8,t-9-dihydroxy-t-10,11-oxy-8,9,10,11-tetrahydrobenz[a] anthracene) is involved in the binding of BA to cellular nucleic acids and show that this diol-epoxide most probably reacts with guanosine and adenosine in RNA and with deoxyguanosine in DNA. The results also show that a 'bay-region' diol-epoxide anti-BA-3,4-diol 1,2-oxide (t-3,-4-dihydroxy-t-1,2-oxy-1,2,3,4-tetrahydrobenz[a]anthracene, which is thought to be involved in the binding of benz[a]anthracene, which is thought to be involved in the binding of benz[a]anthracene to DNA in some situations, reacts mainly with deoxyguanosine.

Adenosine↗