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PubMed1998

Liver tumors induced in B6C3F1 mice by 7-chlorobenz[a]anthracene and 7-bromobenz[a]anthracene contain K-ras protooncogene mutations.

We previously examined the tumorigenicity of 7-chlorobenz[a]anthracene (7-Cl-BA) and 7-bromobenz[a]anthracene (7-Br-BA) in the neonatal mouse bioassay and found that 7-Cl-BA and 7-Br-BA induced hepatocellular adenoma in 92 and 96% of the mice and hepatocellular carcinoma in 100 and 83% of the mice, respectively. In the present study, mRNA was isolated from each of the liver tumors induced by the two compounds and reverse-transcribed to cDNA. Portions of the K- and H-ras oncogene coding sequences were then amplified and analyzed for DNA sequence alterations. Eighty-three percent (20/24) of 7-Cl-BA-induced and 91% (20/22) of 7-Br-BA-induced liver tumors had activated ras protooncogenes. In contrast to the general finding of H-ras mutations in B6C3F1 mouse liver tumors, both compounds had 95% (19/20) of the mutations located at the first base of K-ras codon 13, resulting in a pattern of GGC --> CGC. Thus, our results demonstrate that 7-Cl-BA and 7-Br-BA induce a unique type of ras (K-ras) oncogene activation in liver tumors of B6C3F1 mice.

Adenoma, Liver Cell↗
PubMed1991

Comparative regioselective and stereoselective metabolism of 7-chlorobenz[a]anthracene and 7-bromobenz[a]anthracene by mouse and rat liver microsomes.

Quantitative metabolism of 7-chlorobenz[a]anthracene (7-Cl-BA) and 7-bromobenz[a]anthracene (7-Br-BA) by liver microsomes of uninduced mice and rats was studied. Both enzymatic systems metabolize 7-Cl-BA preferentially at the C-8 and C-9 aromatic double bond region, approximately 42 and approximately 56% respectively, of the total metabolites. 7-Cl-BA and 7-Br-BA were metabolized considerably at C-3 and C-4, C-5 and C-6, C-8 and C-9, and C-10 and C-11. While 7-Cl-BA trans-3,4-dihydrodiol was formed in a 7-8% yield of the total metabolites in both enzymatic systems, 7-Br-BA trans-3,4-dihydrodiol was formed 16.0 and 9.9% respectively, from the mouse and rat liver microsomal metabolism. In mutagenicity assays with the Salmonella typhimurium tester strain TA100 in the presence of S9 activation enzymes, both of these trans-3,4-dihydrodiols exhibited higher mutagenicity than 7-Cl-BA and 7-Br-BA, while the other trans-dihydrodiol metabolites were either essentially inactive or weaker than the parent compounds. These results suggest that 7-Cl-BA trans-3,4-dihydrodiol and 7-Br-BA trans-3,4-dihydrodiol are the proximate metabolites of 7-Cl-BA and 7-Br-BA. Metabolism of 7-Cl-BA and 7-Br-BA by mouse liver microsomes was also in a stereoselective manner, preferentially giving trans-dihydrodiol metabolites an R, R stereochemistry.

Animals↗
PubMed1997

7-Sulfooxymethylbenz[a]anthracene is an ultimate electrophilic and carcinogenic form of 7-hydroxymethylbenz[a]anthracene.

The hypothesis was tested that 7-sulfooxymethylbenz[a]anthracene (7-SBA) is an ultimate electrophilic and carcinogenic form of 7-hydroxymethylbenz[a]anthracene. In conformity with this hypothesis, 7-SBA was more carcinogenic than 7-HBA in inducing sarcomas at the site of repeated subcutaneous injection. These metabolites were individually administered to female Sprague-Dawley rats, beginning at 30 days of age, in 0.2 mumol doses given three times each week for 20 doses. One year after the first injection of 7-SBA, seven of thirteen female Sprague-Dawley rats had developed sarcomas. 7-HBA, on the other hand, had induced sarcomas at the site of injection in only two of tweleve rats. No tumors developed either in the control group given sesame oil:DMSO only or in the untreated control group. It would appear from the results summarized here that the search for an ultimate electrophilic and carcinogenic form of 7-HBA has been successful.

Animals↗
PubMed2001

Benzo(a)pyrene, benzo(a)anthracene, and dibenzo(a,h)anthracene emissions from coal and waste tire energy generation at atmospheric fluidized bed combustion (AFBC).

The main aim of this work was the analyzing of the release to the atmosphere of benzo[a]pyrene (BaP), dibenzo(a,h)anthracene (D(a,h)A), and benzo[a]anthracene (BaA), three of the most carcinogenic PAHs listed by US-EPA as priority pollutants, emitted from combustion at the last generation reactors used nowadays in power generation, fluidized bed reactors, trying to establish their incidence when waste materials are used as "new fuels". BaP, D(a,h)A, and BaA emissions, once collected in the sampling system, have been analyzed by fluorescence spectroscopy in the synchronous mode (FS) after extraction by ultrasonic bath with dimethylformamide (DMF) as solvent. Concerning to the combustion variables influence, the conclusion reached was that, in coal combustion, the lowest emissions of BaP are generated at percentages of excess oxygen of 20%, at flows corresponding to good fluidization conditions, 860 L/h (double of the minimum fluidization velocity) and temperatures out of 850 degrees C; the lowest emission of D(a,h)A are emitted at 20% excess oxygen, 900 L/h and out of 750 degrees C, and the lowest emission of BaA are generated at 20% excess oxygen, 860 L/h and out of the range 750-850 degrees C. Regarding tire as nonfossil fuel, higher emissions of BaP, BaA, and D(a,h)A are detected in comparison to coal combustion. In coal-tire blend, the BaP, BaA, and D(a,h)A emissions are more similar to the values obtained in coal combustion and not intermediate values as it could be expected by the blend composition.

Air Pollutants↗
PubMed1988

Synthesis of the tumorigenic 3,4-dihydrodiol metabolites of dibenz[a,j]anthracene and 7,14-dimethyldibenz[a,j]anthracene.

Syntheses are described of the trans-3,4-dihydrodiol derivatives (2a and 2b) of dibenz[a,j]anthracene and 7,14-dimethyldibenz[a,j]anthracene (1a and 1b), implicated as their proximate carcinogenic metabolites. Conversion of 2a to the bay region anti-diol epoxide derivative 3a, its putative ultimate carcinogenic metabolite, is also reported. The related diol epoxide derivative of 2b could not be prepared due to its chemical instability. Tumorigenicity assays confirm that 1b and 2b are potent carcinogens on mouse skin, while 1a and 2a are only relatively weakly active. The diol epoxide 3a exhibited significantly higher tumorigenicity than its dihydrodiol precursor 2a. These findings are consistent with the hypothesis that the bay region diol epoxide metabolites are the active carcinogenic forms of these hydrocarbons. They also support the generalization that methyl substitution in bay regions enhances the carcinogenic activity of polycyclic aromatic hydrocarbons.

Animals↗
PubMedDate not supplied

Comparative metabolism of dibenz[a,j]anthracene and 7-methyldibenz[a,j]anthracene in primary cultures of mouse keratinocytes.

The identification of several metabolites formed from dibenz[aj]anthracene (DB[aj]A) and 7-methyldibenz[aj]anthracene (7MeDB[aj]A) in primary cultures of mouse keratinocytes is presented. The metabolites were analyzed by coelution with known synthetic standards using high-pressure liquid chromatography. The metabolite identifications were further facilitated by comparisons of fluorescence excitation and emission spectra obtained for isolated metabolites with those for the synthetic standards. Both DB[aj]A and its 7-methyl analog were converted by mouse keratinocytes to the corresponding 3,4- as well as 5,6-dihydrodiols. The 5,6-dihydrodiol of DB[aj]A was the major intracellular metabolite found at all time points up to 24 h. By 48 h, the relative proportion of both intracellular dihydrodiols had decreased, and they were found in approximately equal proportions. In contrast, 7MeDB[aj]A-3,4- dihydrodiol was the major intracellular metabolite of 7MeDB[aj]A at all time points examined up to 48 h. The decreased intracellular retention of DB[aj]A-3,4-dihydrodiol was due, in part, to glucuronide conjugation and subsequent excretion of this metabolite. In this regard, both the 3,4- as well as the 5,6-dihydrodiols of DB[aj]A were found as glucuronides in the extracellular medium, whereas no such conjugates were detected extracellularly in cultures exposed to the 7-methyl derivative. The chromatographic profiles of cell- and medium-associated metabolites from both hydrocarbons also exhibited several other metabolite peaks that remain to be identified. The observed differences in dihydrodiol metabolism by mouse keratinocytes could explain, in part, the greater biological activity of 7MeDB[aj]A relative to DB[aj]A.

Animals↗
PubMed1981

Tumor-initiating activity of the dihydrodiols of 8-methylbenz[a]anthracene and 8-hydroxymethylbenz[a]anthracene.

The tumor-initiating activity of the 3,4-dihydrodiols (diols) as well as other metabolites of 8-methylbenz[a]anthracene (8-MBA) and 8-hydroxymethylbenz[a]anthracene (8-OHMBA) were examined in the classical 2-stage initiation-promotion model on mouse skin. The 3,4-diol of 8-MBA caused 2.2 times as many papillomas/mouse as did 8-MBA. The 3,4-diol of 8-OHMBA was not more tumorigenic than either 8-MBA or 8-OHMBA. None of the other diols tested, including the 5,6- and 8,9-diol of 8-MBA and the 5,6 and 10,11-diol of 8-OHMBA were remarkably tumorigenic. These data indicate that the 3,4-diol of 8-MBA is a good candidate as a proximate carcinogen of 8-MBA and further suggest that the bay region 3,4-diol-1,2-epoxide is a likely ultimate carcinogen of this compound on mouse skin.

Animals↗
PubMed1982

Metabolism of 7-methylbenz[a]anthracene and 7-hydroxymethylbenz[a]anthracene by Cunninghamella elegans.

The fungal metabolism of 7-methylbenz[a]anthracene (7-MBA) and 7-hydroxymethylbenz[a]anthracene (7-OHMBA) was studied. 7-MBA was metabolized by Cunninghamella elegans to form 7-OHMBA-trans-8,9-dihydrodiol and 7-OHMBA-trans-3,4-dihydrodiol as the predominant metabolites. Other metabolites were identified as 7-OHMBA, 7-MBA-trans-8,9-dihydrodiol and 7-MBA-trans-3,4-dihydrodiol, and 7-MBA-8,9,10,11-tetraol. Incubation of 7-OHMBA with C. elegans cells indicated that 7-OHMBA-trans-8,9-dihydrodiol and 7-OHMBA-trans-3,4-dihydrodiol were major metabolites. The metabolism of 7-MBA by rat liver microsomes from 3-methylcholanthrene-treated rats showed that the metabolites were qualitatively similar to those formed by C. elegans, except additional dihydrodiol metabolites were formed at the 5,6 and 10,11 positions. The metabolites formed were isolated by high-performance liquid chromatography and identified by comparing their chromatographic, UV-visible absorption and mass spectral properties with those of reference compounds.

Animals↗
PubMed1979

Comparison of metabolism-mediated binding to DNA of 7-hydroxymethyl-12-methylbenz(a)anthracene and 7, 12-dimethylbenz(a)anthracene.

Comparison of the binding to DNA of 7-hydroxymethyl-12-methylbenza(a)anthracene and 7, 12-dimethylbenz(a)anthracene (DMBA) catalyzed by mouse embryo cells in culture or by rat liver microsomes indicates that the products formed are different for the two hydrocarbons. Thus, the hydroxy compound is not an intermediate in the binding of DMBA to DNA in these systems. Binding of the hydroxy compound to DNA in mouse embryo cells is less efficient than for DMBA and is inhibited by 1,1,1-trichloropropylene 2,3-oxide, an inhibitor of epoxide hydrase. This and the fluorescence spectra of the hydroxy compound-DNA adducts indicate that the hydroxy compound is activated for DNA binding through the formation of a diol-epoxide in the 1,2,3,4-ring. As previously found for DMBA, this is consistent with the activation of this compound through a bay-region diol-epoxide.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1979

Tumorigenicity of the diastereomeric benz[a]anthracene 3,4-diol-1,2-epoxides and the (+)- and (-)-enantiomers of benz[a]anthracene 3,4-dihydrodiol in newborn mice.

The tumorigenic activity of benz[a]anthracene (BA), the (+)- and (-)-enantiomers of trans-3,4-dihydroxy-3,4-dihydrobenz[a]anthracene (BA 3,4-dihydrodiol), and the racemic diastereomers of the BA 3,4-diol-1,2-epoxides [i.e., either or both of the diastereomeric 1,2-epoxides derived from BA 3,4-dihydrodiol in which the epoxide oxygen is cis (diol epoxide-1) or trans (diol epoxide-2) to the benzylic 4-hydroxyl group) was examined in newborn Swiss-Webster mice. The mice were administered ip a total dose of 280 nmoles of compound in divided doses consisting of 40 nmoles within 24 hours of birth, 80 nmoles at 8 days of age, and 160 nmoles at 15 days of age. The experiment was terminated when the animals were 26 weeks of age. BA 3,4-diol-1,2-epoxide-2 was the most potent compound tested. All animals treated with BA 3,4-diol-1,2-epoxide-2 developed pulmonary tumors with an average of 13.3 tumors per mouse. BA 3,4-diol-1,2-epoxide-1 produced pulmonary tumors in 42% of the mice with an average of only 0.56 tumors per mouse. The (-)-enantiomer of BA 3,4-dihydrodiol with [3R,4R] absolute stereochemistry was the second most tumorigenic derivative of BA tested; it produced pulmonary tumors in 71% of the mice with an average of 1.88 tumors per mouse. BA and the (+)-enantiomer of BA 3,4-dihydrodiol had little or no tumorigenic activity at the dose tested. A comparison of the average number of pulmonary tumors per mouse revealed that BA 3,4-diol-1,2-epoxide-2 was about 30-fold more tumorigenic than was BA 3,4-diol-1,2-epoxide-1, 8-fold more tumorigenic than was (-)-BA 3,4-dihydrodiol, and greater than 85-fold more tumorigenic than was BA. These data indicate that in newborn mice BA 3,4-dihydrodiol and a BA 3,4-diol-1,2-epoxide are proximate and ultimate carcinogenic metabolites of BA, respectively.

Animals↗
PubMed1978

Dibenz[a,c]anthracene: a potent inhibitor of skin-tumor initiation by 7,12-dimethylbenz[a]anthracene.

The mechanism by which the weak tumor initiator dibenz[a,c]anthracene (DB[a,c]A) inhibits the skin-tumor-initiating activity of 7,12-dimethylbenz[a]anthracene (DMBA) was investigated. DB[a,c]A was found to be a potent inhibitor of DMBA initiation when given either 5 min, or 1, 12, or 36 hours before DMBA. Pretreatment of mice with unlabeled DB[a,c]A at either 1, 12, or 36 hours before killing increased the in vitro epidermally mediated covalent binding of [3H]DMBA to DNA more than pretreatment with unlabeled DMBA at comparable times. Only when the tumor experiments were mimicked did a decrease in DMBA covalent binding to DNA in vitro occur. The results suggests that some competition at the level of polycyclic hydrocarbon metabolism or at the genome level may exist between metabolites of the weak carcinogen and those of the strong carcinogen.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1979

Shapes of carcinogenic benz[a]anthracenes: the crystal and molecular structure of 1-methylbenz[a]anthracene.

The crystal structure of 1-methylbenz[a]lanthracene, which is weakly carcinogenic, has been determined by application of direct methods to single-crystal X-ray diffractometric data and refined by least squares to R = 0.09 over 845 independent reflections. Crystals are monoclinic, space group P2(1), with a = 8.491(2), b = 7.138(2), c = 10.500(2)ABEta = 95.06(01), Z = 2. As in other benz[a]anthracenes, the K-region bond C(5)-C(6) is short [1.34(1)A]. The distinctive bay geometry, with a methyl group opposite to a hydrogen, H(12), peri to another hydrogen, H(11), has a long bond C(13)--C(18) = 1.47(1)A in the bay, and the angular benz-ring is inclined at 16.5 degrees to the mean plane of the anthracene fragment. The methyl carbon atom is 0.79 A out of the mean molecular plane (or 0.19 A out of the plane of the benz-ring) and the 1.50 A long C(1)-methyl bond makes angles of 117 degrees and 125 degrees at C(1).

Benz(a)Anthracenes↗
PubMed1983

Formation of 7-hydroxymethyl-12-methylbenz(a)anthracene-DNA adducts from 7,12-dimethylbenz(a)anthracene in mouse epidermis.

The formation of DNA adducts from [3H]-7-hydroxymethyl-12-methylbenz(a)anthracene (7-OHM-12-MBA) and [3H]-7,12-dimethylbenz(a)anthracene (DMBA) in the epidermis of Sencar mice was analyzed. Comparison of Sephadex LH-20 chromatographic profiles of DNA samples isolated from mice treated with DMBA or 7-OHM-12-MBA suggested that the DMBA-treated animals contained DNA adduct(s) derived from the further metabolism of 7-OHM-12-MBA. Further analysis of DNA samples from DMBA-treated mice by high-pressure liquid chromatography demonstrated the presence of 5 DNA adducts which were chromatographically indistinguishable from the DNA adducts formed in 7-OHM-12-MBA-treated mice. Epidermal homogenates were utilized to catalyze the covalent binding of [3H]DMBA and [3H]-7-OHM-12-MBA to calf thymus DNA in vitro. Under conditions of limiting concentrations of [3H]DMBA, the majority of the DNA adducts formed chromatographed in regions where 7-OHM-12-MBA-DNA adducts eluted. A major DMBA-DNA adduct formed in this in vitro system eluted with the same retention time as did the major 7-OHM-12-MBA-DNA adduct formed in mouse skin in vivo. These results when coupled with the in vivo data suggest that 7-OHM-12-MBA is an intermediate for at least some of the binding of DMBA to epidermal DNA in Sencar mice.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1981

Metabolism of 7,12-dimethylbenz(a)anthracene and 7-hydroxymethyl-12-methylbenz(a)anthracene by rat liver and microsomes.

The metabolism of 7,12-[14C]dimethylbenz(a)anthracene ([14C]DMBA) and 7-[7-CH2-3H]hydroxymethyl-12-methylbenz(a)anthracene ([7-CH2-3H]7-OHM-12-BMA) by rat liver nuclei and microsomes was studied by high-performance liquid chromatography. DMBA and 7-OHM-12-MBA are metabolized at methyl group(s) and at the aromatic ring carbons to form trans-dihyrodiols at positions 3, 4, 5, 6, 8, 9, and 10,11 and phenols at positions 2, 3, and 4 by both nuclear and microsomal enzymes. Both nuclear and microsomal monooxygenase enzyme activities were inducible by pretreatment of the animals with phenobarbital or 3-methylcholanthrene. The rates of formation of all metabolites by microsomes were five- to 20-fold higher than those by nuclei in metabolizing DMBA or 7-OHM-12-MBA. The presence of a hydroxyl group at the 7-methyl position of DMBA markedly decreased the rate of metabolism. The rate of total metabolism of 7-OHM-12-MBA was only 20 to 70% of that of DMBA under identical in vitro incubation conditions. The 3-methylcholanthrene- and phenobarbital-induced enzymes showed a significantly different regioselectivity toward the metabolism of DMBA or 7-OHM-12-MBA and are attributed to different forms of cytochrome P-450 present in the enzyme preparations.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1976

In vitro malignant transformation of mouse fibroblasts by non-K-region dihydrodiols derived from 7-methylbenz(a)anthracene, 7,12-dimethylbenz(a)anthracene, and benzo(a)pyrene.

The 8,9-dihydrodiols of 7-methylbenz(a)anthracene and 7,12-dimethylbenz(a)anthracene and the 7,8-dihydrodiol of benzo(a)pyrene, which are non-K-region diols with adjacent olefinic double bonds that can be metabolized to diol-epoxides, were more active than the parent hydrocarbons in inducing malignant transformation of M2 mouse fibroblasts; a fourth non-K-region diol, the 9,10-dihydrodiol of benzo(a)pyrene was less active than benzo(a)pyrene. The related K-region dihydrodiols, which lack adjacent olefinic double bonds, and 6-hydroxybenzo(a)pyrene were inactive, 7,8-Dihydrobenzo(a)pyrene, a more potent carcinogen than the 9,10 isomer, induced malignant transformation, but the 9,10 isomer was inactive. Transformed cells with abnormal morphology yielded sarcomas on injection into isologous mice; treated but morphologically normal cells did not. These results support the role of diols and diol-epoxides in the metabolic activation of polycyclic hydrocarbons.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1978

Formation of glucuronic acid conjugates of 7,12-dimethylbenz(a)anthracene phenols in 7,12-dimethylbenz(a)anthracene-treated hamster embryo cell cultures.

Secondary cultures of hamster embryo cells exposed to 0.5 nmol [G-3H]7,12-dimethylbenz(a)anthracene (DMBA) per ml medium metabolized more than 90% of the DMBA within 48 hr. Samples of medium were extracted with chloroform, methanol, and water. The chloroform phases contained about one-third of the DMBA metabolites; the major chloroform-extractable metabolite was 8,9-dihydro-8,9-dihydroxy-7,12-dimethylbenz(a)anthracene. Beta-glucuronidase treatment of the aqueous methanol-soluble metabolites converted almost one-half of them to chloroform-soluble metabolites, of which more than 80% were identified as phenolic derivatives of DMBA. Similar metabolite profiles were obtained by treating the medium with beta-glucuronidase before chloroform extraction. Separation of the methyl group-hydroxylated derivatives of DMBA from the phenolic derivatives was accomplished by high-pressure liquid chromatography. Small amounts of hydroxymethyl derivatives were detected only in the chloroform-extractable material, whereas DMBA phenols were the major component of the beta-glucuronidase-released mateirla. These results indicate that the major pathway of DMBA metabolism in hamster embryo cells is oxidation of the aromatic rings and not oxidation of the methyl groups.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1992

beta-Carotene-mediated inhibition of a DNA adduct induced by 7,12-dimethylbenz(a)anthracene and 7-hydroxymethyl-12-methylbenz(a)anthracene in mouse mammary gland in vitro.

The influence of beta-carotene on the formation of DNA-adducts induced by 7,12-dimethylbenz(a)anthracene (DMBA) and 7-hydroxymethyl-12-methylbenz(a)anthracene (7-OHM-12-MBA) during transformation of mouse mammary cells in organ culture was analysed. Treatment with beta-carotene (10(-8)-10(-5) mol/l) caused inhibition (48.8-94.4%) of an adduct (VI), which was detectable in DNA samples from DMBA-treated mammary glands. Out of six adducts, derived from further analysis of DNA samples from 7-OHM-12-MBA-treated glands, adduct f eluted in the same fraction as adduct (VI), indicating these adducts were analogous. Likewise, adduct f was also inhibited by beta-carotene. Boronate chromatographic analysis revealed this particular adduct was a syn-dihydrodiol epoxide product. Adduct inhibition was detectable both at the start and after DMBA treatment. alpha-Tocopherol and canthaxanthin were ineffective in inhibiting adducts. It is reasonable to conclude that beta-carotene-mediated modification of adducts is associated with the inhibition of a syn-adduct, which is derived from further metabolism of a 7-OHM-12-MBA intermediate.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed2004

Photoaddition of water and alcohols to the anthracene moiety of 9-(2'-hydroxyphenyl)anthracene via formal excited state intramolecular proton transfer.

The title compound undergoes efficient photoaddition of a molecule of a hydroxylic solvent (H(2)O, MeOH, (Me)(2)CHOH) across the 9- and 10-positions of the anthracene moiety to give isolable triphenylmethanol or triphenylmethyl ether type products. The reaction is believed to proceed via a mechanism involving water-mediated formal excited state intramolecular proton transfer (ESIPT) from the phenolic OH to the 10-position of the anthracene ring, generating an o-quinone methide intermediate that is observable by nanosecond laser flash photolysis, and is trappable with nucleophiles. A "water-relay" mechanism for proton transfer seems plausible but cannot be proven directly with the data available. Irradiation in deuterated solvents led to incorporation of one deuterium atom at the methylene position in the photoaddition product, and partial deuterium exchange of the 10-position of recovered starting material, consistent with the proposed formal excited state proton transfer mechanism. The deuterium exchange and photoaddition reach maximum quantum efficiency at approximately 5 M water (in CH(3)CN or CH(3)OH), with no reaction observed in the absence of a hydroxylic solvent, demonstrating the sensitivity of this type of ESIPT to solvent composition.

Journal Article↗