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At least 19 recordsLinked to original sources
PubMed1991

Microbial metabolism of quinoline and related compounds. XII. Isolation and characterization of the quinoline oxidoreductase from Rhodococcus spec. B1 compared with the quinoline oxidoreductase from Pseudomonas putida 86.

Quinoline oxidoreductase from Rhodococcus spec. B1 was purified 39-fold to apparent homogeneity in a 5-step procedure with a recovery of 26%. The Mr of the native enzyme as determined by gel chromatography was 300,000. SDS polyacrylamide gel electrophoresis of the enzyme revealed 3 protein bands corresponding to Mr 82,000, 32,000, and 18,000. The enzyme contains 1.3 atoms of molybdenum, 8 atoms of iron, 8 atoms of acid-labile sulphur, 2 molecules of FAD and 2 molecules of molybdopterin cytosine dinucleotide. Cyanide, 4-hydroxymercuribenzoate and methanol were effective as inhibitors. The amino-terminal protein sequences of the 3 subunits of quinoline oxidoreductase from Rhodococcus B1 compared to those of quinoline oxidoreductase from Pseudomonas putida 86 revealed no difference among 71 amino acids examined.

Amino Acid Sequence↗
PubMed1983

Identification of the metabolites of benzo[f]quinoline and benzo[h]quinoline formed by rat liver homogenate.

Benzo[f]quinoline and benzo[h]quinoline are widespread environmental pollutants which have been found to be mutagenic. The metabolism of benzo[f]quinoline and benzo[h]quinoline was investigated using a liver homogenate from Aroclor-pretreated rats. The metabolites of benzo[f]quinoline which were identified were 7,8-dihydroxy-7,8-dihydrobenzo[f]quinoline, 9,10-dihydroxy-9,10-dihydrobenzo[f]quinoline, 7-hydroxybenzo[f]quinoline, and benzo[f]quinoline-N-oxide. Metabolism studies on benzo[f]quinoline performed in the presence of the epoxide hydratase inhibitor, 3,3,3-trichloropropylene oxide, demonstrated that the formation of both of these dihydrodiols can be inhibited. The major metabolites of benzo[h]quinoline were identified as 5,6-dihydroxy-5,6-dihydrobenzo[h]quinoline and 7,8-dihydroxy-7,8-dihydrobenzo[h]quinoline. Benzo[h]quinoline-N-oxide was not detected as a metabolite. In the presence of an epoxide hydratase inhibitor, the major metabolites of benzo[h]quinoline were 5,6-epoxybenzo[h]quinoline and 7-hydroxybenzo[h]quinoline. The difference in the metabolism to N-oxides observed between benzo[h]quinoline and benzo[f]quinoline is consistent with previous observations in which sterically hindered aromatic ring nitrogen compounds such as benzo[h]quinoline are more resistant to N-oxide formation. The nitrogen atom of these aza-arenes with its lone pair of electrons has a significant influence on sites at which dihydrodiols are formed. The data suggest that the aromatic ring nitrogen of these azaphenanthrenes has an effect similar to that of a methyl substituent in directing their metabolic oxidation.

Animals↗
PubMed1989

Mutagenicity and tumorigenicity of dihydrodiols, diol epoxides, and other derivatives of benzo(f)quinoline and benzo(h)quinoline.

The mutagenic activities of benzo[f]quinoline, benzo[h]quinoline, and a number of their derivatives, including dihydrodiols, K-region oxides, diol epoxides, and tetrahydroepoxides, were assessed in strain TA 100 of Salmonella typhimurium. The dihydrodiol derivatives of benzo[f]quinoline and benzo[h]quinoline were also tested for tumorigenic activity in newborn mice. Benzo[f]quinoline was metabolically activated in the presence of rat liver S-9 preparation to products mutagenic to the bacterial system to a greater extent than was benzo[h]quinoline. However, trans-7,8-dihydro-7,8-dihydroxybenzo[f]quinoline was less mutagenic compared to trans-7,8-dihydroxy-7,8-dihydrobenzo[h]quinoline in the presence of rat liver homogenate. The data on the mutagenic activity of the dihydrodiol derivatives of benzoquinolines were consistent with the intrinsic mutagenicity of the corresponding epoxide derivatives, in that the bay-region diol epoxides and tetrahydroepoxide of benzo[h]quinoline exhibited considerably higher mutagenic activities compared to those of the corresponding derivatives of benzo[f]quinoline at equivalent doses. The K-region oxides of benzo[f]quinoline and benzo[h]quinoline were significantly less mutagenic than their corresponding bay-region diol epoxide and tetrahydroepoxide derivatives. The demonstration that benzo[f]quinoline is significantly more mutagenic than trans-7,8-dihydro-7,8-dihydroxybenzo[f]quinoline, a precursor to the weakly mutagenic bay-region diol epoxide, suggests that the bay-region diol epoxide formation is not the principal pathway for the metabolic activation of benzo[f]quinoline to a mutagen. On the other hand, the isomeric benzo[h]quinoline appears to exert its mutagenic effect via the formation of its bay-region diol epoxide. These results indicate that the position of a nitrogen heteroatom in phenanthrene (the analogous carbocyclic aromatic hydrocarbon) not only has a marked effect on the mutagenic activities of the diol epoxide derivatives, but also can alter the metabolic activation pathways of the parent hydrocarbon. Benzo[f]quinoline, benzo[h]quinoline, and their dihydrodiol derivatives were not tumorigenic in newborn mice.

Animals↗
PubMed1994

Structure-mutagenicity relationships in series of 11H-indolo[3,2-c]quinoline-1,4-diones, tetrahydro-11H-indolo[3,2-c]quinoline-1,4-diones and 11H-pyrido[3',4':4,5]pyrrolo[3,2-c]quinoline-1,4-diones with leukemia cytotoxic properties. Relations with topoisomerase I inhibiting properties.

Six heterocyclic quinones with topoisomerase I inhibiting properties and cytotoxic activities on L1210 leukemia cells were studied for their mutagenicity in four strains of Salmonella typhimurium. The tested compounds are 3-methoxyindolo[3,2-c]quinoline-1,4-diones and their derivatives in which the common pyrroloquinoline nucleus is annelated either with a benzene or a cyclohexane on a pyridine ring. Almost all quinones were found to be direct-acting mutagens at different levels in all strains, mainly TA97a and TA98. Relations were established between their structure and their mutagenic activities. The mutagenicity was found to be influenced (i) by the nature of the fourth nucleus: the pyridinic compounds were the most active, the non-aromatic ones were practically inactive; (ii) by the presence of a methyl group in the 6-position that decreased the mutagenicity. Then, the mutagenic properties were compared with the topoisomerase I inhibiting property that is one of the possible mechanisms of action for these cytotoxic quinones. The results indicated a correlation between mutagenicity and enzyme inhibiting properties.

Animals↗
PubMed1992

Comparison of the mutagenicity of quinoline and all monohydroxyquinolines with a series of arene oxide, trans-dihydrodiol, diol epoxide, N-oxide and arene hydrate derivatives of quinoline in the Ames/Salmonella microsome test.

Fourteen new quinoline derivatives were synthesised and their mutagenicity compared in the Ames test using Salmonella typhimurium TA100 as indicator strain with and without (Aroclor-induced) S9 mix. None of the synthesised quinoline derivatives had to our knowledge been examined before in the Ames test. Quinoline and the monohydroxyquinolines were included as reference compounds. Three of the new derivatives, i.e., quinoline 7,8-oxide, N-methyl-quinoline 5,6-oxide and trans-quinoline-5,6,7,8-dioxide appeared to be mutagenic. Quinoline 7,8-oxide was positive only in the presence of S9 mix, the specific mutagenicity amounting to 2498 +/- 96 and 1289 +/- 120 revertants per mumole with 20 and 10% S9 in the mix, respectively. Both N-methyl-quinoline 5,6-oxide and trans-quinoline-5,6,7,8-dioxide were weakly positive, the former only in the presence of the S9 mix, and the latter irrespective of the presence of S9 mix, the specific mutagenicity amounting to 134 +/- 6 and 123 +/- 10 revertants per mumole, respectively. The mutagenic potency of quinoline 7,8-oxide was of the same order as that of quinoline itself and was distinctly lower than that of 8-hydroxyquinoline. Inconclusive results were obtained with trans-7,8-dihydroxy-7,8-dihydroquinoline, 5,6-dihydroxy-7,8-epoxy-5,6,7,8-tetrahydroquinoline and 8-hydroxyquinoline-N-oxide; if these compounds are mutagenic their mutagenic potency would be at least 20-30 times lower than that of the parent compounds. None of the other chemically synthesised quinoline derivatives showed mutagenic activity with TA100 either in the presence or in the absence of S9 mix. The results obtained with the reference compounds were in accordance with literature data.

Animals↗
PubMed2004

Fungal biotransformation of benzo[f]quinoline, benzo[h]quinoline, and phenanthridine.

Cultures of Umbelopsis ramanniana (=Mucor ramannianus) were grown in fluid Sabouraud medium for 3 days, dosed with 0.23 mM benzo[f]quinoline, benzo[h]quinoline, or phenanthridine (benzo[c]quinoline), and incubated for another 18 days. Cultures were extracted and metabolites (66-75% of the UV absorbance) were separated by high-performance liquid chromatography. They were identified by mass spectrometry and nuclear magnetic resonance spectroscopy. Benzo[f]quinoline was metabolized to benzo[f]quinoline trans-7,8-dihydrodiol, benzo[f]quinoline N-oxide, and 7-hydroxybenzo[f]quinoline, benzo[h]quinoline was metabolized to benzo[h]quinoline trans-5,6-dihydrodiol, benzo[h]quinoline trans-7,8-dihydrodiol, and 7-hydroxybenzo[h]quinoline, and phenanthridine was metabolized to phenanthridine N-oxide and phenanthridin-6(5H)-one. At least one of the metabolites produced from each compound was mutagenic and could not be considered detoxified.

Biotransformation↗
PubMed2001

Structure, stability, and interconversion barriers of the rotamers of cis-[Pt(II)Cl(2)(quinoline)2] and cis-[Pt(II)Cl(2)(3-bromoquinoline)(quinoline)] from X-ray crystallography, NMR spectroscopy and molecular mechanics evidence.

Reported are the preparations of cis-[PtCl(2)(quinoline)(2)] and cis-[PtCl(2)(3-bromoquinoline)(quinoline)] and an investigation of the stabilities and interconversion of the rotamer forms of these complexes. Both head-to-head (HTH) and head-to-tail (HTT) rotamer forms are found in the crystal structure of cis-[PtCl(2)(quinoline)(2)]. The NOESY NMR spectrum of cis-[PtCl(2)(quinoline)(2)] in dmf-d(7) at 300 K is consistent with conformational exchange brought about by rotation about the Pt-N(quinoline) bonds. H.H nonbonded distances between H atoms of the two different quinoline ligands were determined from NOESY data, and these distances are in accord with those observed in the crystal structure and derived from molecular mechanics models. cis-[PtCl(2)(3-bromoquinoline)(quinoline)] was prepared to alleviate the symmetry-imposed absence of inter-ring H2/H2 and H8/H8 NOESY cross-peaks for cis-[PtCl(2)(quinoline)(2)]. Molecular mechanics calculations on the complexes show the HTT rotamers to be 1-2 kJ mol(-)(1) more stable than the HTH forms, consistent with the (1)H spectra where the intensities of resonances for the two forms are approximately equal. Variable-temperature (1)H NMR spectra of cis-[PtCl(2)(quinoline)(2)] in dmf-d(7) indicate a rotational energy barrier of 82 +/- 4 kJ mol(-)(1). Variable-temperature (1)H NMR spectra indicate that the Br substituent on the quinoline ring does not affect the energy barrier to interconversion between the HTT and HTH forms (79 +/- 5 kJ mol(-)(1)). The steric contribution to the rotation barrier was calculated using molecular mechanics calculations and was found to be approximately 40 kJ mol(-)(1), pointing to a possible need for an electronic component to be included in future models.

Journal Article↗
PubMed2005

Synthesis and anticancer evaluation of certain 4-anilinofuro[2,3-b]quinoline and 4-anilinofuro[3,2-c]quinoline derivatives.

Certain linear 4-anilinofuro[2,3-b]quinoline and angular 4-anilinofuro[3,2-c]quinoline derivatives were synthesized and evaluated in vitro against the full panel of NCI's 60 cancer cell lines. For the linear 4-anilinofuro[2,3-b]quinoline derivatives, 1-[4-(furo[2,3-b]quinolin-4-ylamino)phenyl]ethanone (5a) is the most cytotoxic with a mean GI50 value of 0.025 microM. Substitution at either furo[2,3-b]quinoline ring (2a, 2b, and 5b) or 4-anilino moiety (3-7) led to a decrease of cytotoxicity. For the angular 4-anilinofuro[3,2-c]quinoline derivatives, (E)-1-[3-(furo[3,2-c]quinolin-4-ylamino)phenyl]ethanone oxime (14a) exhibited potent inhibitory activities on UO-31, UACC-257, and UACC-62, with GI50 values of 0.03,<0.01, and<0.01 microM respectively. The same cytotoxicity profile was observed for its methyl counterpart, 14b, in which the GI50 values against UO-31, UACC-257, and UACC-62 was<0.01, 0.04 and<0.01 microM respectively. These results deserve full attention especially because 14a and 14b are relatively non-cytotoxic with the mean GI50 value of 7.73 and 8.91 microM respectively.

Antineoplastic Agents↗
PubMed1989

Microbiological degradation of quinoline by Pseudomonas stutzeri: the coumarin pathway of quinoline catabolism.

A Gram-negative, oxidase positive, polar flagellated rod, characterised as Pseudomonas stutzeri, has been isolated from sewage by enrichment culture on quinoline. The organism utilizes quinoline as the sole source of carbon, nitrogen and energy, and liberates UV absorbing and phenolic metabolites during its growth on quinoline. 2-Hydroxyquinoline, 2,8-dihydroxyquinoline, 8-hydroxycoumarin and 2,3-dihydroxyphenylpropionic acid have been isolated as the transformation products of quinoline by this bacterium. Quinoline, 2-hydroxyquinoline, and 8-hydroxycoumarin were rapidly oxidised by quinoline-adapted cells; 2,3-dihydroxyphenylpropionic acid oxidation was also demonstrated by Warburg respirometry but 2,8-dihydroxyquinoline was not oxidised. A pathway for quinoline catabolism by P. stutzeri and the probable mechanisms for formation of 8-hydroxycoumarin are suggested.

Biodegradation, Environmental↗
PubMed2003

Quinolinate dehydrogenase and 6-hydroxyquinolinate decarboxylase involved in the conversion of quinolinic acid to 6-hydroxypicolinic acid by Alcaligenes sp. strain UK21.

In the conversion of quinolinic acid to 6-hydroxypicolinic acid by whole cells of Alcaligenes sp. strain UK21, the enzyme reactions involved in the hydroxylation and decarboxylation of quinolinic acid were examined. Quinolinate dehydrogenase, which catalyzes the first step, the hydroxylation of quinolinic acid, was solubilized from a membrane fraction, partially purified, and characterized. The enzyme catalyzed the incorporation of oxygen atoms of H(2)O into the hydroxyl group. The dehydrogenase hydroxylated quinolinic acid and pyrazine-2,3-dicarboxylic acid to form 6-hydroxyquinolinic acid and 5-hydroxypyrazine-2,3-dicarboxylic acid, respectively. Phenazine methosulfate was the preferred electron acceptor for quinolinate dehydrogenase. 6-Hydroxyquinolinate decarboxylase, catalyzing the nonoxidative decarboxylation of 6-hydroxyquinolinic acid, was purified to homogeneity and characterized. The purified enzyme had a molecular mass of approximately 221 kDa and consisted of six identical subunits. The decarboxylase specifically catalyzed the decarboxylation of 6-hydroxyquinolinic acid to 6-hydroxypicolinic acid, without any co-factors. The N-terminal amino acid sequence was homologous with those of bacterial 4,5-dihydroxyphthalate decarboxylases.

Alcaligenes↗
PubMed2005

Synthesis and cytotoxic evaluation of certain 4-(phenylamino)furo[2,3-b]quinoline and 2-(furan-2-yl)-4-(phenylamino)quinoline derivatives.

Certain 4-(phenylamino)furo[2,3-b]quinoline and 2-(furan-2-yl)-4-(phenylamino)quinoline derivatives were synthesized and evaluated in vitro against the full panel of NCIs 60 cancer cell lines. The preliminary results indicated these tricyclic 4-(phenylamino)furo[2,3-b]quinolines were more cytotoxic than their corresponding 2-(furan-2-yl)-4-(phenylamino)quinoline isomers. For the 4-(phenylamino)furo[2,3-b]quinolines, compounds 2a and 3d are two of the most potent with a mean GI50 value of 0.025 microM in each case. Inactivity of 2b and 2c (positional isomers of 2a) indicated that both electronic environment, and the distance between intercalating pharmacophore and H-bond-donating MeO group are important. For the 2-(furan-2-yl)-4-(phenylamino)quinoline isomers, compound 12 (a mean GI50 of 4.36 microM), which bears a para-COMe substituent, is more active than its meta-substituted counterpart 13 (10.5 microM). However, the electron-donating MeO substituent is preferred at the meta-position, and the cytotoxicity for the meta-substituted derivatives decreased in the order: MeO derivative 14b (3.05 microM) > oxime 16 (6.85 microM) > ketone 13 (10.5 microM) > methyl oxime 18 (20.6 microM).

Aniline Compounds↗
PubMed2000

Some biological properties of new quinoline-4-carboxylic acid and quinoline-4-carboxamide derivatives.

The antimicrobial and morphogenetic effects of fourteen newly synthesized 2-substituted derivatives of quinoline-4-carboxylic acid and quinoline-4-carboxamide were studied using G+ and G- bacteria, yeasts and filamentous fungi. The highest antimicrobial effects were found with substituted quinoline-4-carboxylic acid derivatives. Quinoline-4-carboxamides only weakly influenced the growth of the tested microorganisms. Some derivatives of quinoline-4-carboxylic acid elicited profound changes in the morphology of hyphal tips of Botrytis cinerea, mainly their branching and the release of the cytoplasmic content. Quinoline derivatives, which elicited morphological changes, increased also the permeability of the plasmalemma of plant cells.

Anthocyanins↗
PubMed2000

Synthesis and antitumor cytotoxicity evaluation of pyrido[4,3,2-de]quinolines and isoquinolino[6,5,4,3-cde]quinolines.

A series of novel pyrido[4,3,2-de]quinoline and isoquinolino[6,5,4,3-cde] quinoline compounds was synthesized and evaluated for cytotoxicity in the National Cancer Institute developmental therapeutics program. The tricyclic compound 7 was synthesized by the cyclization of 3,4-diamino-1,2dimethoxybenzene with diethyl 1,3-acetonedicarboxylate. Oxidation of monochloropyrido[4,3,2-de]quinoline 8 selectively produced 2,3-diketopyrido[4,3,2-de]quinoline 9 as deep violet crystals. Compound 9, when treated with acetone or acetophenone, affords the tetracyclic isoquinolino[6,5,4,3-cde]quinolines 13 and 14, respectively. 2,3-Diketopyrido[4,3,2-de]quinolines 9 and 10 exhibit higher cytotoxic potency than isoquinolino[6,5,4,3-cdelquinolines 13, 14, 15 and 16. Compound 9 selectively affects the cell growth against leukemia CCRF-CEM and HL-60 cell lines, the non-small cell lung cancer HOP-92 cell line, and breast cancer MDA-MB231/ ATCC and MDA-MB- 435 cell lines with GI(50) values of <2.0 microM. Modification of compound 9 with an ester group at the N-1 position afforded compound 10, which exhibits a wide spectrum of anticancer activities with a mean graph midpoint value of 1.8 microM against the 60 cancer cell lines.

Antineoplastic Agents↗
PubMed1983

II. Pharmacological studies with derivatives of 2-aminotetralin, benzhydro[f]quinoline, benzhydro[g]quinoline, apomorphine and clonidine suggest a pharmacological dissimilarity between peripheral presynaptic dopamine receptors and alpha-2 adrenoceptors.

This study demonstrates that presynaptic dopamine receptors and alpha-2 adrenoceptors are pharmacologically different. A series of 2-aminotetralins, benzhydro[f]quinolines, benzhydro[g]quinolines, apomorphine and clonidine were studied to determine if they could stimulate presynaptic alpha-2 adrenoceptor and dopamine receptors. Presynaptic dopamine receptor activity was observed in di- and monohydroxy derivatives of 2-aminotetralins, dihydroxy derivatives of benzohydro[f]quinolines and benzohydro[g]quinolines and apomorphine. The greatest presynaptic dopamine receptor activity was observed with agents which maintained the dopamine moiety in the trans coplanar conformation. In contrast to these observations 1) monohydroxy derivatives of 2-aminotetralines were devoid of presynaptic alpha-2 adrenoceptor activity and 2) both cis and trans isomers of dihydroxy derivatives of benzohydro[f]quinolines and benzohydro[g]quinolines exhibited significant presynaptic alpha-2 adrenoceptors activity. These data suggest that presynaptic alpha-2 adrenoceptors and dopamine receptors represent separate functional entities. A discussion on the structure activity relationship associated with presynaptic alpha-2 adrenoceptor and dopamine receptor is provided.

Animals↗
PubMed1972

De novo biosynthesis of nicotinamide adenine dinucleotide in Escherichia coli: excretion of quinolinic acid by mutants lacking quinolinate phosphoribosyl transferase.

The excretion of quinolinic acid was studied in growing and resting cells of Escherichia coli K-12 nadC(13). Under optimal conditions, this organism could synthesize quinolinic acid in several-fold excess of the amount which would be required for normal growth. The excretion of quinolinic acid was controlled by the concentration of nicotinamide adenine dinucleotide (NAD) precursors available to the organism either during growth or during incubation in dense cell suspensions. These observations suggest that biosynthesis of NAD de novo is regulated by both repression and feedback inhibition. Analogues of niacin which inhibit bacterial growth also inhibited and repressed the synthesis (excretion) of quinolinic acid. The pH optimum for quinolinic acid excretion agreed favorably with the optimum observed for its synthesis in vitro. The rate of quinolinic acid excretion was strongly influenced by the concentration of ribose or glycerol in the medium.

Amino Acids↗
PubMed1988

Localization of quinolinic acid metabolizing enzymes in the rat brain. Immunohistochemical studies using antibodies to 3-hydroxyanthranilic acid oxygenase and quinolinic acid phosphoribosyltransferase.

Specific antibodies raised in rabbits against 3-hydroxyanthranilic acid oxygenase (EC 1.13.11.6) and quinolinic acid phosphoribosyltransferase (EC 1.13.11.6) and quinolinic acid phosphoribosyltransferase (EC 2.4.2.19) were used in immunohistochemical studies to map the cellular localization of the quinolinic acid metabolizing enzymes in the adult male rat brain. 3-Hydroxyanthranilic acid oxygenase immunoreactivity was found to be present in glial cells of presumed astroglial identity, as judged by co-localization with glial fibrillary acidic protein. 3-Hydroxyanthranilic acid oxygenase-immunoreactive glial cells were present in all brain regions and within major fiber tracts. The density of 3-hydroxyanthranilic acid oxygenase-immunoreactive glial cells as well as the intensity of staining of these cells differed among brain regions. In general, telencephalic acid diencephalic areas harbored a larger number of 3-hydroxyanthranilic acid oxygenase-positive cells than did mesencephalic regions. In the former regions the caudate nucleus, septum, nucleus accumbens, neocortex and hippocampus were particularly enriched in 3-hydroxyanthranilic acid oxygenase-immunoreactive cells. In the thalamus, regional differences were noted with regard to the intensity of staining among glial cells with high densities of 3-hydroxyanthranilic acid oxygenase cells in the anteroventral, reticular and ventromedial nuclei. In the inferior and superior colliculi, numerous 3-hydroxyanthranilic acid oxygenase-positive glial cells were found in all layers. In the hypothalamus, 3-hydroxyanthranilic acid oxygenase-immunoreactive glial cells were encountered in the zona incerta, the lateral hypothalamic area, the caudal preoptic region and in the dorsomedial nucleus. In the mesencephalon, the substantia nigra contained numerous, moderately stained cells. At caudal levels of the brain-stem, a relatively large number of cells was detected in the nucleus of the solitary tract, the pontine nucleus and in the fascial nerve nucleus, while other nuclei, such as the reticular formation and the area postrema were relatively poor in 3-hydroxyanthranilic acid oxygenase-immunoreactive cells. In addition to staining of glial cells, neuronal cell bodies containing 3-hydroxyanthranilic acid oxygenase immunoreactivity were detected in the main and in the accessory olfactory bulb, as well as in the ventromedial nucleus of the hypothalamus. Quinolinic acid phosphoribosyltransferase immunoreactivity was observed within glial cells and in association with neuronal cell bodies. Some, but not all, quinolinic acid phosphoribosyltransferase positive glial cells contained glial fibrillary acidic protein (Köhl

3-Hydroxyanthranilate 3,4-Dioxygenase↗