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1

Mclntyre, G. S., and R. H. Gooding. "Variation in the pteridine content in the heads of tsetse flies (Diptera: Glossinidae: Glossina Wiedemann): evidence for genetic control." Canadian Journal of Zoology 74, no. 4 (1996): 621–26. http://dx.doi.org/10.1139/z96-071.

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The pteridine content of the head capsule of teneral flies from 11 genetically selected lines (including eye-color mutants) of Glossina morsitans morsitans Westwood and Glossina palpalis palpalis Robineau-Desvoidy was examined using fluorescence spectroscopy. Wild-type G. p. palpalis had a greater pteridine content than did wild-type G. m. morsitans. Within G. m. morsitans there was a 25% variation in fluorescence values between genetic lines. Wild-type G. p. palpalis had the same pteridine content as brick mutants but more than tan mutants; in G. m. morsitans the salmon mutants had a higher pteridine content than did wild-type flies. Pteridine content did not account for the difference in eye color between male and female brick mutants. Accumulation of pteridines was not influenced by genotype in young flies, but in older flies salmon mutants accumulated pteridines more rapidly than did wild-type flies. Young flies, both wild type and salmon, accumulated pteridines more rapidly than did old flies. The results of the analysis of head capsule fluorescence in males from the parental lines and F1 and F2 generations of reciprocal crosses of the G. m. morsitans lines with the highest and lowest pteridine contents revealed that genetic control of pteridine content lies on the X chromosome and on one autosome.
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2

Burton, Casey, and Yinfa Ma. "The role of urinary pteridines as disease biomarkers." Pteridines 28, no. 1 (2017): 1–21. http://dx.doi.org/10.1515/pterid-2016-0013.

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AbstractPteridines and their derivatives function as intermediates in the metabolism of several vitamins and cofactors, and their relevance to disease has inspired new efforts to study their roles as disease biomarkers. Recent analytical advances, such as the emergence of sensitive mass spectrometry techniques, new workflows for measuring pteridine derivatives in their native oxidation states and increased multiplexing capacities for the simultaneous determination of many pteridine derivatives, have enabled researchers to explore the roles of urinary pteridines as disease biomarkers at much lower levels with greater accuracy than with previous technologies or methods. As a result, urinary pteridines are being increasingly studied as putative cancer biomarkers with promising results being reported from exploratory studies. In addition, the role of urinary neopterin as a universal biomarker for immune system activation is being investigated in new diseases where it is anticipated to become a useful supplementary marker in clinical diagnostic settings. In summary, this review provides an overview of recent developments in the clinical study of urinary pteridines as disease biomarkers, covers the most promising aspects of advanced analytical techniques being developed for the determination of urinary pteridines and discusses the major challenges associated with implementing pteridine biomarkers in clinical laboratory settings.
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3

Goldberg, M., F. Gassner, and M. Merkenschlager. "Studies and Comparison of Urinary Pteridine Patterns in Dogs and Cats and their Alteration in Various Neoplasias and Virus Infections." Pteridines 1, no. 1 (1989): 29–35. http://dx.doi.org/10.1515/pteridines.1989.1.1.29.

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Summary Urinary excretion levels of five pteridines in healthy cats and dogs and in 14 groups of animals with tumours or virus infections were determined by HPLC after partial purification by ion exchange chromatography. Healthy cats and dogs produce species specific differences. In contrary to cats 6-hydroxymethylpterin was not detectable in dogs. Whereas in dogs biopterin presents the main part of pteridines (about 70%), cats contain about 53% catabolic isoxanthopterin in the pteridine pattern. In the various tumours no qualitative but quantitative alterations in the pteridine concentrations could be detected. The changes in the different tumours were not applied to all pteridines, so that each type of tumour shows an own pattern of pteridines.In the parvovirosis of the dog neopterin, biopterin and isoxanthopterin increased significantly. In the virusfree parvovirosis suspicious dogs only pterin was elevated. In the feline leucosis and feline infectious peritonitis a significant rise of all five measured pteridines were observed.Altogether, the data show, that increased urinary pteridines present a real additional aid for the suspicion of neoplasias or viral infections in the veterinary medicine.
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4

Girgin, Gözde, Terken Baydar, Dietmar Fuchs, Gönül Sahin, Elif Özmert, and Kadriye Yurdakök. "Evaluation of Serum and Urinary Levels of some Pteridine Pathway Components in Healthy Turkish Children." Pteridines 23, no. 1 (2012): 90–95. http://dx.doi.org/10.1515/pteridines.2012.23.1.90.

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Abstract Neopterin, as a non-conjugated pteridine, is synthesized from guanosine triphosphate and its production is upregulated upon the activation of cellular immune response. Alterations of pteridines in body fluids are known to correlate well with existing diseases and stages, prognosis, clinical outcomes and survival data. It is of advantage to have a pteridine database of healthy volunteers to determine normal values. Thereby, especially in children there is no detailed study on pteridine levels. The aim of this study is to initiate the establishment of pteridine database of healthy children in our country. Serum neopterin levels were analysed by enzyme-linked immunosorbent assay. Urinary neopterin and biopterin levels and serum kynurenine, tryptophan levels and kynurenine/tryptophan ratio as an estimate of tryptophan breakdown were assessed with high-pressure liquid chromatography in serum and urine samples of 55 children aged between 3 months and 10 years. The results were evaluated within the subgroups of different ages and sex. Pteridine pathway components were found to be higher in children compared to adults. Higher levels of pteridine pathway components observed within the first years of life may reflect the rapid maturation of the immune system, and environmental adaptation and/or insufficiency of defence systems. On the other hand, it may also relate to a higher frequency of infections not (yet) manifested clinically.
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5

Soyka, Rainer, and Wolfgang Pfleiderer. "Pteridines, XCVI. Synthesis and Reactions of 6-(1,2,3-Trihydroxypropyl)pteridines." Pteridines 2, no. 2 (1990): 63–74. http://dx.doi.org/10.1515/pteridines.1990.2.2.63.

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Summary Various hydropyrano [3.2-g] pteridines (7, 10, 12, 21 , 33) were oxidized to the corresponding 6-(1,2,3- trihydroxypropyl)pteridine derivatives (8,9, 11, 13,32, 34), which are valuable intermediates for the synthesis of new 6-substituted pteridines (15 - 46). Periodate oxidation led to pteridine-6-carboxaldehydes (15, 16, 17, 38), which easily formed oximes (19 - 22, 39, 40). The aldehydes were further oxidized to 6-carboxylic acids (25,26,42) or reduced to 6-hydroxymethyl derivatives (27, 28, 43). Reductive condensations of the aldehydes (15, 16, 38) with p-aminobenzoylglutamic acid afforded folic acid analogues (29, 30, 44). Dehydration of the oximes (19, 20, 39) resulted in the formation of 6-carbonitriles (23, 24, 41, 46). The newly synthesized compounds were characterized by elemental analysis and by UV and NMR spectra.
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6

Rinkevich, Frank D., Joseph W. Margotta, Jean M. Pittman, James A. Ottea, and Kristen B. Healy. "Pteridine levels and head weights are correlated with age and colony task in the honey bee,Apis mellifera." PeerJ 4 (June 30, 2016): e2155. http://dx.doi.org/10.7717/peerj.2155.

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Background.The age of an insect strongly influences many aspects of behavior and reproduction. The interaction of age and behavior is epitomized in the temporal polyethism of honey bees in which young adult bees perform nurse and maintenance duties within the colony, while older bees forage for nectar and pollen. Task transition is dynamic and driven by colony needs. However, an abundance of precocious foragers or overage nurses may have detrimental effects on the colony. Additionally, honey bee age affects insecticide sensitivity. Therefore, determining the age of a set of individual honey bees would be an important measurement of colony health. Pteridines are purine-based pigment molecules found in many insect body parts. Pteridine levels correlate well with age, and wild caught insects may be accurately aged by measuring pteridine levels. The relationship between pteridines and age varies with a number of internal and external factors among many species. Thus far, no studies have investigated the relationship of pteridines with age in honey bees.Methods.We established single-cohort colonies to obtain age-matched nurse and forager bees. Bees of known ages were also sampled from colonies with normal demographics. Nurses and foragers were collected every 3–5 days for up to 42 days. Heads were removed and weighed before pteridines were purified and analyzed using previously established fluorometric methods.Results.Our analysis showed that pteridine levels significantly increased with age in a linear manner in both single cohort colonies and colonies with normal demography. Pteridine levels were higher in foragers than nurses of the same age in bees from single cohort colonies. Head weight significantly increased with age until approximately 28-days of age and then declined for both nurse and forager bees in single cohort colonies. A similar pattern of head weight in bees from colonies with normal demography was observed but head weight was highest in 8-day old nurse bees and there was no relationship of head weight with age of foragers.Discussion.Although the relationship between pteridine levels and age was significant, variation in the data yielded a +4-day range in age estimation. This allows an unambiguous method to determine whether a bee may be a young nurse or old forager in colonies with altered demographics as in the case of single cohort colonies. Pteridine levels in bees do not correlate with age as well as in other insects. However, most studies used insects reared under tightly controlled laboratory conditions, while we used free-living bees. The dynamics of head weight change with age is likely to be due to growth and atrophy of the hypopharyngeal glands. Taken together, these methods represent a useful tool for assessing the age of an insect. Future studies utilizing these methods will provide a more holistic view of colony health.
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7

Döring, Thomas, Romesh C. Boruah, and Wolfgang Pfleiderer. "Synthesis of 7-Acyl-2,4-disubstituted Pteridines by Radical Nucleophilic Substitution and Displacement Reactions." Pteridines 15, no. 4 (2004): 129–48. http://dx.doi.org/10.1515/pteridines.2004.15.4.129.

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Abstract 2,4-Disubstituted pteridine derivatives (1-3) react with acyl radicals very selectively in position 7 by a nucleophilic Substitution mechanism (4-10). Oxidation of the 2-methylthio group proceeds with m-chloroperbenzoic acid in good yields to the corresponding 7-acyl-2-methylsulfonyl-4-aminopteridines (11-16). The methylsulfonyl group can easily been displaced by nucleophiles such as aliphatic amines (27, 29, 32-42, 45), cyclic amines (56-61), aromatic amines (30, 31) and amino acids (43-54). Oxygen nucleophiles lead to 7-acyl-isopterin derivatives (62-66). The acyl side-chain is also prone to structural modifications leading to the corresponding secondary alcohols on NaBH4 reduction (74-77) or to imino derivatives on reactions with amines (67-73) which can analogously been reduced to 2,4-disubstituted 7-( l-aminoalkyl)pteridines (80-85). An interesting H-shift was observed during heating of 32, 78 and 79 with benzylamine leading not to the benzylimines but the isomeric benzylideneamino derivatives 86-88. Various acetylations by acetic anhydride (AC2O) gave 89-93 and reduction of the pyrazine moiety to the 5,6,7,8-tetrahydro-pteridine derivatives 94-96 proceeded in the expected manner. The characterization of ther newly synthesized pteridine derivatives was performed by 1H-NMR spectra, UV-spectra and elemental analyses. Measurements of the basic pKa values of a selection of 2,4,7-trisubstituted pteridines were pteridines to characterize the dication, monocation and the neutral species by their UV-spectra.
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8

Edalat, Hamideh, Mohammad Akhoundi, and Hamidreza Basseri. "Age-dependance of pteridines in the malaria vector, Anopheles stephensi." Pteridines 28, no. 3-4 (2017): 157–61. http://dx.doi.org/10.1515/pterid-2017-0009.

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AbstractDetermining the accurate age of malaria vectors is crucial to measure the risk of malaria transmission. A group of fluorescent chemicals derived from a pyrimidine-pyrazine ring structure known as pteridines from the head, thorax and whole body of adult female Anopheles stephensi were identified and evaluated as a tool for chronological and physiological age determination of malaria vectors. The female mosquitoes were collected from an insectary colony at an interval of every 5 days, up to 30 days, and the pteridines of head, thorax and whole body were detected fluorometrically by high-pressure liquid chromatography (HPLC) using excitation and emission wavelengths of 365 and 455 nm, respectively. In addition, alteration of the pteridines compounds was compared between blood and sugar fed mosquito groups. Although four pteridines including pterin-6-carboxylic acid, biopterin, xanthopterin and isoxanthopterin were detected, some of them were absent in the head or thorax of mosquitoes. Levels of all four pteridines were similarly decreased in a linear manner throughout 30 days. No significant difference in alteration of pteridine compounds was observed between the two groups of blood or sugar fed mosquitoes. This result indicates that diet has a little effect on pteridines alteration. Age determination based on pteridines, as an age-grading technique, could be used for field collected mosquitoes, which have either sugar or blood meal. In addition, analyzing total pteridine fluorescence from only whole body could be a convenient method to estimate the age.
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9

Tsusué, M., S. Kuroda, and H. Sawada. "Localization of Sepiapterin Deaminase and Pteridines In the Granules In Epidermal Cells of the Silkworm, Bombyx mori." Pteridines 2, no. 3 (1990): 175–82. http://dx.doi.org/10.1515/pteridines.1990.2.3.175.

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Summary A new method for assay of sepiapterin deaminase (3.5.4.24) activity by use of high performance liquid chromatography (HPLC) was developed. By this sensitive method the enzyme activity in the cell organelle was assayed. After cell fractionation, the enzyme was extracted with deoxycholate from pteridine granules of epidermal cells of the lemon mutant silkworm. On stepwise sucrose gradient centrifugation, most of the enzyme activity localized in the aggregated pteridine granules fraction, while the soluble fraction contained only one fourth of the total enzyme activity. The enzyme in the granule fraction had the same properties as the previously reported sepiapterin deaminase. These data show that the enzyme is localized in pteridine granules in the living cells. The attachment of the enzyme to the granule membrane is rather loose and previous papers studied the enzyme released from the granules. Cell fractionation and morphological observation showed that sepiapterin, sepialumazine and other pteridines were also localized in the granules together with uric acid.
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10

Ochoa, C., M. Rodríguez, L. Domínguez, et al. "Nematocide activity of 6,7-diarylpteridines in three experimental models." Journal of Helminthology 73, no. 4 (1999): 333–36. http://dx.doi.org/10.1017/s0022149x99000554.

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Thein vitronematocide activity of seventeen 6,7-diarylpteridines has been tested using three different experimental models,Caenorhabditis elegans,Nippostrongylus brasiliensisandHeligmosomoides polygyrus. The method of evaluation of inhibition in the secretion of acetylcholinesterase byH. polygyrusseems to be the most indicated to avoid false positives. Thein vivoactivities, againstTrichinella spiralis, of the mostin vitroactive pteridines have been assayed. All pteridine derivatives bearing 6,7-di-p-bromophenyl substituents have shownin vitronematocide activites in the three experimental models used. Amongst all the pteridines testedin vivo, only 2,4-pteridinedithione derivatives exhibited moderate activity.
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11

NARE, B., J. LUBA, L. W. HARDY, and S. BEVERLEY. "New approaches to Leishmania chemotherapy: pteridine reductase 1 (PTR1) as a target and modulator of antifolate sensitivity." Parasitology 114, no. 7 (1997): 101–10. http://dx.doi.org/10.1017/s0031182097001133.

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Leishmania and other trypanosomatid protozoa require reduced pteridines (pterins and folates) for growth, suggesting that inhibition of these pathways could be targeted for effective chemotherapy. This goal has not yet been realized, indicating that pteridine metabolism may be unusual in this lower eukaryote. We have investigated this possibility using both wild type and laboratory-selected antifolate-resistant strains, and with defined genetic knockouts of several pteridine metabolic genes. In Leishmania, resistance to the antifolate methotrexate is mediated through several mechanisms singly or in combination, including alterations in transport leading to reduced drug influx, overproduction (R-region amplification) or point mutation of dihydrofolate reductase-thymidylate synthase (DHFR-TS), and amplification of a novel pteridine reductase (PTR1, encoded by the H-region). All of the proteins involved are potential targets for antifolate chemotherapy. Notably, parasites in which the gene encoding dihydrofolate reductase (DHFR) has been deleted (dhfr-ts− knockouts) do not survive in animal models, validating this enzyme as a target for effective chemotherapy. However, the properties of pteridine reductase 1 (PTR1) suggest a reason why antifolate chemotherapy has so far not been successful in trypanosomatids. PTR1, by its ability to provide reduced pterins and folates, has the potential to act as a by-pass and/or modulator of DHFR inhibition under physiological conditions. Moreover, PTR1 is less sensitive to many antifolates targeted primarily against DHFR. These findings suggest that successful antifolate chemotherapy in Leishmania will have to target simultaneously both DHFR and PTR1.
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12

Estévez Dimitrov, Ronja, Jens Amendt, Florian Rothweiler, and Richard Zehner. "Age determination of the adult blow fly Lucilia sericata (Diptera: Calliphoridae) through quantitative pteridine fluorescence analysis." Forensic Science, Medicine and Pathology 16, no. 4 (2020): 641–48. http://dx.doi.org/10.1007/s12024-020-00295-4.

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AbstractDetermination of a minimal postmortem interval via age estimation of necrophagous diptera has been restricted to the juvenile stages and the time until emergence of the adult fly, i.e. up until 2–6 weeks depending on species and temperature. Age estimation of adult flies could extend this period by adding the age of the fly to the time needed for complete development. In this context pteridines are promising metabolites, as they accumulate in the eyes of flies with increasing age. We studied adults of the blow fly Lucilia sericata at constant temperatures of 16 °C and 25 °C up to an age of 25 days and estimated their pteridine levels by fluorescence spectroscopy. Age was given in accumulated degree days (ADD) across temperatures. Additionally, a mock case was set up to test the applicability of the method. Pteridine increases logarithmically with increasing ADD, but after 70–80 ADD the increase slows down and the curve approaches a maximum. Sex had a significant impact (p < 4.09 × 10−6) on pteridine fluorescence level, while body-size and head-width did not. The mock case demonstrated that a slight overestimation of the real age (in ADD) only occurred in two out of 30 samples. Age determination of L. sericata on the basis of pteridine levels seems to be limited to an age of about 70 ADD, but depending on the ambient temperature this could cover an extra amount of time of about 5–7 days after completion of the metamorphosis.
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13

Burgmayer, Sharon J. Nieter, and Edward I. Stiefel. "Transition-metal pteridine complexes. Preparation and characterization of cobalt(II) pteridines." Inorganic Chemistry 27, no. 22 (1988): 4059–65. http://dx.doi.org/10.1021/ic00295a033.

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14

Escriche, B., and F. J. Silva. "An in vitro System for Studying Pteridine Biosynthesis In Drosophila melanogaster." Pteridines 3, no. 3 (1991): 171–76. http://dx.doi.org/10.1515/pteridines.1991.3.3.171.

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In vitro organ culture is a system especially useful for the study of metabolic pathways and their regulation. This report applies such a system to the study of the biosynthesis of pteridines in Drosophila melanogaster, determining in vitro optimal conditions for head cultures, in relation to this metabolic pathway. The validity of the system was tested by applying it to the study of a well-known enzyme, xanthine dehydrogenase, which catalyzes the transformation of pterin into isoxanthopterin. Supplementation experiments with pterin were carried out, determining that, as expected, only those strains having xanthine dehydrogenase activity were able to transform this compound into isoxanthopterin. These results confirm the usefulness of this system for future studies on pteridine metabolism.
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15

Albert, Adrien, and H. C. S. Wood. "Pteridine syntheses. II.isoxanthopterin." Journal of Applied Chemistry 3, no. 11 (2007): 521–23. http://dx.doi.org/10.1002/jctb.5010031107.

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16

Maier, Josef, Thomas Werner, and Helga Ninnemann. "Homology Cloning of GTP-cydohydrolase I from Fungi and Plants by Reverse-transcription PCR Using a General Set of Degenerate Primers." Pteridines 6, no. 3 (1995): 112–15. http://dx.doi.org/10.1515/pteridines.1995.6.3.112.

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Summary Unconjugated pteridines are present in fungi, algae and plants. However, the functions of pteridines in these organisms are not thoroughly investigated. The biosynthesis follows the same steps as were shown for animals and eubacteria. One possible function of pteridines in these organisms is participation in blue-light reception. To analyze this or other functions of pteridines it would be useful to inhibit pteridine synthesis specifically by genetic engineering. GTP-cyclohydrolase I is the primary enzyme of tetrahydrobiopterin and folic acid biosynthesis. A comparison of amino acid sequences of GTP-cyclohydrolase I (EC 3.5.4.16) previously known from various species allowed the construction of degenerate primers, based on highly conserved regions. The same consensus primers are able to bind to cDNAs of unrelated eukaryotes. By reverse-transcriptase PCR cDNAs of the conserved C-terminal part of the fungi Neurospora and Phycomyces, the phytoflagellate Euglena and the higher plant Mucuna hassjoo were amplified and cloned. Similarities between the sequences agreed with the evolutionary relationship of the investigated organisms. Various regions strictly conserved between unrelated eukaryotes and bacteria were observed, which could be essential for the function of GTP-cyclohydrolase I.
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17

Hoekstra, R., and D. Fekkes. "Pteridines and affective disorders." Acta Neuropsychiatrica 14, no. 3 (2002): 120–26. http://dx.doi.org/10.1034/j.1601-5215.2002.140305.x.

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The pteridine tetrahydrobiopterin (BH4) is an essential cofactor in the biosynthesis of dopamine, (nor)epinephrine, serotonin and nitric oxide (NO). Furthermore, BH4 has a direct influence on release mechanisms of these neurotransmitters and on serotonin receptor binding activity immunology. The synthesis of BH4 is stimulated by interferon-gamma and hence there is a close relationship with the immune system HPA-axis. In animal experiments it was also found that the hypothalamus–pituitary–adrenal axis influences the pteridine metabolism. In clinical studies, so far, no evidence has been found for this relationship diseases. A congenital biopterin deficiency results in atypical phenylketonuria with severe neuropsychiatric symptoms. In several neurological diseases, such as Parkinson's disease, decreased levels of BH4 are found depression. Since 1984 there have been reports on decreased biopterin and increased neopterin levels in urine and plasma of depressed patients. Conflicting results have also been found, however, due probably to methodological problems therapy. Until now, oral administration of BH4 to depressed patients has been performed by two investigators, which resulted in mainly temporal clinical improvement discussion. Understanding of biochemical mechanisms in which pteridines are involved may contribute to our knowledge of the pathogenesis and treatment of affective disorders. This paper aims to provide an overview of the relevant literature and warrant for further research on this intriguing compound.
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18

McLean, Claire A., Adrian Lutz, Katrina J. Rankin, Adam Elliott, Adnan Moussalli, and Devi Stuart-Fox. "Red carotenoids and associated gene expression explain colour variation in frillneck lizards." Proceedings of the Royal Society B: Biological Sciences 286, no. 1907 (2019): 20191172. http://dx.doi.org/10.1098/rspb.2019.1172.

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A long-standing hypothesis in evolutionary ecology is that red–orange ornamental colours reliably signal individual quality owing to limited dietary availability of carotenoids and metabolic costs associated with their production, such as the bioconversion of dietary yellow carotenoids to red ketocarotenoids. However, in ectothermic vertebrates, these colours can also be produced by self-synthesized pteridine pigments. As a consequence, the relative ratio of pigment types and their biochemical and genetic basis have implications for the costs and information content of colour signals; yet they remain poorly known in most taxonomic groups. We tested whether red- and yellow-frilled populations of the frillneck lizard, Chlamydosaurus kingii, differ in the ratio of different biochemical classes of carotenoid and pteridine pigments, and examined associated differences in gene expression. We found that, unlike other squamate reptiles, red hues derive from a higher proportion of ketocarotenoids relative to both dietary yellow carotenoids and to pteridines. Whereas red frill skin showed higher expression of several genes associated with carotenoid metabolism, yellow frill skin showed higher expression of genes associated with steroid hormones. Based on the different mechanisms underlying red and yellow signals, we hypothesize that frill colour conveys different information in the two populations. More generally, the data expand our knowledge of the genetic and biochemical basis of colour signals in vertebrates.
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19

Frost, S. K., L. G. Epp, and S. J. Robinson. "The pigmentary system of developing axolotls." Development 92, no. 1 (1986): 255–68. http://dx.doi.org/10.1242/dev.92.1.255.

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The albino mutant in the Mexican axolotl (Ambystoma mexicanum) is analysed with respect to the differentiation of pigment cells. Pigment cells were observed with the transmission electron microscope in order to determine any unusual structural characteristics and to determine what happens to each of the cell types as development proceeds. Chemical analyses of pteridine pigments were also carried out, and the pattern of pteridines in albino animals was found to be more complex than, and quantitatively enhanced (at all developmental stages examined) over, the pattern observed in comparable wild-type axolotls. The golden colour of albino axolotls is due primarily to sepiapterin (a yellow pteridine) and secondarily to riboflavin (and other flavins). Coincident with enhanced levels of yellow pigments, xanthophore pigment organelles (pterinosomes) in albino skin reach a mature state earlier than they do in wild-type axolotl skin. This morphology is conserved throughout development in albino animals whereas it is gradually lost in the wild type. Unpigmented melanophores from albino axolotls are illustrated for the first time, and in larval albino axolotls the morphology of these cells is shown to be very similar to xanthophore morphology. In older albino animals xanthophores are easily distinguished from unpigmented melanophores. Iridophores seem to appear in albino skin at an earlier stage than they have been observed in wild-type skin. Morphologically, wild-type and albino iridophores are identical.
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20

Rong, Yikang S., and Kent G. Golic. "Dominant Defects in Drosophila Eye Pigmentation Resulting From a Euchromatin-Heterochromatin Fusion Gene." Genetics 150, no. 4 (1998): 1551–66. http://dx.doi.org/10.1093/genetics/150.4.1551.

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Abstract We have isolated a dominant mutation, pugilistDominant (pug D), that causes variegated reductions in pteridine and ommochrome pigmentation of the Drosophila eye. The effect of pugD on pteridine pigmentation is most dramatic: the only remaining pigment consists of a thin ring of pigment around the periphery of the eye with a few scattered spots in the center. The pugD mutation disrupts a gene that encodes a Drosophila homolog of the trifunctional enzyme methylenetetrahydrofolate dehydrogenase (MTHFD; E.C.1.5.1.5, E.C.3.5.4.9, E.C.6.3.4.3). This enzyme produces a cofactor that is utilized in purine biosynthesis. Because pteridines are derived from GTP, the pigment defect may result from an impairment in the production of purines. The mutant allele consists of a portion of the MTHFD coding region fused to ∼1 kb of highly repetitive DNA. Transcription and translation of both parts are required for the phenotype. The repetitive DNA consists of ∼140 nearly perfect repeats of the sequence AGAGAGA, a significant component of centric heterochromatin. The unusual nature of the protein produced by this gene may be responsible for its dominance. The repetitive DNA may also account for the variegated aspect of the phenotype. It may promote occasional association of the pugD locus with centric heterochromatin, accompanied by inactivation of pugD, in a manner similar to the proposed mode of action for brownDominant.
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21

Murata, Shizuaki, and Ning Chen. "Difference of DNA Compaction Performed by Two kinds of Oncopterin-Mimic Pteridine - Polyamine Conjugates." Pteridines 17, no. 1 (2006): 1–4. http://dx.doi.org/10.1515/pteridines.2006.17.1.1.

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Abstract Two types of pteridine - polyamine conjugates designed on oncopterin perform different actions to DNA. The most obvious difference is their actions in DNA compaction. One of the pteridine - polyamine conjugates, PT- 2R, containing a polyamine substituent (R) on the C(2) position of pterin (PT) compacts a DNA molcculc in an all-or-none fashion without the intervention of an intermediate. The othcr (PT-4R: R exists on the c(4) position of PT) carries out the DNA compaction via partially compacted intermediates. The difference is discussed based on various interaction modes of the pteridine - polyamine conjugates to DNA.
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22

PFEIFFER, Silvia, C. F. Antonius GORREN, Eva PITTERS, Kurt SCHMIDT, R. Ernst WERNER, and Bernd MAYER. "Allosteric modulation of rat brain nitric oxide synthase by the pterin-site enzyme inhibitor 4-aminotetrahydrobiopterin." Biochemical Journal 328, no. 2 (1997): 349–52. http://dx.doi.org/10.1042/bj3280349.

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We investigated the functional and allosteric effects of the 4-amino analogue of tetrahydrobiopterin, (6R)-2,4-diamino-5,6,7,8-tetrahydro-6-(l-erythro-1,2-dihydroxypropyl)pteridine (4-amino-H4biopterin) on pteridine-free rat neuronal nitric oxide synthase. In the presence of added (6R)-5,6,7,8-tetrahydro-L-erythrobiopterin (H4biopterin; 10 μM), 4-amino-H4biopterin completely inhibited the conversion of both L-arginine and NG-hydroxy-L-arginine with half-maximally effective concentrations of 1.1±0.09 and 1.3±0.09 μM, respectively. Inhibition was reversible, as shown by a time-dependent restoration of citrulline formation upon dilution of the inhibitor-treated enzyme (t1/2 = 3.0 min). Binding of 4-amino-H4biopterin led to a complete conversion of the haem from low-spin to high-spin state, and to the formation of stable homodimers which partially survived electrophoresis under denaturating conditions. These results show that oxidation of both L-arginine and NG-hydroxy-L-arginine is pteridine-dependent, and that the allosteric effects of H4biopterin do not fully explain the essential role of the pteridine cofactor in nitric oxide biosynthesis.
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23

Gourley, David G., James Luba, Larry W. Hardy, Stephen M. Beverley, and William N. Hunter. "Crystallization of recombinant Leishmania major pteridine reductase 1 (PTR1)." Acta Crystallographica Section D Biological Crystallography 55, no. 9 (1999): 1608–10. http://dx.doi.org/10.1107/s0907444999008999.

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The enzyme pteridine reductase (PTR1) has recently been discovered in the protozoan parasite Leishmania and validated as a target for therapeutic intervention. PTR1 is responsible for the salvage of pteridines and also contributes to antifolate drug resistance. Structural analysis, in combination with ongoing biochemical characterization will assist the elucidation of the structure–activity relationships of this important enzyme and support a structure-based approach to discover novel inhibitors. Recombinant L. major PTR1 has been purified from an Escherichia coli expression system and used in crystallization experiments. Orthorhombic crystals have been obtained and data to 2.8 Å has been measured. The space group is P21212 or P212121 with unit-cell dimensions of a = 103.9, b = 134.7, c = 96.2 Å. One homotetramer, of molecular mass approximately 120 kDa, probably constitutes the asymmetric unit and gives a Matthews coefficient, Vm , of 2.8 Å3 Da−1 and 56% solvent volume. Self-rotation function calculations show a single well defined non-crystallographic twofold axis with features that might represent additional elements of non-crystallographic symmetry. The detail of exactly what constitutes the asymmetric unit will be resolved by structure determination.
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24

Tillinghast, H. S., and P. C. Newell. "Chemotaxis towards pteridines during development of Dictyostelium." Journal of Cell Science 87, no. 1 (1987): 45–53. http://dx.doi.org/10.1242/jcs.87.1.45.

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Following a previous study indicating a sensitivity to folate during the developmental phase of Dictyostelium discoideum, a series of pteridines were investigated for their ability to induce amoebal chemotaxis during development of this organism. Several compounds were found to resemble folate in their ability to induce chemotaxis of both vegetative amoebae and amoebae developing during the first few hours of starvation. One compound, L-monapterin, was distinct in showing chemotactic activity only during the developmental phase after approximately 12 h of starvation. Tests using the polymerization of cytoskeletal actin as an assay for a cellular response correlated with chemotaxis showed that 10 nM-L-monapterin was a potent inducer of this response and that responsiveness appeared only after 12 h of development. The timing of these events may be correlated with the formation of tips containing stalk cells that occurs in multicellular aggregates at approximately 12 h, and suggests a role for L-monapterin (or a naturally occurring, closely related pteridine) in cell sorting. The evolutionary significance of the roles of pteridines is discussed.
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25

Werner-Felmayer, G., G. Golderer, E. R. Werner, P. Gröbner, and H. Wachter. "Pteridine biosynthesis and nitric oxide synthase in Physarum polycephalum." Biochemical Journal 304, no. 1 (1994): 105–11. http://dx.doi.org/10.1042/bj3040105.

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Physarum polycephalum, an acellular slime mould, serves as a model system to study cell-cycle-dependent events since nuclear division is naturally synchronous. This organism was shown to release isoxanthopterin which is structurally related to tetrahydrobiopterin, a cofactor of aromatic amino acid hydroxylases and of nitric oxide synthases (NOSs) (EC 1.14.13.39). Here, we studied Physarum pteridine biosynthesis in more detail and found that high amounts of tetrahydrobiopterin are produced and NOS activity is expressed. Physarum pteridine biosynthesis is peculiar in as much as 7,8-dihydroneopterin aldolase (EC 4.1.2.25), an enzyme of folic acid biosynthesis usually not found in organisms producing tetrahydrobiopterin, is detected in parallel. NOS purified from Physarum depends on NADPH, tetrahydrobiopterin and flavins. Enzyme activity is independent of exogenous Ca2+ and is inhibited by arginine analogues. The purified enzyme (with a molecular mass of 130 kDa) contains tightly bound tetrahydrobiopterin and flavins. During the synchronous cell cycle of Physarum, pteridine biosynthesis increases during S-phase whereas NOS activity peaks during mitosis, drops at telophase and peaks again during early S-phase. Our results characterize Physarum pteridine biosynthesis and NOS and suggest a possible link between NOS activity and mitosis.
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26

Murata, Shizuaki, Kenji Kiguchi, and Takashi Sugimoto. "Highly Regioselective Alkylation of Pteridine." HETEROCYCLES 35, no. 2 (1993): 639. http://dx.doi.org/10.3987/com-92-s(t)103.

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27

Helliwell, M., A. Dinsmore, C. D. Garner, and J. A. Joule. "A 1-alkylated pteridine, C15H19ClN6O3." Acta Crystallographica Section C Crystal Structure Communications 55, no. 2 (1999): 254–56. http://dx.doi.org/10.1107/s0108270198011883.

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28

McIntyre, G. S., and R. H. Gooding. "Pteridine accumulation in Musca domestica." Journal of Insect Physiology 41, no. 4 (1995): 357–68. http://dx.doi.org/10.1016/0022-1910(94)00105-p.

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29

Warhurst, D. C. "Pteridine synthesis in malaria parasites." Parasitology Today 2, no. 3 (1986): 57–58. http://dx.doi.org/10.1016/0169-4758(86)90154-7.

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30

Corona, Paola, Federica Gibellini, Andrea Cavalli, et al. "Structure-Based Selectivity Optimization of Piperidine–Pteridine Derivatives as Potent Leishmania Pteridine Reductase Inhibitors." Journal of Medicinal Chemistry 55, no. 19 (2012): 8318–29. http://dx.doi.org/10.1021/jm300563f.

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31

Millán, J. M., and C. Nájera. "Mutagenesis at Five Pteridine Pathway Loci In Drosophila melanogaster: Genetic and Biochemical Characterization." Pteridines 4, no. 3 (1993): 131–37. http://dx.doi.org/10.1515/pteridines.1993.4.3.131.

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SummaryIn order to carry out a genetic and biochemical analysis of pteridin pathway eye colour loci, sixteen strains of five eye colour mutants of Drosophila melanogaster (2 dke, 7 sf. 3 se, 3 Hnr and 1 bw) from natural populations were used. Four EMS mutagenesis experiments were carried out to produce induced mutants of the same loci. 54 mutants (mosaics and completes) were obtained but only 7 (4 sf, 1 bw, 1 Hnr and I dke) could be isolated. The 40.48% of the mutations were mosaics. The percentage of mutants appeared during the four first days (85.19%) was significatively higher to the percentage of mutants appeared during the four following (14.18%). Viabilities of EMS-induced mutants were similar to that of the natural ones. For the induced mutants viability at 25°C was higher than at 16°C and heterozygotes had a higher Viability than mutant homozygotes. The low mutagenesis frequencies and the lack of some metabolites for Hnr and se mutants suggest an important role of these mutants in the pteridine pathway.
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32

Cieślik, Ewa, and Iwona Cieślik. "Occurrence and significance of folic acid." Pteridines 29, no. 1 (2018): 187–95. http://dx.doi.org/10.1515/pteridines-2018-0017.

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AbstractFolic acid is a naturally occurring pteridine, which was originally isolated from plants. Folic acid (pteroyl-glutamic acid) is composed of pteridine (6-methylptero), p-aminobenzoic acid (PABA) and glutamic acid. Folic acid (folacin) is a compound of major importance for the proper functioning of the human body. Its adequate supply is essential for the proper course of many biochemical processes in the body, including the process of neural tube closure in the fetus, DNA and amino acid synthesis, growth of red blood cells, and the function of the nervous system. Folic acid is a compound of a high sensitivity to physical and chemical factors, and its bioavailability is limited by interactions with multiple food components. Therefore, folate deficiency is one of the most common deficiencies. This paper presents the structure and characteristics of folic acid as a pteridine, it also discusses dietary sources of folate and the effects of its deficiency.
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33

Togo, Kazuyuki, Toshiya Ishihara, Kenji Yamamoto, and Hideyuki Sawada. "Older-onset levodopa-responsive parkinsonism with normal DAT-SPECT and pterin hypometabolism." BMJ Case Reports 14, no. 5 (2021): e240067. http://dx.doi.org/10.1136/bcr-2020-240067.

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Pterin species participate in dopamine biosynthesis, and abnormal pteridine metabolism contributes to reduced dopamine. GTP cyclohydrolase 1 (GCH-1) deficiency, which triggers pteridine hypometabolism and normally develops in childhood, can mediate an adult-onset decrease in levodopa production and dopa-responsive dystonia (DRD), with normal dopamine transporter single-photon emission computed tomography (DAT-SPECT). A recent study described normal DAT-SPECT in adult-onset cases with GCH-1 mutations, clinically diagnosed with Parkinson’s disease, which raises the possibility that the abnormal metabolism of pteridine may be a differential diagnosis for adult-onset parkinsonism. We report an older patient with levodopa-responsive parkinsonism with normal DAT-SPECT, or scans without evidence of dopamine deficit (SWEDD), whose biochemical analysis showed pterin hypometabolism, which occurs in GCH-1-deficient DRD. Surprisingly, this patient presented no dystonia or GCH-1 gene mutation or deletion. This case suggests that low pterin metabolism should be considered in older-onset levodopa-responsive parkinsonism with normal DAT-SPECT, even without GCH-1 mutations or deletions.
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34

Hiranrat, Asadhawut, Darren C. Holland, Wilawan Mahabusarakam, John N. A. Hooper, Vicky M. Avery, and Anthony R. Carroll. "Tedaniophorbasins A and B—Novel Fluorescent Pteridine Alkaloids Incorporating a Thiomorpholine from the Sponge Tedaniophorbas ceratosis." Marine Drugs 19, no. 2 (2021): 95. http://dx.doi.org/10.3390/md19020095.

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Two new fluorescent pteridine alkaloids, tedaniophorbasins A (1) and B (2), together with the known alkaloid N-methyltryptamine, were isolated, through application of mass directed purification, from the sponge Tedaniophorbas ceratosis collected from northern New South Wales, Australia. The structures of tedaniophorbasins A and B were deduced from the analysis of 1D/2D NMR and MS data and through application of 13C NMR DFT calculations. Tedaniophorbasin A possesses a novel 2-imino-1,3-dimethyl-2,3,7,8-tetrahydro-1H-[1,4]thiazino[3,2-g]pteridin-4(6H)-one skeleton, while tedaniophorbasin B is its 2-oxo derivative. The compounds show significant Stokes shifts (~14,000 cm−1) between excitation and emission wavelengths in their fluorescence spectra. The new compounds were tested for bioactivity against chloroquine-sensitive and chloroquine-resistant strains of the malaria parasite Plasmodium falciparum, breast and pancreatic cancer cell lines, and the protozoan parasite Trypanosoma brucei brucei but were inactive against all targets at 40 µM.
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35

Paudel, Hari Ram, Ranjita Das, Chia-Hua Wu та Judy I. Wu. "Self-assembling purine and pteridine quartets: how do π-conjugation patterns affect resonance-assisted hydrogen bonding?" Organic & Biomolecular Chemistry 18, № 6 (2020): 1078–81. http://dx.doi.org/10.1039/c9ob02412c.

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36

Bartke, Michael, and Wolfgang Pfleiderer. "Pteridines, IXC. Synthesis, Oxidations and Reactions of 6- and 7-Hydroxy-2-thiolumazines Selective Cytotoxicity of Carboxypeptidase-activated Methotrexate ex-Peptides." Pteridines 1, no. 1 (1989): 57–63. http://dx.doi.org/10.1515/pteridines.1989.1.1.57.

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Summary Various 6-(10, 11) and 7-hydroxy-2-thiolumazines (8,9) have been synthesized and oxidations of the thioamide function studied . H20 2 Oxidation of 7-hydroxy-2-thiolumazine (8) in basic medium leads to pteridine-4,7- dione-2-sulfinate (12), which eliminates S02 in anhydrous acids. Oxidative desulfurization of 8 and its 8- methyl derivative 9 proceeds directly in formic acid with H20 2 and m-chloroperbenzoic acid to give 16 and 17 respectively. KMn04 oxidation forms the pteridine-4,7,dione-2-sulfonates (14, 15), which react under hydrolytic conditions to give the corresponding 2-hydroxy derivtives (18, 19) and on displacement with ammonium acetate/ammonia at elevated temperature form the pterin derivatives 20 and 21.2-Thio-pteridine-4,6-dione (10) oxidizes also to the corresponding 2-sulfonate (22), which could only be isolated after addition of potassium bisulfite in the form of the dipotassium 7,8-dihydropteridine-4,6-dione- 2,7-disulfonate (23) adduct.The newly synthesized compounds have been characterized by elemental analyses, pKa determinations, UVand IH-NMR-spectra.
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37

Soyka, Rainer, Wolfgang Pfleiderer, and Roland Prewo. "Pteridine. Teil XCIV. Synthese und Eigenschaften von 5,6-Dihydro-6-(1,2,3-trihydroxypropyl)pteridinen: Kovalente intramolekulare Addukte." Helvetica Chimica Acta 73, no. 4 (1990): 808–26. http://dx.doi.org/10.1002/hlca.19900730407.

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38

Shahzad, Shabnam, Muhammad Abdul Qadir, Mahmood Ahmed, et al. "Folic acid-sulfonamide conjugates as antibacterial agents: design, synthesis and molecular docking studies." RSC Advances 10, no. 70 (2020): 42983–92. http://dx.doi.org/10.1039/d0ra09051d.

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39

Petukh, M. G., G. N. Semenkova, D. Fuchs, and S. N. Cherenkevich. "Pteridine-dependent oxygen activation in neutrophils." Cell and Tissue Biology 3, no. 6 (2009): 538–43. http://dx.doi.org/10.1134/s1990519x09060066.

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40

Albert, Adrien, and H. C. S. Wood. "Pteridine syntheses. I. Leucopterin and xanthopterin." Journal of Applied Chemistry 2, no. 10 (2007): 591–92. http://dx.doi.org/10.1002/jctb.5010021005.

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41

Cha, K. W., S. I. Park, Y. K. Lee, and J. J. Yim. "Capillary Electrophoretic Separation of Pteridine Compounds." Pteridines 4, no. 4 (1993): 210–13. http://dx.doi.org/10.1515/pteridines.1993.4.4.210.

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42

ASAHI, Yutaka, Masami TANAKA, and Naohiro YAMAMOTO. "Voltammetry of the Pteridine Derivative, Triamterene." CHEMICAL & PHARMACEUTICAL BULLETIN 44, no. 5 (1996): 1115–18. http://dx.doi.org/10.1248/cpb.44.1115.

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43

Choi, Yong Kee, Yoon Kyung Hwang, Yong Han Kang, and Young Shik Park. "Chemical structure of 1-O-(L-erythro-biopterin-2'-yl)-a-glucose isolated from a cyanobacterium Synechococcus sp. PCC 7942." Pteridines 12, no. 3 (2001): 121–25. http://dx.doi.org/10.1515/pteridines.2001.12.3.121.

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Abstract A pteridine glycoside in Synechococcus sp. PCC 7942, the structure of which had been tentatively identified as biopterin-glucoside, was isolated and characterized for its exact chemical structure by 2D-NMR spectroscopy. The determined structure is 1-0-(L-erythro-biopterin-2'-yl)-α-glucose. It is the first report on the occurrence of a biopterin-glucoside having a α-configured sugar directly attached at the pteridine ring. This result also supports that the previously purified UDP-glucose: BH4 glucosyltransferase from Synechococcus sp. PCC 7942, which catalyzes the synthesis of BH4-glucoside from UDP-glucose and BH4, is a α-glucosyltransferase.
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44

Palabiyik, Saziye Sezin, Gozde Girgin, Ali Asci, et al. "Folate, neopterin and kynurenine pathway in patients with statin therapy." Pteridines 27, no. 1-2 (2016): 7–12. http://dx.doi.org/10.1515/pterid-2015-0011.

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AbstractStatins, widely used antihyperlipidemic drugs, also have immunomodulatory properties independent from their lipid lowering effect. Even with slight modulations in the immune system, pteridine levels can display changes. The effect of statins on pteridines and related pathways has been demonstrated in a limited number of studies. The aim of the study was to evaluate the possible changes in neopterin and folate levels, and tryptophan (Trp) degradation in hyperlipidemic patients. Patients who were admitted to the cardiology clinic were randomly grouped if they were having statin treatment (n=69) or not (n=36). Serum Trp and kynurenine (Kyn), erythrocyte folate, and urinary neopterin levels were measured. It was found that urinary neopterin levels were significantly higher in patients on statin treatment (p<0.05) while levels of folate, Trp, Kyn, and Kyn-to-Trp ratios (Kyn/Trp) presented no significant changes (all, p>0.05). The correlation of the measured parameters was also evaluated and neopterin, folate and tryptophan degradation were found to be positively correlated. According to the results, neopterin levels, folate status and Trp degradation were altered in patients with statin treatment in comparison with the patients not receiving statin therapy. In order to point out the direct effect of statins on pteridines, further studies presenting both pre- and post-statin treatment of these parameters are needed.
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45

Schormann, Norbert, Olga Senkovich, Subramaniam Ananthan, and Debasish Chattopadhyay. "Docking and biological activity of pteridine analogs: search for inhibitors of pteridine reductase enzymes from Trypanosoma cruzi." Journal of Molecular Structure: THEOCHEM 635, no. 1-3 (2003): 37–44. http://dx.doi.org/10.1016/s0166-1280(03)00403-2.

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46

Xu, Shenzheng, Xiaoyu Jia, Jiaxin Lu, et al. "Pteridine derivatives: novel low-molecular-weight organogelators and their piezofluorochromism." New Journal of Chemistry 44, no. 8 (2020): 3382–91. http://dx.doi.org/10.1039/c9nj05922a.

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47

Shintaku, Haruo. "Early Diagnosis of 6-Pyruvoyl-tetrahydropterin Synthase Deficiency." Pteridines 5, no. 1 (1994): 18–27. http://dx.doi.org/10.1515/pteridines.1994.5.1.18.

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Summary 6-Pyruvoyl-tetrahydropterin synthase (PTPS) deficiency, which used to be called dihydrobiopterin synthase deficiency, is the most common kind of tetrahydrobiopterin deficiency. Early treatment by administration of tetrahydrobiopterin and neurotransmitter precursors helps to prevent neurological injury, so prompt diagnosis of neonates with hyperphenylalaninemia discovered by screening for phenylketonuria is necessary. Three patients with PTPS deficiency were diagnosed by pteridine analysis. All patients had low biopterin and high neopterin levels in the urine, resulting in a neopterin to biopterin ratio (N/B)much higher than that of age-matched controls. The mean NIB in the parents of these patients was twice that of healthy unrelated adults. PTPS activity was measured in one of these patients with PTPS deficiency and in his family members; the patient was homozygous and his parents were heterozygous for PTPS deficiency. This result meant that N/Bcould be used as an index of PTPS activity. In healthy subjects studied cross-sectionally, urinary levels of pteridine decreased in groups of increasing age, and the same change was found in subjects with hyperphenylalaninemia studied cross-sectionally. Thus, pteridine values of patients can be compared meaningfully only with age-matched controls. The urinary N/Bis useful for the diagnosis of homozygotes and heterozygotes for PTPS deficiency.
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48

Takeda, Taisuke, Takashi Hamazaki, Ryohei Wakahara, Hiroki Fujioka, Shizuhiro Niihira, and Haruo Shintaku. "Oxidative Stress and Pteridines in Pediatric Asthma: Relationship to Exhaled Nitric Oxide." Pteridines 23, no. 1 (2012): 104–9. http://dx.doi.org/10.1515/pteridines.2012.23.1.104.

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Abstract Fractional exhaled nitric oxide (FeNO) is a useful marker of airway inflammation in asthmatics. Nitric oxide synthase (NOS) requires tetrahydrobiopterin as a cofactor and produces superoxide during NO generation. Therefore, we investigated the relationship of FeNO to pteridine biosynthesis and oxidative stress in pediatric asthma patients. We recruited 67 asthmatic children for FeNO measurement and examined neopterin, biopterin, and Diacron-reactive oxygen metabolites (d-ROMs) as an oxidative stress marker in both summer and winter. Although d-ROMs levels did not show significant correlation with FeNO levels in summer, d-ROMs and FeNO were positively correlated in winter (p <0.05). Both neopterin and biopterin levels in the blood tended to be lower in patients who showed higher FeNO. Multivariate analysis revealed that increased IgE levels correlated with increased FeNO (p <0.01) and decreased neopterin (p <0.05) levels. This data supports a mechanism by which decreased levels of pteridines promote reactive oxygen species production upon NO generation, resulting in airway injury in asthmatic patients. Correlation with IgE level indicates that Th2-mediated allergic inflammation is involved in this process.
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49

Oettl, K., and G. Reibnegger. "Pteridine Derivatives as Modulators of Oxidative Stress." Current Drug Metabolism 3, no. 2 (2002): 203–9. http://dx.doi.org/10.2174/1389200024605127.

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50

Giori, Paolo, Chiara B. Vicentini, Augusto C. Veronese, and Mario Guarneri. "Synthesis of 6,7-Disubstituted Pteridine-2,4-diones." HETEROCYCLES 32, no. 1 (1991): 79. http://dx.doi.org/10.3987/com-90-5617.

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