Relevant bibliographies by topics / Kynurenine

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  1. Journal articles
  2. Dissertations / Theses
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  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Kynurenine'

Author: Grafiati
Published: 4 June 2021
Last updated: 7 July 2024

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Journal articles on the topic "Kynurenine"

1

Maget, Alexander, Martina Platzer, Susanne A. Bengesser, Frederike T. Fellendorf, Armin Birner, Robert Queissner, Carlo Hamm, et al. "Differences in Kynurenine Metabolism During Depressive, Manic, and Euthymic Phases of Bipolar Affective Disorder." Current Topics in Medicinal Chemistry 20, no. 15 (June 1, 2020): 1344–52. http://dx.doi.org/10.2174/1568026619666190802145128.

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Background & Objectives: The kynurenine pathway is involved in inflammatory diseases. Alterations of this pathway were shown in psychiatric entities as well. The aim of this study was to determine whether specific changes in kynurenine metabolism are associated with current mood symptoms in bipolar disorder. Methods: Sum scores of the Hamilton Depression Scale, Beck Depression Inventory, and Young Mania Rating Scale were collected from 156 bipolar individuals to build groups of depressive, manic and euthymic subjects according to predefined cut-off scores. Severity of current mood symptoms was correlated with activities of the enzymes kynurenine 3-monooxygenase (ratio of 3-hydroxykynurenine/ kynurenine), kynurenine aminotransferase (ratio of kynurenic acid/ kynurenine) and kynureninase (ratio of 3-hydroxyanthranilic acid/ 3-hydroxykynurenine), proxied by ratios of serum concentrations. Results: Individuals with manic symptoms showed a shift towards higher kynurenine 3-monooxygenase activity (χ2 = 7.14, Df = 2, p = .028), compared to euthymic as well as depressed individuals. There were no differences between groups regarding activity of kynurenine aminotransferase and kynureninase. Within the group of depressed patients, Hamilton Depression Scale and kynurenine aminotransferase showed a significant negative correlation (r = -0.41, p = .036), displaying lower metabolism in the direction of kynurenic acid. Conclusion: Depression severity in bipolar disorder seems to be associated with a decreased synthesis of putative neuroprotective kynurenic acid. Furthermore, higher kynurenine 3-monooxygenase activity in currently manic individuals indicates an increased inflammatory state within bipolar disorder with more severe inflammation during manic episodes. The underlying pathophysiological mechanisms of the different affective episodes could represent parallel mechanisms rather than opposed processes.
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2

Chen, Yiquan, and Gilles J. Guillemin. "Kynurenine Pathway Metabolites in Humans: Disease and Healthy States." International Journal of Tryptophan Research 2 (January 2009): IJTR.S2097. http://dx.doi.org/10.4137/ijtr.s2097.

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Tryptophan is an essential amino acid that can be metabolised through different pathways, a major route being the kynurenine pathway. The first enzyme of the pathway, indoleamine-2,3-dioxygenase, is strongly stimulated by inflammatory molecules, particularly interferon gamma. Thus, the kynurenine pathway is often systematically up-regulated when the immune response is activated. The biological significance is that 1) the depletion of tryptophan and generation of kynurenines play a key modulatory role in the immune response; and 2) some of the kynurenines, such as quinolinic acid, 3-hydroxykynurenine and kynurenic acid, are neuroactive. The kynurenine pathway has been demonstrated to be involved in many diseases and disorders, including Alzheimer's disease, amyotrophic lateral sclerosis, Huntington's disease, AIDS dementia complex, malaria, cancer, depression and schizophrenia, where imbalances in tryptophan and kynurenines have been found. This review compiles most of these studies and provides an overview of how the kynurenine pathway might be contributing to disease development, and the concentrations of tryptophan and kynurenines in the serum, cerebrospinal fluid and brain tissues in control and patient subjects.
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Badawy, Abdulla A. B., and Samina Bano. "Tryptophan Metabolism in Rat Liver after Administration of Tryptophan, Kynurenine Metabolites, and Kynureninase Inhibitors." International Journal of Tryptophan Research 9 (January 2016): IJTR.S38190. http://dx.doi.org/10.4137/ijtr.s38190.

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Rat liver tryptophan (Trp), kynurenine pathway metabolites, and enzymes deduced from product/substrate ratios were assessed following acute and/or chronic administration of kynurenic acid (KA), 3-hydroxykynurenine (3-HK), 3-hydroxyanthranilic acid (3-HAA), Trp, and the kynureninase inhibitors benserazide (BSZ) and carbidopa (CBD). KA activated Trp 2,3-dioxygenase (TDO), possibly by increasing liver 3-HAA, but inhibited kynurenine aminotransferase (KAT) and kynureninase activities with 3-HK as substrate. 3-HK inhibited kynureninase activity from 3-HK. 3-HAA stimulated TDO, but inhibited kynureninase activity from K and 3-HK. Trp (50 mg/kg) increased kynurenine metabolite concentrations and KAT from K, and exerted a temporary stimulation of TDO. The kynureninase inhibitors BSZ and CBD also inhibited KAT, but stimulated TDO. BSZ abolished or strongly inhibited the Trp-induced increases in liver Trp and kynurenine metabolites. The potential effects of these changes in conditions of immune activation, schizophrenia, and other disease states are discussed.
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Majláth, Zsófia, and László Vécsei. "A kinureninrendszer és a stressz." Orvosi Hetilap 156, no. 35 (August 2015): 1402–5. http://dx.doi.org/10.1556/650.2015.30246.

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The kynurenine pathway is the main route of tryptophan degradation which gives rise to several neuroactive metabolites. Kynurenic acid is an endogenous antagonist of excitatory receptors, which proved to be neuroprotective in the preclinical settings. Kynurenines have been implicated in the neuroendocrine regulatory processes. Stress induces several alterations in the kynurenine metabolism and this process may contribute to the development of stress-related pathological processes. Irritable bowel disease and gastric ulcer are well-known disorders which are related to psychiatric comorbidity and stress. In experimental conditions kynurenic acid proved to be beneficial by reducing inflammatory processes and normalizing microcirculation in the bowel. Further investigations are needed to better understand the relations of stress and the kynurenines, with the aim of developing novel therapeutic tools for stress-related pathologies. Orv. Hetil., 2015, 156(35), 1402–1405.
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Hafstad Solvang, Stein-Erik, Jan Erik Nordrehaug, Dag Aarsland, Johannes Lange, Per Magne Ueland, Adrian McCann, Øivind Midttun, Grethe S. Tell, and Lasse Melvaer Giil. "Kynurenines, Neuropsychiatric Symptoms, and Cognitive Prognosis in Patients with Mild Dementia." International Journal of Tryptophan Research 12 (January 2019): 117864691987788. http://dx.doi.org/10.1177/1178646919877883.

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Introduction: Circulating tryptophan (Trp) and its downstream metabolites, the kynurenines, are potentially neuroactive. Consequently, they could be associated with neuropsychiatric symptoms and cognitive prognosis in patients with dementia. Objective: The objective of this study was to assess associations between circulating kynurenines, cognitive prognosis, and neuropsychiatric symptoms. Methods: We measured baseline serum Trp, neopterin, pyridoxal 5′-phosphate (PLP), and 9 kynurenines in 155 patients with mild dementia (90 with Alzheimer’s disease, 65 with Lewy body dementia). The ratios between kynurenine and Trp and kynurenic acid (KA) to kynurenine (KKR) were calculated. The Mini-Mental State Examination (MMSE) and the Neuropsychiatric Inventory (NPI) were administered at baseline and annually over 5 years. Associations between baseline metabolite concentrations with MMSE and the NPI total score were assessed using a generalized structural equation model (mixed-effects multiprocess model), adjusted for age, sex, current smoking, glomerular filtration rate, and PLP. Post hoc associations between KKRs and individual NPI items were assessed using logistic mixed-effects models. False discovery rate (0.05)–adjusted P values ( Q values) are reported. Results: Kynurenine had a nonlinear quadratic relationship with the intercept of the MMSE scores over 5 years ( Q < 0.05), but not with the slope of MMSE decline. Kynurenine was associated with a higher NPI total score over time ( Q < 0.001). Post hoc, both KKR and KA were associated with more hallucinations ( Q < 0.05). Conclusions: Kynurenine has a complex relationship with cognition, where both low and high levels were associated with poor cognitive performance. A higher KKR indicated risk for neuropsychiatric symptoms, especially hallucinations.
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Gawel, Kinga. "A Review on the Role and Function of Cinnabarinic Acid, a “Forgotten” Metabolite of the Kynurenine Pathway." Cells 13, no. 5 (March 5, 2024): 453. http://dx.doi.org/10.3390/cells13050453.

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In the human body, the majority of tryptophan is metabolized through the kynurenine pathway. This consists of several metabolites collectively called the kynurenines and includes, among others, kynurenic acid, L-kynurenine, or quinolinic acid. The wealth of metabolites, as well as the associated molecular targets and biological pathways, bring about a situation wherein even a slight imbalance in the kynurenine levels, both in the periphery and central nervous system, have broad consequences regarding general health. Cinnabarinic acid (CA) is the least known trace kynurenine, and its physiological and pathological roles are not widely understood. Some studies, however, indicate that it might be neuroprotective. Information on its hepatoprotective properties have also emerged, although these are pioneering studies and need to be replicated. Therefore, in this review, I aim to present and critically discuss the current knowledge on CA and its role in physiological and pathological settings to guide future studies.
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Büki, Alexandra, Gabriella Kekesi, Gyongyi Horvath, and László Vécsei. "A Potential Interface between the Kynurenine Pathway and Autonomic Imbalance in Schizophrenia." International Journal of Molecular Sciences 22, no. 18 (September 16, 2021): 10016. http://dx.doi.org/10.3390/ijms221810016.

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Schizophrenia is a neuropsychiatric disorder characterized by various symptoms including autonomic imbalance. These disturbances involve almost all autonomic functions and might contribute to poor medication compliance, worsened quality of life and increased mortality. Therefore, it has a great importance to find a potential therapeutic solution to improve the autonomic disturbances. The altered level of kynurenines (e.g., kynurenic acid), as tryptophan metabolites, is almost the most consistently found biochemical abnormality in schizophrenia. Kynurenic acid influences different types of receptors, most of them involved in the pathophysiology of schizophrenia. Only few data suggest that kynurenines might have effects on multiple autonomic functions. Publications so far have discussed the implication of kynurenines and the alteration of the autonomic nervous system in schizophrenia independently from each other. Thus, the coupling between them has not yet been addressed in schizophrenia, although their direct common points, potential interfaces indicate the consideration of their interaction. The present review gathers autonomic disturbances, the impaired kynurenine pathway in schizophrenia, and the effects of kynurenine pathway on autonomic functions. In the last part of the review, the potential interaction between the two systems in schizophrenia, and the possible therapeutic options are discussed.
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Szűcs, Edina, Azzurra Stefanucci, Marilisa Pia Dimmito, Ferenc Zádor, Stefano Pieretti, Gokhan Zengin, László Vécsei, Sándor Benyhe, Marianna Nalli, and Adriano Mollica. "Discovery of Kynurenines Containing Oligopeptides as Potent Opioid Receptor Agonists." Biomolecules 10, no. 2 (February 12, 2020): 284. http://dx.doi.org/10.3390/biom10020284.

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Kynurenine (kyn) and kynurenic acid (kyna) are well-defined metabolites of tryptophan catabolism collectively known as “kynurenines”, which exert regulatory functions in host-microbiome signaling, immune cell response, and neuronal excitability. Kynurenine containing peptides endowed with opioid receptor activity have been isolated from natural organisms; thus, in this work, novel opioid peptide analogs incorporating L-kynurenine (L-kyn) and kynurenic acid (kyna) in place of native amino acids have been designed and synthesized with the aim to investigate the biological effect of these modifications. The kyna-containing peptide (KA1) binds selectively the μ-opioid receptor with a Ki = 1.08 ± 0.26 (selectivity ratio μ/δ/κ = 1:514:10,000), while the L-kyn-containing peptide (K6) shows a mixed binding affinity for μ, δ, and κ-opioid receptors, with efficacy and potency (Emax = 209.7 + 3.4%; LogEC50 = −5.984 + 0.054) higher than those of the reference compound DAMGO. This novel oligopeptide exhibits a strong antinociceptive effect after i.c.v. and s.c. administrations in in vivo tests, according to good stability in human plasma (t1/2 = 47 min).
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Myint, A. M. "Role of Tryptophan-kynurenine Pathway in Depression: Psychopathological Aspect." European Psychiatry 24, S1 (January 2009): 1. http://dx.doi.org/10.1016/s0924-9338(09)70521-8.

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It was reported that cytokines such as IFN-γ reduce the synthesis of 5-HT by stimulating the activity of indoleamine 2,3 dioxygenase (IDO) enzyme which degrades tryptophan to kynurenine. Kynurenine is further metabolized to kynurenic acid (KYNA), 3-hydroxykynurenine (3OHK) and quinolinic acid (QA) by kynurenine aminotransferase (KAT), kynurenine 3-monooxygenase (KMO) and kynureninase. Both KMO and kynureninase are also shown to be activated by IFNγ. The 3OHK is neurotoxic apoptotic while QA is the excitotoxic N-methyl-D-aspartate (NMDA) receptor agonist. Conversely KYNA is an antagonist of all three ionotropic excitatory amino acid receptors and considered neuroprotective. In the brain, tryptophan catabolism occurs in the astrocytes and. The astrocytes are shown to produce mainly KYNA whereas microglia and macrophages produced mainly 3OHK and QA. The astrocytes have been demonstrated to metabolise the QA produced by the neighbouring microglia.Tryptophan breakdown has been found to be increased but KYNA, the neuroprotective metabolite is decreased in both blood and cerebrospinal fluid of the patients with major depression compared to healthy controls. Moreover, the ratio between KYNA and 3OHK showed significant correlation with response to treatment. These findings lead to the hypothesis an imbalance neuroprotection-neurodegener-ation in terms of kynurenine metabolites and their immunological and biochemical interactions in the brain might further induce the apoptosis of the neuroprotective astrocytes and the vulnerability to stress is thereby enhanced.
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Zakharov, Gennady A., Alexander V. Zhuravlev, Tatyana L. Payalina, Nikolay G. Kamyshev, and Elena V. Savvateeva-Popova. "The influence of D. melanogaster mutations of the kynurenine pathway of tryptophan metabolism on locomotor behavior and expression of genes belonging to glutamatergic and cholinergic systems." Ecological genetics 9, no. 2 (June 15, 2011): 65–73. http://dx.doi.org/10.17816/ecogen9265-73.

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Disbalance of kynurenines produced by Drosophila mutations of the kynurenine pathway of tryptophan metabolism influences the locomotor behavior in larvae. The most pronounced is the effect of accumulation of kynurenic acid in the mutant cinnabar manifested as sharp reduction of general level of locomotor activity. The mutations seem to act through modulatory influences of kynurenines on signal cascades governed by ionotropic glutamatergic and cholinergic receptors. Expression of receptor genes in the mutants shows age-related changes pointing to gradual evolvement of consequences of kynurenines disbalance.
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Dissertations / Theses on the topic "Kynurenine"

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Milne, Gavin D. S. "Inhibition studies of kynurenine 3-monooxygenase." Thesis, University of St Andrews, 2013. http://hdl.handle.net/10023/4101.

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Kynurenine 3-monooxygenase (K3MO) lies on the kynurenine pathway, the major pathway for the catabolism of L-tryptophan. It converts kynurenine to 3-hydroxy kynurenine. Inhibition of K3MO is important in several neurological diseases and there is evidence that inhibition of K3MO could also be targeted for the prevention of multiple organ failure, secondary to acute pancreatitis. A structure activity relationship based upon the 1,2,4-oxadiazoles motif was carried out which revealed amide 207 as an inhibitor of P. fluorescens K3MO. Further structure activity relationships were developed based upon 207. This revealed 3,4-dichloro substitution in 235 and 245 as optimum for inhibition. Co-crystalisation of these inhibitors with P. fluorescens K3MO revealed their interactions with the enzyme. It also highlighted new, potential interactions between the inhibitors and K3MO. This led to the synthesis of 271 and 272, which were also potent inhibitors of K3MO. These amides were successfully co-crystalised with P. fluorescens K3MO. Further development of the amides followed, with amide 282 providing the most potent inhibitor of P. fluorescens K3MO to date (Kᵢ = 29.1 nM).
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Thevandavakkam, Mathuravani Aaditiyaa. "Deciphering the kynurenine-3-monooxygenase interactome." Thesis, University of Leicester, 2011. http://hdl.handle.net/2381/10070.

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Kynurenine-3-monooxygenase (KMO) is a mitochondrial enzyme in the kynurenine pathway (KP) through which tryptophan is degraded to NAD+. The central KP is altered in neurodegenerative diseases and other CNS disorders. The causative role of KP metabolites has been particularly well studied in the neurodegenerative disorder Huntington’s disease (HD), a fatal adult onset condition inherited in an autosomal dominant manner. In HD, flux in the KP is perturbed such that neurotoxic metabolites (3-hydroxykynurenine and quinolinic acid) of the pathway are increased relative to a neuroprotective metabolite (kynurenic acid). KMO lies at a critical branching point in the KP such that inhibition of KMO activity ameliorates this metabolic perturbation. Consequently, several recent studies have found that KMO inhibition is protective in models of HD. These findings have widespread implications in treating several neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease where the KP is implicated in pathogenesis. The focus of this project was to better understand the cellular role(s) and interactions of KMO. To this end, a novel membrane yeast two hybrid approach was established and optimised to identify protein interaction partners for outer mitochondrial membrane proteins. This approach was implemented to identify protein interaction partners of human KMO and its yeast orthologue Bna4, which were confirmed by biochemical approaches. Additionally, genetic interaction partners of BNA4 identified by systematic genetic screens were individually validated by classic genetic manipulations. Bioinformatic tools were then used to identify enriched interaction networks for KMO using this novel interaction data. These analyses suggested possible roles for KMO in many processes, including energy metabolism, cytoskeleton organisation and response to infection and inflammation, providing evidence that KMO plays roles in diverse cellular pathways in addition to the KP.
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Bell, Helen Barbara. "Characterisation of the active site of kynurenine 3-monooxygenase." Thesis, University of Edinburgh, 2016. http://hdl.handle.net/1842/20397.

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Kynurenine 3-monooxygenase (KMO) is a flavoprotein which has been implicated in Huntington’s disease, Alzheimer’s disease and acute pancreatitis. Recently there has been important research published about this enzyme including the structure of a truncated Saccharomyces cerevisiae KMO enzyme and KMO inhibition studies in animal models of disease. In previous work from this research group the complete Pseudomonas fluorescens KMO enzyme has been successfully crystallised both with and without the substrate, L-kynurenine, from which significant insights were gained into function and the potential role of domain movement. To examine substrate binding in KMO and to consolidate previous structural studies, key residues in the active site have been investigated using site directed mutagenesis, crystallography and kinetic analysis using steady-state techniques. This analysis has identified the interactions between the enzyme and the substrate and provides a basis for inhibitor design. The residues implicated in substrate binding are N369, Y404 and R84. For N369 and Y404, minor changes to the amino acid in the mutations N369S and Y404F were shown to cause a decrease in binding affinity of the substrate but the enzyme remained active. For the mutations Y404A and R84K enzyme activity was significantly affected. Crystal structures of N369S, Y404F and R84K were also obtained. Another residue in the active site studied was H320 which is the only amino acid to differ in the active sites of the human and Pseudomonas fluorescens enzymes. This residue was therefore of interest to determine whether the bacterial enzyme used in this work is likely to be a good model for the human enzyme, which has not yet been successfully isolated in significant quantities for in vitro research. Modifying this residue to obtain H320F KMO revealed that this residue does not have a significant role in substrate binding. Potent inhibitor molecules have been studied with this enzyme and shown in kinetic assays to have nanomolar Ki values. These inhibitors are the most potent inhibitors studied with Pseudomonas fluorescens to date and continue previous inhibitor studies carried out with this enzyme. This group of inhibitors contain different substituents in the part of the molecule shown to bind closest to the C-terminal domain of the protein. These novel inhibitors do not allow the flavin to be reduced by NADPH (which results in unwanted peroxide production) unlike a number of previously studied molecules and therefore have the potential to be clinically useful. This research therefore answers many questions about this enzyme, in particular about the role of particular residues in the active site, substrate recognition and inhibition of this important drug target.
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Wilkinson, Martin. "Structural dynamics and ligand binding in kynurenine-3-monooxygenase." Thesis, University of Edinburgh, 2013. http://hdl.handle.net/1842/7965.

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Kynurenine 3-monooxygenase is a FAD-dependent aromatic hydroxylase (FAH) which is a widely suggested therapeutic target for controlling the balance of bioactive metabolite levels produced by the mammalian kynurenine pathway (KP). Prior to starting this work no structural information was known for the enzyme, with studies of the human form complicated by the presence of a C-terminal transmembrane helix. The bacterial Pseudomonas fluorescens enzyme (PfKMO) lacks the transmembrane region and has been previously characterised by Crozier-Reabe and Moran [1, 2]. Therefore PfKMO, which shares 32 % sequence identity with the human enzyme, was selected as a target for structure solution. Initial substrate bound PfKMO crystals showed poor X-ray diffraction. Subsequent growth optimisation and the generation of a C252S/C461S PfKMO mutant (dm2) yielded crystals suitable for structure solution. Selenomethioninelabelled substrate bound dm2 crystals were used to solve the first structure to a resolution of 3.40 Å. With just one protein molecule per asymmetric unit, a high solvent content was responsible for the poor diffraction properties of this crystal form. The overall fold resembled that of other FAH enzymes with a Rossmann-fold based FADbinding domain above a buried substrate binding pocket. Interestingly PfKMO possesses an additional, novel C-terminal domain that caps the back of the substrate-binding pocket on the opposite side to the flavin. Residues proposed to be involved in substrate binding were identified and shown to be highly conserved among mammalian KMO sequences. Subsequently single crystals of substrate-free dm2 PfKMO were obtained and showed significantly stronger diffraction due to new lattice packing in an orthorhombic space group bearing four molecules per asymmetric unit. The structure was solved to a resolution of 2.26 Å and revealed a clear conformational change of the novel C-terminal domain. This movement opens a potential route of substrate/product exchange between bulk solvent and the active site. The investigation of a set of C-terminal mutants further explored the relevance and mechanics of the conformational change. In addition the presence of chloride ions in the substrate-free crystal growth solution caused a small number of localised subtle alterations to the structure, with a potential chloride binding site identified adjacent to the flavin cofactor. This may have relevance for the observed inhibition of PfKMO activity by monovalent anions – a feature widely common to FAH enzymes [3]. The first discovered KMO inhibitors were analogues of the substrate L-Kyn, however one such compound (m-NBA) was recently shown to instigate uncoupled NADPH oxidation leading to the release of cytotoxic hydrogen peroxide [1]. A set of substrate analogues were tested and characterised for inhibition of PfKMO. The picture was shown to be complex as some substrate analogues completely inhibited the enzyme whilst the binding of some still stimulated low-levels of NADPH oxidation. Crystallographic studies with m-NBA and 3,4-dichlorobenzoylalanine (3,4-CBA) bound revealed indistinguishable structures from that of substrate-bound PfKMO. These studies suggest that the analogue 3,4CBA is a potent PfKMO inhibitor whose therapeutic potential may be re-visited. The previous most potent KMO inhibitor whose structure was not analogous to the substrate was Ro 61-8048 [4], which unfortunately did not pass pre-clinical safety tests. A novel series of 1,2,4-oxadiazole amides based on the structure of Ro 61-8048 was created by Gavin Milne (PhD, University of St Andrews) and tested on PfKMO. Rounds of refinement led to the discovery and refinement of low nanomolar competitive inhibitors of the bacterial enzyme. PfKMO was co-crystallised with each of the four most potent compounds forming a third different lattice arrangement, which yielded structures to resolutions of 2.15-2.40 Å. The structures displayed conformational changes resembling the substrate-free fold possibly caused by displacement of a crucial substrate-binding residue, R84. Overall the wealth of structural data obtained may be transferable to predictions about the structural features of human KMO and to the rational design of therapeutic inhibitors. The potent novel inhibitors tested may additionally present a new exciting development for the therapeutic inhibition of human KMO.
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Owe-Young, Robert School of Medicine UNSW. "Kynurenine pathway metabolism at the blood-brain barrier." Awarded by:University of New South Wales. School of Medicine, 2006. http://handle.unsw.edu.au/1959.4/26183.

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A major product of HIV-infected and cytokine-stimulated monocytic-lineage cells is quinolinic acid (QUIN), a neurotoxic metabolite of the kynurenine pathway (KP) of L-tryptophan (L-Trp) metabolism. Despite the large number of neurotoxins found in HIV patients with AIDS Dementia Complex (ADC), only QUIN correlates with both the presence and severity of ADC. With treatment, cerebrospinal fluid (CSF) QUIN concentrations decrease proportionate to the degree of clinical and neuropsychological improvement. As endothelial cells (EC) of the blood-brain barrier (BBB) are the first brain-associated cell that a bloodborne pathogen would encounter, this project examined the BBB response to KP metabolites, as these are implicated in damage of the CNS associated with ADC. Using RT-PCR and HPLC/gas chromatographymass spectrometry (GC-MS), I found that cultured primary human BBB EC and pericytes constitutively expressed the KP. EC synthesised kynurenic acid (KA) constitutively, and after immune activation, kynurenine (KYN). Pericytes produced small amounts of picolinic acid and after immune activation, KYN. An SV40-transformed BBB EC showed no KP expression. By contrast, human umbilical vein EC only expressed low levels of KA after immune activation, however human dermal microvascular EC showed a similar constitutive and inducible KP to that in BBB EC. As T cells are central to primary HIV infection, I also examined KP expression in two CD4+ and one CD4- cell lines, but none showed either constitutive or inducible KP expression. I next examined how QUIN might interact with BBB EC. There was no binding of 3H-QUIN to cultured primary human BBB EC, however a biologically relevant concentration of QUIN induced changes in gene expression which adversely affected EC function, possibly mediated by lipid peroxidation and oxidative stress. The upregulated genes were of the heat shock protein family, and the downregulated genes were associated with regulation of cell adhesion, tight junction and cytoskeletal stability, metalloproteinase (MMP) regulation, apoptosis and G protein signaling. Immunofluorescence showed that QUIN induced morphological changes in BBB EC consistent with the changes in gene expression. Gelatin zymography showed that this was not mediated by MMPs, as constitutive MMP expression was unchanged. These data provide strong evidence for QUIN directly damaging the BBB in the context of HIV infection.
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Taylor, Mark Robert Duncan. "High-resolution structural studies of kynurenine 3-monooxygenase." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/28913.

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The kynurenine pathway produces NAD+ from L-tryptophan. Metabolites known as the kynurenines are produced within the pathway. The effects of the kynurenines have been associated with a number of diseases including cancer, Alzheimer’s disease, Huntington’s disease, and acute pancreatitis. Kynurenine monooxygenase (KMO) is an enzyme that catalyses the conversion of L-kynurenine to 3-hydroxy-L-kynurenine, the downstream product of which is the neurotoxic quinolinic acid. L-kynurenine is positioned at a branching point within the pathway. Metabolism via KMO leads to quinolinic acid production whereas conversion via kynurenine aminotransferase (KAT) produces the neuroprotective kynurenic acid. Inhibition of KMO leads to an increase in kynurenic acid concentration. This has also been shown to ameliorate the symptoms of neurological diseases in a number of animal models as well as to protect against multiple organ dysfunction caused by acute pancreatitis in rodent models. These findings present KMO as a promising drug target. Due to the hydrophobic nature of human KMO (hKMO) it has been necessary to utilise other forms of KMO as models. Past studies have produced crystal structures of a truncated Saccharomyces cerevisiae KMO and of Pseudomonas fluorescens KMO (PfKMO). Previous work in this research group has resulted in the structure of variants of PfKMO bound to either inhibitor molecules or substrate. These structures identified residues involved in substrate binding and the presence of a highly mobile section of the C-terminus, giving rise to open and closed conformations. It was surmised the movement of the C-terminus was dependent upon the presence of substrate and an interactive network between the C-terminus and the rest of the protein. Using improved crystallising conditions high-resolution structures of PfKMO have been produced that allow for further study of residues involved in substrate binding and the interactive network within the C-terminus. The mutants R84K and Y404F showed severely decreased enzyme activity. Crystal structures of these proteins showed disrupted interactions between substrate and active site. These findings underline the importance of residues R84 and Y404 in substrate binding. An H320F mutation gives an analogous active site to hKMO. Crystallographic and kinetic study of this mutant proved very similar to PfKMO, supporting the use of PfKMO as a model for hKMO. Throughout the work each structure had a P21221 space group with two molecules in the asymmetric unit. The presence of an open and closed molecule within each structure, including substrate-free molecules refuted the connection between C-terminus and substrate. R386K and E372T mutations were separately introduced in order to interrupt the interactive network. The presence of both open and closed conformations in the structures of R386K and E372T refutes the necessity for the interactive network in C-terminus movement. The data analysed throughout the project suggest simple mobility and thermal motion as the cause of the movement of the C-terminus. This work, in conjunction with kinetic data from the thesis of Helen Bell, presents structural data to characterise the role of binding residues within the active site of KMO as well as the mechanistic role of the C-terminus. It also highlights the importance of certain binding residues and countered the previously held hypotheses surrounding the significance of the C-terminus. The mechanistic role of the C-terminus therefore remains unclear and requires further study.
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Swaih, Aisha Mahmod O. "Functional and localization studies of human kynurenine 3-monooxygenase." Thesis, University of Leicester, 2016. http://hdl.handle.net/2381/37835.

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Kynurenine 3-monooxygensae (KMO) is an outer mitochondrial membrane protein which plays a critical regulatory role in the kynurenine pathway (KP), catalysing the production of 3-hydroxykynurenine (3-HK). Increased KMO activity likely contributes to the excitotoxicity seen in neurodegenerative disorders by elevating the levels of the neurotoxic KP metabolites 3-HK and quinolinic acid. Studies employing models of Huntington’s disease (HD) have shown that inhibition of KMO is neuroprotective, making KMO a potential therapeutic target for this disorder. This study interrogates the subcellular localisation of human KMO and dissects the interaction between KMO and the huntingtin (HTT) protein, mutations in which cause HD. Confocal microscopy based co-localisation studies of KMO demonstrated that full length KMO (flKMO) was exclusively localised to the mitochondria when expressed in HEK293T cells. Notably, deleting a C-terminal portion of flKMO which contains a putative transmembrane domain mis-localised the remaining protein (tKMO) to other cellular compartments. Localization of flKMO to the outer mitochondrial membrane was further confirmed via transmission electron microscopy. To study potential interactions between flKMO and HTT in living cells, bimolecular fluorescence complementation (BiFC) assay was utilised, which is based upon reconstitution of split fluorescence proteins. The BiFC approach allowed visualisation and quantification of flKMO interaction with both WT HTT and soluble mHTT fragments at the mitochondria. The strength of this interaction is inversely correlated to the length of the HTT polyglutamine expansion. Increased mitochondrial sub-cellular localisation of BiFC HTT constructs was confirmed via microscopy. tKMO however did not interact with HTT via the BiFC system, indicating that the C-terminal region of flKMO is important for both mitochondrial localisation and protein interaction. In total, these data suggest that flKMO-HTT interactions at the mitochondria may be biologically significant and could play a role in regulating KMO activity, and that in HD this regulatory process is impaired.
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Kolodziej, Lukasz. "An investigation of the kynurenine pathway in experimental arthritis." Thesis, Imperial College London, 2011. http://hdl.handle.net/10044/1/9641.

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The kynurenine pathway is a catabolic biochemical pathway responsible for degradation of tryptophan, an essential amino acid. As a consequence, biologically active molecules, kynurenines, are produced. These chemical entities can influence immune responses. Previously, it has been shown that pharmacological inhibition of the initial step on the pathway increases the severity of collagen-induced arthritis (CIA), an animal model of rheumatoid arthritis. In contrast, treatment with kynurenine, a major by product of tryptophan degradation, effectively ameliorated the disease. This project was based around the hypothesis that tryptophan metabolism via the kynurenine pathway represents an endogenous regulatory mechanism that is activated in response to inflammation. To test this hypothesis, I carried out a comprehensive analysis of the kynurenine pathway in the immune system in CIA as well as in the liver or kidneys, organs in which kynurenine pathway is the most active under normal conditions. In this study, the endogenous activity of the kynurenine pathway in the immune system (lymph nodes and spleen), inflamed paws, liver, and kidneys was monitored during the induction phase of CIA (day 14 after immunisation) and during the period of disease resolution (day 10 after disease onset). In addition, the concentration of tryptophan, kynurenine and its selected catabolites anthranilic acid (AA) and 3-hydroxyanthranilic acid (3-HAA) was determined in the sera. All results were compared with naive tissues.Increased expression of all enzymes along the kynurenine pathway was observed locally in draining lymph nodes during the pre-arthritic phase of arthritis and this was accompanied by reduced levels of tryptophan. In contrast, during the resolution phase of arthritis not only was there decreased tryptophan concentration, but also there was an accumulation of the downstream tryptophan metabolites, kynurenine, AA, and 3-HAA in lymph nodes. In addition, the accumulation of kynurenine and its downstream metabolites observed during the resolution of arthritis was accompanied by reduced expression of enzymes involved in kynurenine catabolism (kynureninase, kynurenine 3-monooxygenase, and 3-hydroxyanthranilate 3,4 dioxygenase) towards the levels found in naïve mice. These findings provide for the first time evidence of an association between resolution of arthritis and the local accumulation of kynurenines in lymph nodes. However, in the paws and spleens of mice with CIA, there was no evidence of activation of the kynurenine pathway. Surprisingly, however, kynurenine catabolism was increased in the kidneys and liver during CIA which may explain why in sera from mice with CIA, the tryptophan concentration was not changed, whereas levels of kynurenine, AA, and 3-HAA actually decreased, despite the increased levels found in lymph nodes at the same time points. Based on these findings I assessed the potential therapeutic effect of exogenous administration of AA and 3-HAA in mice with established CIA and in order to facilitate this study I established a novel method of assessment of bone integrity based on 3-dimensional imaging using micro-computed tomography. Using in vivo observations, micro-computed tomography and histological sectioning with hematoxylin and eosin staining, I showed that neither AA nor 3-HAA treatment was effective in established CIA. However, treatment with etanercept, a potent inhibitor of TNF, profoundly reduced the severity of bone and cartilage damage. I also confirmed previous findings that tranilast, a derivative of 3-HAA which exhibits kynurenine-like activity and has a longer half-life than naturally occurring tryptophan metabolite, was effective in established CIA. Thus, taken together, activation of the kynurenine pathway in the lymph nodes may constitute a fine tuning mechanism involved in resolution of inflammation. However, exogenous administration of naturally occurring kynurenines is unlikely to be an effective therapeutic strategy to reduce inflammation in arthritis, possibly because of their rapid clearance from the circulation.
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Skouras, Christos. "Kynurenine metabolism and organ dysfunction in human acute pancreatitis." Thesis, University of Edinburgh, 2017. http://hdl.handle.net/1842/28898.

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BACKGROUND: Acute pancreatitis (AP) is a sterile initiator of systemic inflammation that can trigger multiple organ dysfunction syndrome (MODS). In the acute phase of AP, the kynurenine pathway of tryptophan metabolism plays an important role in the genesis of AP-MODS in experimental animal models, but it is unknown whether the pathway is activated in human AP. Human data are required to support the rationale for kynurenine 3- monooxygenase (KMO) inhibition as a treatment for AP-MODS and reinforce the translational potential. Additionally, as respiratory dysfunction is frequent in severe AP, the role of lung ultrasonography in severity stratification deserves investigation. Furthermore, the effect of AP-MODS on long-term survival is unknown. OBJECTIVES: My objectives were to: 1) Define the temporal and quantitative relationship of kynurenine metabolites with the onset and severity of APMODS, 2) Investigate the value of lung ultrasonography in the early diagnosis of respiratory dysfunction in human AP-MODS, and 3) Examine whether early AP-MODS impacts on long-term survival. METHODS: 1) A prospective, observational, clinical experimental medicine study titled “Inflammation, Metabolism, and Organ Failure in Acute Pancreatitis” (IMOFAP) was performed. For 90 days, consecutive patients with a potential diagnosis of AP were recruited and venous blood was sampled at 0, 3, 6, 12, 24, 48, 72 and 168 hours post-recruitment. Kynurenine metabolite concentrations were measured by liquid chromatography–tandem mass spectrometry (LC-MS/MS) and analysed in the context of clinical data, disease severity indices, and cytokine profiles. 2) In a nested cohort within IMOFAP, 41 participants underwent lung ultrasonography to evaluate whether this imaging modality can detect respiratory dysfunction in AP. 3) Survival data for a prospectively maintained database of patients with AP was analysed after accounting for in-hospital deaths. RESULTS: 1) During the IMOFAP study, 79 patients were recruited with an elevated serum amylase, of which 57 patients met the diagnostic criteria for AP; 9 had severe disease. Temporal profiling revealed early tryptophan depletion and contemporaneous elevation of plasma concentrations of 3- hydroxykynurenine, which paralleled systemic inflammation and AP severity. 2) Lung ultrasonography findings correlated with respiratory dysfunction. 3) 694 patients were followed up for a median of 8.8 years. AP-MODS conferred a deleterious effect on overall survival which persisted after the exclusion of inhospital deaths (10.0 years, 95% C.I. = 9.4-10.6 years) compared to AP without MODS (11.6 years, 95% C.I. = 11.2-11.9 years; P = 0.001). This effect was independent of age. CONCLUSIONS: In the acute phase of AP, metabolic flux through KMO is elevated and proportionate to AP severity. Lung ultrasonography may be a useful technique for evaluating AP-MODS. AP-MODS is an independent predictor of long-term mortality. Together, this work reinforces the rationale for investigating early phase KMO inhibition as a therapeutic strategy in humans.
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Urenjak, Jutta A., and Tihomir P. Obrenovitch. "Accumulation of quinolinic acid with euro-inflammation: does it mean excitotoxicity?" Thesis, Kluwer Academic, Plenum Publishers, New York, 2003. http://hdl.handle.net/10454/2833.

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Books on the topic "Kynurenine"

1

Schwarcz, Robert, Simon N. Young, and Raymond R. Brown, eds. Kynurenine and Serotonin Pathways. Boston, MA: Springer New York, 1991. http://dx.doi.org/10.1007/978-1-4684-5952-4.

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Mittal, Sandeep, ed. Targeting the Broadly Pathogenic Kynurenine Pathway. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-11870-3.

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W, Stone T., ed. Quinolinic acid and the kynurenines. Boca Raton, Fla: CRC Press, 1989.

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Robert, Schwarcz, Young Simon N, and Brown Raymond R, eds. Kynurenine and serotonin pathways: Progress in tryptophan research. New York: Plenum Press, 1991.

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Rickards, Edward Hugh Galbraith. Plasma kynurenine tryptophan metabolites and associated substances in Gilles de la Tourette's Syndrome. Birmingham: University of Birmingham, 1999.

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Lázló, Vécsei, ed. Kynurenines in the brain: From experiments to clinics. Hauppauge, NY: Nova Science Publishers, 2005.

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Mirza, Sarwarbeg. The hepatic and the peripheral metabolism of tryptophan via the kynurenine pathway in children with biliary atresiaand with orthotopic liver transplant: The assessment of the relationship between the levels of the kynurenine metabolites, neopterin, biopterin and liver function tests. [Guildford]: University of Surrey, 1995.

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Naleem, Wazeer A. A study of urinary kynurenine metabolites in pre-pubertal, pubertal and post-pubertal male offsprings of families with family history negative and family history positive of alcoholism. [Guildford]: University of Surrey, 1995.

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Lapin, Izjaslav P. The neuroactivities of kynurenines: Stress, anxiety, depression, alcoholism, epilepsy : the 2000 Oswald Schmiedeberg lecture. Tartu: Tartu Ülikool, 2000.

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Mittal, Sandeep. Targeting the Broadly Pathogenic Kynurenine Pathway. Springer, 2016.

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Book chapters on the topic "Kynurenine"

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Schomburg, Dietmar, and Dörte Stephan. "Kynurenine 3-monooxygenase." In Enzyme Handbook, 433–36. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-57942-4_91.

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Schomburg, Dietmar, and Dörte Stephan. "Kynurenine-oxoglutarate transaminase." In Enzyme Handbook 13, 235–38. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-59176-1_46.

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Schomburg, Dietmar, and Dörte Stephan. "Kynurenine-glyoxylate transaminase." In Enzyme Handbook 13, 491–93. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-59176-1_98.

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Okuno, E., and R. Kido. "Kynureninase and Kynurenine 3-Hydroxylase in Mammalian Tissues." In Advances in Experimental Medicine and Biology, 167–76. Boston, MA: Springer New York, 1991. http://dx.doi.org/10.1007/978-1-4684-5952-4_15.

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Minatogawa, Y., C. Kawai, S. Hatada, and M. Sato. "Liver Specific Kynurenine (Alanine)." In Advances in Experimental Medicine and Biology, 471–76. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-0381-7_73.

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Schomburg, Dietmar, and Dörte Stephan. "Kynurenine 7, 8-hydroxylase." In Enzyme Handbook, 745–47. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-57942-4_154.

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Rudzite, V., and E. Jurika. "Kynurenine and Lipid Metabolism." In Advances in Experimental Medicine and Biology, 463–66. Boston, MA: Springer New York, 1991. http://dx.doi.org/10.1007/978-1-4684-5952-4_45.

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Majláth, Zsófia, Levente Szalárdy, Dénes Zádori, Péter Klivényi, Ferenc Fülöp, József Toldi, and László Vécsei. "Neuroprotection by Kynurenine Metabolites." In Handbook of Neurotoxicity, 1403–16. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-5836-4_165.

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Majláth, Zsófia, Levente Szalárdy, Dénes Zádori, Péter Klivényi, Ferenc Fülöp, József Toldi, and László Vécsei. "Neuroprotection by Kynurenine Metabolites." In Handbook of Neurotoxicity, 1067–80. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-15080-7_165.

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Weil-Fugazza, J. "Endogenous Kynurenine Derivatives and Pain." In Advances in Experimental Medicine and Biology, 83–87. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-0381-7_11.

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Conference papers on the topic "Kynurenine"

1

Gosker, Harry R., Gerard Clarke, John F. Cryan, and Annemie M. Schols. "Impaired skeletal muscle kynurenine metabolism in patients with COPD." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa940.

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Tharawadeephimuk, Waranan, Chaiyavat Chaiyasut, Sasithorn Sirilun, and Phakkharawat Sittiprapaporn. "Preliminary Study of Probiotics and Kynurenine Pathway in Autism Spectrum Disorder." In 2019 16th International Conference on Electrical Engineering/Electronics, Computer, Telecommunications and Information Technology (ECTI-CON). IEEE, 2019. http://dx.doi.org/10.1109/ecti-con47248.2019.8955380.

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Triplett, Todd A., Kendra Triplett, Everett Stone, Michelle Zhang, Mark Manfredi, Candice Lamb, Yuri Tanno, Lauren Ehrlich, and George Georgiou. "Abstract 5571: Immune-checkpoint inhibition via enzyme-mediated degradation of kynurenine." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-5571.

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Pinto, Sheena, Christoph Steeneck, Michael Albers, Simon Anderhub, Manfred Birkel, Larisa Buselic-Wölfel, Gisela Eisenhardt, Claus Kremoser, Thomas Hoffmann, and Ulrich Deuschle. "Abstract 1210: Targeting the IDO1-Kynurenine-AhR pathway for cancer immunotherapy." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-1210.

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Pinto, Sheena, Christoph Steeneck, Michael Albers, Simon Anderhub, Manfred Birkel, Larisa Buselic-Wölfel, Gisela Eisenhardt, Claus Kremoser, Thomas Hoffmann, and Ulrich Deuschle. "Abstract 1210: Targeting the IDO1-Kynurenine-AhR pathway for cancer immunotherapy." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-1210.

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Botticelli, Andrea, Bruna Cerbelli, Luana Lionetto, Ilaria Zizzari, Annalina Pisano, Michela Roberto, Elisa Onesti, et al. "Abstract 5705: The key role of kynurenine in anti-PD-1 failure." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-5705.

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Breda, Carlo, Aisha M. Swaih, Mariaelena Repici, and Flaviano Giorgini. "A29 Kynurenine 3-monooxygenase interacts with huntingtin at the outer mitochondrial membrane." In EHDN 2018 Plenary Meeting, Vienna, Austria, Programme and Abstracts. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/jnnp-2018-ehdn.27.

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Poulain-Godefroy, Odile, Mélina Le Roux, Gwenola Kervoaze, Anais Ollivier, Muriel Pichavant, and Philippe Gosset. "Kynurenine pathway as a modulator of inflammation in COPD and its exacerbations." In ERS Lung Science Conference 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/23120541.lsc-2022.61.

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Wangpaichitr, Medhi, Chunjing Wu, Dan JM Nguyen, Ying-Ying Li, Lynn G. Feun, and Niramol Savaraj. "Abstract 5478: Targeting kynurenine pathway for the treatment of cisplatin-resistant lung cancer." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-5478.

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Bessede, Alban, Antoine Italiano, Assia Chaïbi, Christophe Rey, Imane Nafia, Sylvestre le Moulec, Sophie Cousin, Maud Toulmonde, Céline Auzanneau, and Marina Pulido. "Abstract 5716: Functional evidence for an immunosuppressive role of kynurenine in cancer patients." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-5716.

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