Relevant bibliographies by topics / Biotransformation of drugs

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters

Academic literature on the topic 'Biotransformation of drugs'

Author: Grafiati
Published: 4 June 2021
Last updated: 12 February 2022

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Journal articles on the topic "Biotransformation of drugs"

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Svensson, Craig K. "Biotransformation of Drugs in Human Skin." Drug Metabolism and Disposition 37, no. 2 (November 12, 2008): 247–53. http://dx.doi.org/10.1124/dmd.108.024794.

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Tong, Wang-Yu, and Xiang Dong. "Microbial Biotransformation: Recent Developments on Steroid Drugs." Recent Patents on Biotechnology 3, no. 2 (June 1, 2009): 141–53. http://dx.doi.org/10.2174/187220809788700157.

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Velı́k, J., V. Baliharová, J. Fink-Gremmels, S. Bull, J. Lamka, and L. Skálová. "Benzimidazole drugs and modulation of biotransformation enzymes." Research in Veterinary Science 76, no. 2 (April 2004): 95–108. http://dx.doi.org/10.1016/j.rvsc.2003.08.005.

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Fink-Gremmels, J., and A. S. J. P. A. M. van Miert. "Veterinary drugs: disposition, biotransformation and risk evaluation." Analyst 119, no. 12 (1994): 2521. http://dx.doi.org/10.1039/an9941902521.

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Tang, Xia, Jerry W. Hayes, II, Louis Schroder, William Cacini, John Dorsey, R. C. Elder, and Katherine Tepperman. "Determination of Biotransformation Products of Platinum Drugs in Rat and Human Urine." Metal-Based Drugs 4, no. 2 (January 1, 1997): 97–109. http://dx.doi.org/10.1155/mbd.1997.97.

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Cisplatin is an extremely effective cancer chemotherapeutic agent, but its use is often accompanied by toxicity. Second generation drugs such as carboplatin are becoming more widely used because of reduced toxicity. Since biotransformation products have been implicated in the toxic responses, we have begun to investigate the reactions of cisplatin and carboplatin with potential biological ligands. Reaction products were characterized using HPLC with inductively coupled plasma - mass spectrometry (HPLC-ICP-MS), H1 and C13 NMR and fast atom bombardment - mass spectrometry (FAB-MS). Three Pt-creatinine complexes, cis-[Pt(NH3)2Cl(Creat)]+, cis-[Pt(NH3)2(H2O)(Creat)]2+ and cis-[Pt(NH3)2(Creat)2]2+, were synthesized and the platinum was shown to coordinate to the ring nitrogen, N(3). Human urine samples from patients on cisplatin chemotherapy were shown to contain cisplatin, its hydrolysis product and biotransformation products containing Pt-creatinine, Pt-urea and Pt-uric acid complexes. Urine from carboplatin patients shows fewer biotransformation products. Studies with control and diabetic (protected against cisplatin toxicity) rats showed systematic differences in the biotransformation products formed on administration of cisplatin.
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Ravindran, Selvan, Amlesh J. Tambe, Jitendra K. Suthar, Digamber S. Chahar, Joyleen M. Fernandes, and Vedika Desai. "Nanomedicine: Bioavailability, Biotransformation and Biokinetics." Current Drug Metabolism 20, no. 7 (August 7, 2019): 542–55. http://dx.doi.org/10.2174/1389200220666190614150708.

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Background: Nanomedicine is increasingly used to treat various ailments. Biocompatibility of nanomedicine is primarily governed by its properties such as bioavailability, biotransformation and biokinetics. One of the major advantages of nanomedicine is enhanced bioavailability of drugs. Biotransformation of nanomedicine is important to understand the pharmacological effects of nanomedicine. Biokinetics includes both pharmacokinetics and toxicokinetics of nanomedicine. Physicochemical parameters of nanomaterials have extensive influence on bioavailability, biotransformation and biokinetics of nanomedicine. Method: We carried out a structured peer-reviewed research literature survey and analysis using bibliographic databases. Results: Eighty papers were included in the review. Papers dealing with bioavailability, biotransformation and biokinetics of nanomedicine are found and reviewed. Bioavailability and biotransformation along with biokinetics are three major factors that determine the biological fate of nanomedicine. Extensive research work has been done for drugs of micron size but studies on nanomedicine are scarce. Therefore, more emphasis in this review is given on the bioavailability and biotransformation of nanomedicine along with biokinetics. Conclusion: Bioavailability results based on various nanomedicine are summarized in the present work. Biotransformation of nanodrugs as well as nanoformulations is also the focus of this article. Both in vitro and in vivo biotransformation studies on nanodrugs and its excipients are necessary to know the effect of metabolites formed. Biokinetics of nanomedicine is captured in details that are complimentary to bioavailability and biotransformation. Nanomedicine has the potential to be developed as a personalized medicine once its physicochemical properties and its effect on biological system are well understood.
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Da Silva, Vinicius Barreto, Daniel Fábio Kawano, Ivone Carvalho, Edemilson Cardoso Conceição, Osvaldo Freitas, and Carlos Henrique Tomich de Paula Silva. "Psoralen and Bergapten: In Silico Metabolism and Toxicophoric Analysis of Drugs Used to Treat Vitiligo." Journal of Pharmacy & Pharmaceutical Sciences 12, no. 3 (December 9, 2009): 378. http://dx.doi.org/10.18433/j3w01d.

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PURPOSE: to discuss the contribution of psoralen and bergapten metabolites on psoralens toxicity. METHODS: Computational chemistry prediction of metabolic reactions and toxicophoric groups based on the expert systems Derek and Meteor. RESULTS: a total of 15 metabolites were suggested for both psoralen and bergapten based on phase 1 and 2 biotransformations until the 3rd generation. Five toxicophoric substructures were shared among psoralen, bergapten and their corresponding metabolites; one toxicophoric marker (resorcinol) was only identified in bergapten and its biotransformation products. CONCLUSION: Although the toxic effects of psoralens are well known and documented, there is little information concerning the role of their metabolites in this process. We believe this work add to the knowledge of which molecular substructures are relevant to the process of metabolism and toxicity induction, thus guiding the search and development of more effective and less toxic drugs to treat vitiligo.
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Rekka, Eleni A., Panos N. Kourounakis, and Maria Pantelidou. "Xenobiotic Metabolising Enzymes: Impact on Pathologic Conditions, Drug Interactions and Drug Design." Current Topics in Medicinal Chemistry 19, no. 4 (April 11, 2019): 276–91. http://dx.doi.org/10.2174/1568026619666190129122727.

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Background: The biotransformation of xenobiotics is a homeostatic defensive response of the body against bioactive invaders. Xenobiotic metabolizing enzymes, important for the metabolism, elimination and detoxification of exogenous agents, are found in most tissues and organs and are distinguished into phase I and phase II enzymes, as well as phase III transporters. The cytochrome P450 superfamily of enzymes plays a major role in the biotransformation of most xenobiotics as well as in the metabolism of important endogenous substrates such as steroids and fatty acids. The activity and the potential toxicity of numerous drugs are strongly influenced by their biotransformation, mainly accomplished by the cytochrome P450 enzymes, one of the most versatile enzyme systems. Objective: In this review, considering the importance of drug metabolising enzymes in health and disease, some of our previous research results are presented, which, combined with newer findings, may assist in the elucidation of xenobiotic metabolism and in the development of more efficient drugs. Conclusion: Study of drug metabolism is of major importance for the development of drugs and provides insight into the control of human health. This review is an effort towards this direction and may find useful applications in related medical interventions or help in the development of more efficient drugs.
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Klinger, W. "Biotransformation of Drugs and other Xenobiotics during Postnatal development." Experimental and Toxicologic Pathology 48 (June 1996): 1–88. http://dx.doi.org/10.1016/s0940-2993(96)80104-7.

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PINZA, M., and G. PIFFERI. "ChemInform Abstract: Synthesis and Biotransformation of 3-Hydrazinopyridazine Drugs." ChemInform 26, no. 17 (August 18, 2010): no. http://dx.doi.org/10.1002/chin.199517276.

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Dissertations / Theses on the topic "Biotransformation of drugs"

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Hung, Yi-Feng. "Microbial biotransformation of 2-arylpropionic acids." Thesis, University of Brighton, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.361579.

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Blankert, Bertrand. "Développement de méthodes électroanalytiques hybrides pour l'étude de la biotransformation des médicaments." Doctoral thesis, Universite Libre de Bruxelles, 2006. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/210863.

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Le thème principal de notre travail consistait en la mise en exergue de l'efficience de la mise en œuvre de techniques hybrides associant l’électrochimie à l’élément biologique (biocapteur) ou l’électrochimie aux performances de la spectrométrie de masse (couplage EC-MS). Les informations fournies, jointes aux résultats des mesures en voltampérométrie sur électrodes solides, permettent une bonne compréhension mécanistique quant au devenir oxydatif de substances médicamenteuses.

Notre champ d'investigation s'est plus spécifiquement focalisé sur deux familles de molécules psychotropes (les phénothiazines, et une dibenzoazépine). Celles-ci connaissent un usage thérapeutique intensif et un regain d’intérêt pour des applications nouvelles, mais leur utilisation optimale souffre de l’existence d'effets secondaires physiopathologiques importants et dont l’étiologie est encore mal connue.

En premier lieu, les résultats de la voltampérométrie cyclique et les différentes modulations en ligne d'une cellule électrochimique couplée à la détection par spectrométrie de masse, nous ont permis de mettre en évidence des différences essentielles dans le devenir des phénothiazines quant aux produits d'oxydations générés. Plus précisément, un comportement clairement distinct entre les phénothiazines garnies de deux (2C) ou trois carbones (3C) entre les deux azotes au niveau de leur chaîne latérale a pu être mis en évidence. Les phénothiazines 3C s'oxydent de manière classique en leur sulfoxyde correspondant. Par contre, les phenothiazines 2C, conjointement à la formation de leur sulfoxyde, souffrent dans des conditions énergiques d’oxydation (persulfate, potentiel élevé) d'une rupture de la chaîne latérale et libèrent la phénothiazine base aisément oxydable et donc subissant elle-même une oxydation. Au vu des structures moléculaires en trois dimensions, nous émettons l’hypothèse que volume trop important de la chaîne latérale des phénothiazines 2C empêcherait le déploiement aisé des structures aromatiques en un radical cation coplanaire lors du phénomène d'oxydation. Les tensions intrastructurelles apparues conduiraient au bris de la chaîne latérale. Différents modes d'oxydation (chimique, électrochimique, enzymatique) ont été utilisés et laissent chacun apparaître la dépendance directe entre la puissance de l'agent oxydant appliqué et les produits d'oxydation obtenus. Chaque technique de détection, de manière individuelle, a bien confirmé la dualité entre les deux groupes de molécules. La mise en commun des divers résultats nous a permis l'identification irrévocable des espèces intermédiaires instables et des composés finaux. Par corollaire, nous avons pu postuler un schéma général d'oxydation pour les dérivés phénothiaziniques. Il nous paraît intéressant de transposer nos résultats aux biotransformations des phénothiazines car les produits identifiés ne possèdent pas l'activité pharmacologique du composé parent mais présentent un profil toxicologique bien répertorié dans la littérature. Nos résultats suggèrent d’approfondir les études de biotransformation afin de déterminer si ‘l’éclatement’ oxydatif des phénothiazines 2C est également observé in vivo. Une relation cause/effet de ces métabolites pourrait ainsi être établie.

En deuxième point, au travers de l'association CE/SM ou CE/CL/SM, nous avons étudié l’électroxydation de la clozapine. La génération et l'identification des principaux métabolites de phases I et II, illustre un mimétisme certain avec le CYP450, et nous a permis de confirmer de nombreuses données de la littérature quant à l'oxydation in vivo et in vitro de la clozapine. L'oxydation électrochimique ne génère cependant pas l'ensemble des réactions de métabolisation prises en charge par le système CYP450. Lors de la combinaison CE/SM, par l'absence de séparation chromatographique dans cette configuration, le spectre de masse présente un pic correspondant à un intermédiaire à demi-vie courte, difficilement et rarement mis en évidence: l'ion nitrénium. Cette espèce hautement réactive envers les fonctions thiols des petites molécules et des protéines, se trouve très régulièrement tenue pour responsable majeur de la toxicité avérée de la clozapine.

L'apparition plus abondante de dérivés déméthylés démontre l'influence du potentiel appliqué à l'électrode de travail lors de l'oxydation électrochimique. En effet, les processus de déméthylation nécessitent des potentiels élevés pour être observés. En présence de glutathion, aux différents pics antérieurement identifiés, des pics supplémentaires relatifs à la formation d'adduits de GSH sur la CLZ apparaissent. Les courbes voltampérométriques réalisées sur la clozapine suggèrent la distinctement la formation de l'ion nitrénium et d'une nouvelle espèce aisément électroréduite, probablement une structure quinone imine. L'addition de GSH provoque la disparition des pics de réduction de la CLZ. Ces comportements en VC corroborent les interprétations issues des mesures par couplage EC/CL/SM.

La dernière partie de notre travail a consisté en la construction d'un biocapteur à pâte de carbone solide avec inclusion au sein de cette matrice de peroxydase de raifort. Basé sur la capacité reconnue de l'HRP à reproduire in vitro des produits d'oxydation similaires à la métabolisation in vivo, nous avons exploité un tel biocapteur pour l'analyse de la clozapine et de composés thiols. Une compréhension fine du mécanisme opérationnel intrinsèque du biocapteur a pu être suggérée. La génération à la surface de l'électrode de l'ion nitrénium par oxydation enzymatique de la clozapine par l'HRP, suivie de sa réduction immédiate fournit un courant ampérométrique substantiel. Sous des conditions de pH optimales, ce courant de réduction autorise la détermination quantitative de la clozapine dans un domaine de linéarité compris entre 1 x 10-5 M et 1 x 10-6 M. L'addition de composés thiols dans le milieu occasionne une chute de courant par action de ceux-ci sur la structure radical cation ou nitrénium par addition nucléophile. La disparition de l'ion nitrénium et la formation d'un adduit GSH-CLZ inhibent tout processus de réduction à l'électrode du biocapteur. Cette diminution de courant proportionnelle aux concentrations en thiols introduits, permet la détermination quantitative de dérivés thiols. Les courbes de calibration exprimées en pourcentage d'inhibition conduisent facilement à l'évaluation de la constante d'inhibition (Ki) et de CI50. L'étude de la réponse ampérométrique de la clozapine à l'EPC/HRP en l'absence ou présence d'un dérivé thiol envisagé permet la détermination de Km et de caractériser le type d'inhibition qui entre en jeu. De tels paramètres cinétiques nous ont habilités à classer les thiols considérés en fonction de leur puissance réactionnelle envers les substances oxydées de la clozapine.

Au terme de ce travail, nous espérons avoir illustré, par l’étude de quelques molécules modèles, l’intérêt de la mise en œuvre des techniques électrochimiques couplées à l’élément biologique ou à la spectrométrie de masse. Des améliorations au niveau de la cellule électrochimique sont envisageables par l’emploi d’électrodes modifiées, elles laissent entrevoir la possibilité de mimer totalement le système CYP450.

Les résultats fournis par ces techniques hybrides et par voltampérométrie cyclique sont complémentaires, ils procurent un éventail d'informations d'une utilité estimable pour une application dans des études prédictives précoces de candidats médicament.
Doctorat en Sciences biomédicales et pharmaceutiques
info:eu-repo/semantics/nonPublished

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Chipiso, Kudzanai. "Biomimetic Tools in Oxidative Metabolism: Characterization of Reactive Metabolites from Antithyroid Drugs." PDXScholar, 2016. http://pdxscholar.library.pdx.edu/open_access_etds/3083.

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Toxicities of sulfur-based drugs have been attributed to formation of highly reactive sulfur oxo-acids and depletion of glutathione by the formation of reactive metabolites. Metabolic activation of these sulfur centers to conceivably toxic reactive metabolites (RMs) that can covalently modify proteins is considered the initial step in drug-induced toxicity. Despite considerable effort and research, detection and characterization of these RMs during drug development and therapy remains a challenge. Methimazole (MMI) and 6-propyl-2-thiouracil (PTU) are two commonly used antithyroid, sulfur-based drugs. Though effective, these drugs are associated with idiosyncratic toxicity. PTU has acquired a black box warning and physicians are calling for its withdrawal. RMs resulting from bioactivation of these drugs have been implicated in the aforementioned adverse reactions. Unfortunately, isolating and detecting RMs using traditional analytical techniques has not been successful due to their high reactivity and short life span, typically less than a minute. Current approaches in drug metabolism studies use microsomal incubations to generate RMs, which are then trapped using nucleophiles. Antithyroid drugs, however, are known to deactivate enzymes involved in their oxidation. Moreover, due to the complex nature of biological matrices and low abundance of possible toxic conjugates, this technique results in poor selectivity and sensitivity. This study developed and optimized an analytical method based on coupling electrochemical redox reactions and mass spectrometry to generate, detect and identify RMs from antithyroid drugs. The metabolites were also compared to those that were generated using chemical oxidants and biological microsomes. Mimicry of enzymatic oxidation of the antithyroid drugs was carried out by electrochemically oxidizing them using a coulometric cell coupled on-line to electrospray ionization mass spectrometry (EC/ESI-MS). Oxidation of MMI and subsequent trapping with nucleophile resulted in formation of adducts with N-acetylcysteine, revealing reactive metabolites. The most-postulated metabolite, sulfenic acid, had never been isolated or detected until now, using electrochemistry on-line with electrospray ionization. The results showed that bioactivation of MMI proceeds predominantly through the S-oxide and not through formation of thiyl radicals. These same trapping experiments were also conducted with PTU, but no conjugates were detected. The lack of conjugates from PTU does not preclude formation of RMs, but asserts radical pathway might be dominant in EC oxidation. A double mixing stopped flow was used to investigate the kinetics and mechanism of reaction of the MMI and the biologically relevant hypochlorous acid (HOCl), a product of oxidation of chloride (Cl-) ions by myeloperoxidase. The products from the chemical oxidations were compared to the electrochemically generated metabolites, some differences were apparent. Human liver microsomes (HLM) were also used, to investigate oxidation of PTU. Oxidation of PTU, resulted in the supposedly toxic S-oxide, but this has never been isolated, save for speculation. A comparison of metabolites that were found with HLM to those generated electrochemically showed some degree of similarity. These results show that in vitro techniques such as chemical oxidations and electrochemistry coupled to mass spectrometry can be used to mimic oxidative metabolism and subsequent high throughput screening of reactive metabolites.
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Schiffer, Lina Maria Klara Renate [Verfasser], and Rita [Akademischer Betreuer] Bernhardt. "Human steroidogenic cytochromes P450 : biotransformation of drugs and biotechnological application / Lina Maria Klara Renate Schiffer. Betreuer: Rita Bernhardt." Saarbrücken : Saarländische Universitäts- und Landesbibliothek, 2016. http://d-nb.info/1099282020/34.

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Mardal, Marie [Verfasser]. "Studies on the biotransformation/degradation pathways of drugs of abuse and their main human metabolites in wastewater / Marie Mardal." Saarbrücken : Saarländische Universitäts- und Landesbibliothek, 2017. http://d-nb.info/1227925484/34.

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Al-Attrache, Houssein. "Etude de la toxicité idiosyncratique de médicaments sur cellules HepaRG et levure : influence du stress inflammatoire et de la biotransformation." Thesis, Rennes 1, 2016. http://www.theses.fr/2016REN1B049/document.

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Chez l’homme, de nombreux médicaments ne sont toxiques que chez un petit nombre de patients traités. Divers facteurs de susceptibilité, génétiques et autres (doses quotidiennes, stress inflammatoire, réaction immune, maladie hépatique,…), favoriseraient la survenue de ces toxicités de type idiosyncratique, non prévisibles par des études chez l’animal. Leur prédiction et la caractérisation des mécanismes impliqués représentent donc un challenge majeur. Dans ce travail, nous avons étudié in vitro l’influence d’un stress inflammatoire sur le potentiel cytotoxique, cholestatique et stéatosique de trois médicaments connus par leurs effets de type idiosyncratique au niveau du foie, le diclofenac (DCF), la trovafloxacine (TVX) et l’amiodarone (AMD) en utilisant comme modèles expérimentaux les cellules humaines HepaRG différenciées, métaboliquement compétentes, et pour comparaison les cellules HepaRG non différenciées, les cellules HepG2, les hépatocytes humains primaires ainsi qu’un autre modèle cellulaire eucaryote la levure Saccharomyces cerevisiae. Nos résultats montrent que les cellules HepaRG différenciées sont moins sensibles au DCF que les cellules métaboliquement non compétentes et que cette toxicité implique la voie intrinsèque de l’apoptose, associée à la génération de ROS et d’un stress du réticulum endoplasmique. Elle est aggravée par le TNF-α via la voie apoptotique extrinsèque. La toxicité de DCF est aussi augmentée lors d’un co-traitement avec TVX et encore plus en présence de TNF-α. En revanche, cette cytokine ne potentialise pas les effets cholestatiques des 2 molécules, caractérisés notamment par une dilatation des canalicules biliaires et une inhibition de l’activité de certains transporteurs d’acides biliaires (BSEP, NTCP). Un stress inflammatoire induit par le lipopolysaccharide bactérien aggrave aussi les effets cytotoxiques et stéatosiques de l’AMD via une production de ROS, une inhibition de l’oxydation des acides gras et une accumulation des triglycérides, aboutissant à un contexte de stéatohépatite. De plus, une aggravation de la toxicité de DCF a également été observée dans Saccharomyces cerevisiae portant une mutation au niveau de certains transporteurs de la phase III, tel que Pdr5, et surtout après co-traitement avec la N-acétyl-cystéine via une voie qui pourrait être dépendante des perturbations des ponts di-sulfure au niveau de certaines protéines clés (transporteurs, protéines de signalisation ou facteurs de transcription, ...). Au total, tous ces résultats suggèrent que des facteurs environnementaux tel qu’un stress inflammatoire, et génétiques peuvent moduler la réponse toxique à des médicaments non seulement en induisant des stress oxydants et du réticulum endoplasmique mais aussi en modifiant leur métabolisme et donc les interactions entre médicaments, et certaines voies de signalisation essentielles
In human, many drugs are toxic for only rare patients. Genetic and various other factors (daily doses, inflammatory stress, immune reaction, liver diseases) are thought to favor such idiosyncratic toxicity that is not predictable in animals. Its prediction and mechanisms involved are very challenging. In this work, we have investigated in vitro the influence of an inflammatory stress on cytotoxic, cholestatic and steatotic effects of 3 drugs which are known to cause idiosyncratic hepatotoxicity, i.e. diclofenac (DCF), trovafloxacin (TVX) and amiodarone (AMD), using as experimental models, metabolically competent differentiated HepaRG cells, and for comparison, undifferentiated HepaRG cells, HepG2 cells, primary human hepatocytes as well as a non hepatic eukaryotic cell, the yeast Saccharomyces cerevisiae. Our results show that differentiated HepaRG cells were less sensitive than their undifferentiated counterparts and that toxicity involved intrinsic apoptosis., associated with ROS generation and endoplasmic reticulum stress and was aggravated with TNF-α via extrinsic apoptosis.. DCF toxicity was augmented by co-treatment with TVX and further by co-addition of TNF-α. By contrast, this cytokine did not potentiate cholestatic effects of either drug, typified by dilatation of bile canaliculi and inhibition of some bile acids transporters (BSEP, NTCP). An inflammatory stress induced by the bacterial lipopolysaccharide aggravated cytotoxicity and steatosis induced by AMD, via ROS generation, fatty acid oxidation and triglycerides accumulation leading to a steatohepatitis-like state. Moreover, DCF toxicity was also augmented in S. cerevisiae containing mutations of transporters of phase III, such as Pdr5, and especially after co-treatment with N-acetyl cysteine, via a pathway that is probably dependent on alterations of di-sulfure bounds in critical proteins (transporters, signaling proteins, transcription factors). Together, all the results suggest that environmental factors, such as inflammatory stress or genetic factors can modulate the toxic response to drugs by inducing oxidative and endoplasmic reticulum stress as well as by modifying metabolism, drug-drug interactions and key signaling pathways
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Thorén, Hanna. "The investigation of the biotransformation products formed by Cunninghamella elegans for different classes of drugs by the use of UPLC Q-TOF MS." Thesis, Uppsala universitet, Avdelningen för analytisk farmaceutisk kemi, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-248510.

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The fungus Cunninghamella elegans has in many studies shown to have abiotransformation similar to the metabolism of mammals. If the biotransformation isgeneral, it enables the production of metabolites by the fungus and the use asreference material. The purpose of the project were to examine whether themetabolic process of C. elegans is general, with respect to the formation ofglucosides, and can be applied to different classes of drugs. During the project, theanalyses were performed on a UPLC Q-TOF, run in both MSE and MSMS mode. Themobile phase used consisted of MeOH and 0.1 % formic acid in MQ water. Toincrease the concentration of possible glucosides, the samples were subjected to anacidic or alkaline SPE. Glucosides were detected in the fungal incubates of diclofenac,buprenorphine, norbuprenorphine and oxazepam. For diclofenac, besides twodifferent glucosides (diclofenac glucoside and hydroxylated diclofenac glucoside), ahydroxylated metabolite and a hydroxylated metabolite conjugated with sulfate werediscovered. In the samples containing buprenorphine, the phase I metabolitenorbuprenorphine was also encountered. Further, in the fungal incubates ofdexamethasone a defluorinated metabolite was identified, which is a metabolicpathway never before described for C. elegans.ISSN: 1650
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Reddivari, Muralidhar. "Microbiological biotransformations for drug synthesis." Thesis, University of Ulster, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.274094.

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Yu, DONGHUI. "Development of magnetic particle based biosensors and microreactors for drug analysis and biotransformation studies." Doctoral thesis, Universite Libre de Bruxelles, 2008. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/210517.

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In the first part of this work, magnetized nanoporous silica based microparticles (MMPs) are used for horseradish peroxidase (HRP) immobilization and applied in amperometric peroxidase-based biosensors. A homemade magnetized carbon paste electrode permits the MMPs attraction close to the electrode surface. The resulting original biosensor is applied to the investigation of enzymatic oxidation of model drug compounds namely, clozapine (CLZ) and acetaminophen (APAP) by HRP in the presence of hydrogen peroxide. The biosensor operates at a low applied potential and the signal corresponds to the electro-reduction of electroactive species enzymatically generated. The biosensor allows performing the quantitation of the two drug compounds in the micromolar concentration range. It allows also the study of thiol compounds based on the inhibition of the biosensor response. Interestingly, distinct inhibition results are observed for HRP entrapped in the silica microparticles compared to the soluble HRP.

We expect that this type of biosensors holds high promise in quantitative analysis and in biotransformation studies of drug compounds.

In the second part of this thesis work, HRP immobilized magnetic nanoparticles are injected on-line and magnetically retained, as a microreactor, in the capillary of a CE setup. The purpose of such a configuration is to develop an analytical tool for studying “in vitro” drug biotransformation. The advantages expected are (i) minimum sample (drug compound) and biocomponent (enzyme) consumption, (ii) high analysis throughput, (iii) selectivity and sensitivity. In order to illustrate the potential of such an instrumental configuration, it has been applied to study acetaminophen as model drug compound. The mechanistic information obtained by the HRP/H2O2 system is in agreement with literature data on acetaminophen metabolization. Horseradish peroxidase kinetic studies are realized by this setup and the apparent Michaelis constant is determined. Capillary electrophoresis permitted the identification of APAP off-line biotransformed products such as N-acetyl-p-benzoquinone imine (NAPQI), the APAP dimer and APAP polymers as inferred from literature data. The formation of the APAP dimer was further confirmed by electrospray ionization mass spectrometry.


Doctorat en Sciences biomédicales et pharmaceutiques
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Yagnik, Asutosh Trilochan. "Molecular modelling applications in rational drug design and the study of enzyme-ligand interactions." Thesis, University of Exeter, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.245931.

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Books on the topic "Biotransformation of drugs"

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Albert, Adrien. Xenobiosis: Foods, drugs, and poisons in the human body. London: Chapman and Hall, 1987.

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Xenobiosis: Foods, drugs and poisons in the human body. London: Chapman and Hall, 1987.

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International Congress on Cellular and Molecular Aspects of Glucuronidation. (1988 Montpellier, France). Cellular and molecular aspects of glucuronidation =: Aspects cellulaires et moleculaires de la glucuronoconjugaison : proceedings of the International Congress on Cellular and Molecular Aspects of Glucuronidation, held in Montpellier (France), 27-29 April 1988. London: Libbey, 1988.

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Mrazek, David. Psychiatric pharmacogenomics. New York: Oxford University Press, 2010.

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Gibson, G. Gordon. Introduction to drug metabolism. London: Chapman and Hall, 1986.

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Paul, Skett, ed. Introduction to drug metabolism. 2nd ed. Cheltenham: Stanley Thornes, 1999.

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Gibson, G. Gordon. Introduction to drug metabolism. 2nd ed. London: Blackie Academic & Professional, 1994.

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Paul, Skett, ed. Introduction to drug metabolism. 3rd ed. Cheltenham, UK: Nelson Thornes Publishers, 2001.

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1922-, Alexander Peter, Gielen Jacques, and Sartorelli Alan C, eds. Bioreduction in the activation of drugs: Proceedings of the Second Biochemical Pharmacology Symposium, Oxford, UK, 25-26 July 1985. Oxford: Pergamon Press, 1986.

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Reddivari, Muralidhar. Microbiological biotransformations for drug synthesis. [S.l: The author], 2002.

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Book chapters on the topic "Biotransformation of drugs"

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Ellison, Corie A., Alice L. Crane, and James R. Olson. "Biotransformation of Insecticides." In Metabolism of Drugs and Other Xenobiotics, 685–702. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2012. http://dx.doi.org/10.1002/9783527630905.ch25.

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Iwainsky, H. "Mode of Action, Biotransformation and Pharmacokinetics of Antituberculosis Drugs in Animals and Man." In Antituberculosis Drugs, 399–553. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-72873-0_6.

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Klinger, Wolfgang. "Developmental Regulation of Biotransformation of Drugs and other Xenobiotics." In Molecular Aspects of Oxidative Drug Metabolizing Enzymes, 237–48. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79528-2_13.

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Shyam Prasad, G., and B. Sashidhar Rao. "Fungal Biotransformation of Drugs: Potential Applications in Pharma Industry." In Microbial Biotechnology, 387–407. Toronto ; New Jersey : Apple Academic Press, 2015.: Apple Academic Press, 2017. http://dx.doi.org/10.1201/b19978-25.

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Husser, Christophe, Erich Koller, Andreas Brink, and Simone Schadt. "Studying the Biotransformation of Phosphorothioate-Containing Oligonucleotide Drugs by LC-MS." In Methods in Molecular Biology, 307–15. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9670-4_18.

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Guengerich, F. P., A. Bondon, R. G. Böcker, and T. L. Macdonald. "Roles of aminium radical intermediates in the biotransformation of dihydropyridines, cycloalkylamines, and N,N-dimethylanilines by cytochrome P-450 enzymes." In N-Oxidation of Drugs, 141–55. Dordrecht: Springer Netherlands, 1991. http://dx.doi.org/10.1007/978-94-011-3112-4_9.

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Ibragimova, Nailya, Marina Lyu, Aitugan Sabitov, Saltanat Jumabayeva, and Roza Karzhaubayeva. "The Study of Biotransformation Products and Microbiological Activity of Antibacterial Drugs In Vivo." In Recent Advances in Environmental Science from the Euro-Mediterranean and Surrounding Regions (2nd Edition), 723–27. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-51210-1_114.

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Tallarida, Ronald J., Robert B. Raffa, and Paul McGonigle. "Drug Metabolism (Biotransformation)." In Springer Series in Pharmacologic Science, 61–95. New York, NY: Springer New York, 1988. http://dx.doi.org/10.1007/978-1-4612-3778-5_4.

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Khojasteh, Siamak Cyrus, Harvey Wong, and Cornelis E. C. A. Hop. "Biotransformation and Bioactivation." In Drug Metabolism and Pharmacokinetics Quick Guide, 97–125. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-5629-3_6.

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Wen, Bo, and Sidney D. Nelson. "Common Biotransformation Reactions." In Mass Spectrometry in Drug Metabolism and Disposition, 13–41. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9780470929278.ch2.

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