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Relevant bibliographies by topics / Drugs Xenobiotics

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Journal articles
Dissertations / Theses
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Academic literature on the topic 'Drugs Xenobiotics'

Author: Grafiati

Published: 4 June 2021

Last updated: 17 February 2022

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Journal articles on the topic "Drugs Xenobiotics"

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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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Nakov, Radislav, and Tsvetelina Velikova. "Chemical Metabolism of Xenobiotics by Gut Microbiota." Current Drug Metabolism 21, no. 4 (June 25, 2020): 260–69. http://dx.doi.org/10.2174/1389200221666200303113830.

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: Among the gut microbiota’s newly explored roles in human biology is the ability to modify the chemical structures of foreign compounds (xenobiotics). A growing body of evidence has now provided sufficient acumen on the role of the gut microbiota on xenobiotic metabolism, which could have an intense impact on the therapy for various diseases in the future. Gut microbial xenobiotic metabolites have altered bioavailability, bioactivity and toxicity and can intervene with the actions of human xenobiotic-metabolizing enzymes to affect the destiny of other ingested molecules. These modifications are diverse and could lead to physiologically important consequences. : In the current manuscript we aim to review the data currently available on how the gut microbiota directly modifies drugs, dietary compounds, chemicals, pollutants, pesticides and herbal supplements.

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Besseghir, Kamel, and Françoise Roch-Ramel. "Renal Excretion of Drugs and Other Xenobiotics." Kidney and Blood Pressure Research 10, no. 5 (1987): 221–41. http://dx.doi.org/10.1159/000173131.

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Hayes, J. R., and J. F. Borzelleca. "Nutrient interaction with drugs and other xenobiotics." Journal of the American Dietetic Association 85, no. 3 (March 1985): 335–39. http://dx.doi.org/10.1016/s0002-8223(21)03609-9.

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Negishi, Masahiko, Kaoru Kobayashi, Tsutomu Sakuma, and Tatsuya Sueyoshi. "Nuclear receptor phosphorylation in xenobiotic signal transduction." Journal of Biological Chemistry 295, no. 45 (August 11, 2020): 15210–25. http://dx.doi.org/10.1074/jbc.rev120.007933.

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Nuclear pregnane X receptor (PXR, NR1I2) and constitutive active/androstane receptor (CAR, NR1I3) are nuclear receptors characterized in 1998 by their capability to respond to xenobiotics and activate cytochrome P450 (CYP) genes. An anti-epileptic drug, phenobarbital (PB), activates CAR and its target CYP2B genes, whereas PXR is activated by drugs such as rifampicin and statins for the CYP3A genes. Inevitably, both nuclear receptors have been investigated as ligand-activated nuclear receptors by identifying and characterizing xenobiotics and therapeutics that directly bind CAR and/or PXR to activate them. However, PB, which does not bind CAR directly, presented an alternative research avenue for an indirect ligand-mediated nuclear receptor activation mechanism: phosphorylation-mediated signal regulation. This review summarizes phosphorylation-based mechanisms utilized by xenobiotics to elicit cell signaling. First, the review presents how PB activates CAR (and other nuclear receptors) through a conserved phosphorylation motif located between two zinc fingers within its DNA-binding domain. PB-regulated phosphorylation at this motif enables nuclear receptors to form communication networks, integrating their functions. Next, the review discusses xenobiotic-induced PXR activation in the absence of the conserved DNA-binding domain phosphorylation motif. In this case, phosphorylation occurs at a motif located within the ligand-binding domain to transduce cell signaling that regulates hepatic energy metabolism. Finally, the review delves into the implications of xenobiotic-induced signaling through phosphorylation in disease development and progression.

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Kanai, Yoshikatsu, and Hitoshi Endou. "Molecular biology of transporters for drugs and xenobiotics." Japanese Journal of Pharmacology 76 (1998): 22. http://dx.doi.org/10.1016/s0021-5198(19)40217-5.

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Roberts, D. F. "Ethnic Differences in Reactions to Drugs and Xenobiotics." Journal of Medical Genetics 24, no. 9 (September 1, 1987): 574–75. http://dx.doi.org/10.1136/jmg.24.9.574-b.

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Ghersi-Egea, Jean-FranÇois, and Nathalie Strazielle. "Choroid Plexus Transporters for Drugs and Other Xenobiotics." Journal of Drug Targeting 10, no. 4 (January 2002): 353–57. http://dx.doi.org/10.1080/10611860290031859.

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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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HATTIS, D. "Pharmacogenetics: Ethnic Differences in Reactions to Drugs and Xenobiotics." Science 234, no. 4773 (October 10, 1986): 222–23. http://dx.doi.org/10.1126/science.234.4773.222-a.

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Dissertations / Theses on the topic "Drugs Xenobiotics"

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Ngulube, Thabale Jack. "The interaction of anti-malarial drugs and steroid hormone metabolism." Thesis, University of Leeds, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.329825.

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Arranz, Calderon M. J. "Genetic variation in the response of mice to xenobiotics, in vitro." Thesis, Open University, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.315324.

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Morrison, Roxanne. "The development of an in vitro system for the production of drug metabolites using microsomal enzymes from bovine liver." Thesis, Rhodes University, 2011. http://hdl.handle.net/10962/d1007698.

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Drug metabolism is a specialised subset of xenobiotic metabolism, pertaining to the breakdown and elimination of pharmaceutical drugs. The enzymes involved in these pathways are the cytochrome P450 family of isozymes. Metabolism is an important factor in determining the pharmacological effects of drugs. The main aim of this study was to develop a system whereby the major metabolites of drugs can be produced in vitro. An in vitro system was developed and optimised using commercially prepared microsomes from rat liver and coumarin (by monitoring its conversion to 7-hydroxycoumarin) as a model. The optimum running conditions for the incubations were 50 μM coumarin, 50 μg protein/ml microsomes, 1 mM NADP⁺, 5 mM G6P and 1U/ml G6PDH incubated for 30 minutes at 38℃. The HPLC method for the detection of coumarin and 7-hydroxycoumarin was also validated with respect to linearity, reproducibility, precision, accuracy and lower limits of detection and quantification. The system developed was then tested using microsomes prepared from fresh bovine liver on these ten drugs of interest in doping control in horse racing: diazepam, nordiazepam, oxazepam, promazine, acepromazine, chlorpromazine, morphine, codeine, etoricoxib and lumiracoxib. The bovine liver microsomes were prepared using differential centrifugation and had activity on a par with the commercial preparations. This in vitro system metabolised the drugs and produced both phase I and II metabolites, similar to those observed in humans and horses in vivo. For example, the major metabolites of the benzodiazepine drug, diazepam, nordiazepam, temazepam and oxazepam as well as the glucuronidated phase II products were all found after incubations with the bovine liver microsomes. The metabolism of the drugs was also investigated in silico using the computational procedure, MetaSite. MetaSite was able to successfully predict known metabolites for most of the drugs studied. Differences were observed from the in vitro incubations and this is most likely due to MetaSite using only human cytochrome P450s for analysis.

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Oliveira, Nícolas Gustavo Matias de. "Soroprevalência de toxoplasmose e avaliação de genotoxicidade em indivíduos diagnosticados com esquizofrenia expostos a xenobióticos." Universidade Federal de Goiás, 2018. http://repositorio.bc.ufg.br/tede/handle/tede/8295.

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - CAPES
Schizophrenia (EQZ) is a chronic mental illness that affects about 1% of the world population and is characterized by behavioral domains such as positive symptoms characterized by hallucinations and delusions and negative symptoms that involve apathy, anhedonia and social blunting. The cause of EQZ remains unknown, but it is known to be a disease whose etiology involves environmental and genetic factors. Several studies seek to identify factors that clarify the etiology of the disease. The agent that causes toxoplasmosis, Toxoplasma gondii, seems to be related to the development and progression of the disease, evidenced by studies that argue that T. gondii infection may be a triggering factor for psychosis in some individuals, since the parasite has a certain tropism by the central nervous system. Furthermore, studies have reported parasite infection as a factor related to genotoxicity, including toxoplasma infection in an animal model. Based on the foregoing, the present study aimed to evaluate the seropositivity to T. gondii (IgM or IgG) and the avidity of IgG in a group of individuals diagnosed with EQZ in the city of Goiânia and to evaluate the occurrence of genotoxicity in these, of genotoxicity with exposure to xenobiotics such as tobacco, alcohol, especially drugs, and / or T. gondii infection. Seropositivity was observed above 70% among individuals diagnosed with EQZ in relation to the controls, with avidity above 50%, indicating that individuals had contact with T. gondii at some time prior to the survey. Despite the genotoxic damage found, there was no significant difference in genotoxic damage among the infected individuals evaluated. The present study did not demonstrate that T. gondii may be a contributing factor to the occurrence of DNA damage, and the use of antipsychotic drugs, tobacco and alcohol, despite being a risk factor for genotoxicity, did not demonstrate an influence significant difference in the present study. However, it is necessary to carry out other analyzes and investigate parameters such as the time of drug use and exposure to other xenobiotics. In order to know better the life habits of individuals, it may help to provide more information about this relationship between T. gondii and EQZ.
A esquizofrenia (EQZ) é uma doença mental crônica que afeta cerca de 1% da população mundial e se caracteriza por domínios comportamentais, como sintomas positivos, caracterizados por alucinações e delírios e sintomas negativos, que envolvem apatia, anedonia e embotamento social. A causa da EQZ ainda permanece desconhecida, mas sabe-se que se trata de uma doença que cuja etiologia envolve fatores ambientais e genéticos. Vários estudos buscam identificar fatores que esclareçam a etiologia da doença. O agente causador da toxoplasmose, Toxoplasma gondii, parece ter relação com o desenvolvimento e progressão da doença, evidenciado por estudos que defendem que a infecção por T. gondii pode ser um fator desencadeante de psicoses em alguns indivíduos, já que o parasito apresenta um certo tropismo pelo sistema nervoso central. Ainda, estudos tem reportado a infecção por parasitos como fator relacionado a genotoxicidade, incluindo a infecção pelo toxoplasma em um modelo animal. Com base no exposto, o presente trabalho teve por objetivo avaliar a soropositividade para T. gondii (IgM ou IgG) e a avidez da IgG em um grupo de indivíduos diagnosticados com EQZ do município de Goiânia e avaliar a ocorrência de genotoxicidade nestes, procurando relação da genotoxicidade com a exposição a xenobióticos como tabaco, álcool, especialmente medicamentos, e/ou com a infecção pelo T. gondii. Observou- se soropositividade acima de 70% entre os indivíduos diagnosticados com EQZ em relação aos controles, com avidez acima de 50%, indicando que os indivíduos tiveram contato com o T. gondii em algum momento anterior a pesquisa. Apesar do dano genotóxico encontrado, não houve diferença significativa no dano genotóxico entre os indivíduos infectados avaliados. O presente estudo não demonstrou que T. gondii pode ser um fator contribuinte para a ocorrência de danos ao DNA, e o uso de fármacos antipsicóticos, o fumo e o álcool, apesar de serem um fator de risco para a genotoxicidade, não demonstraram uma influência significativa no presente estudo. Entretanto, há a necessidade de realizar outras análises e investigar parâmetros como o tempo de uso dos fármacos, e de exposição a outros xenobióticos, enfim, o melhor conhecimento dos hábitos de vida dos indivíduos pode ajudar a trazer mais informações acerca dessa relação entre T. gondii e a EQZ.

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McKay, Judith A. "The expression of xenobiotic metabolising enzymes in human tumours." Thesis, University of Aberdeen, 1996. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU078740.

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The cytochromes P450 (CYPs), epoxide hydrolases (EHs) and glutathione S-transferases (GSTs) are three of the major families of enzymes involved in the metabolism of xenobiotics in the human body. Immunohistochemical analysis revealed a high frequency of expression of xenobiotic metabolising enzymes in all tumour types studied, in contrast to corresponding normal tissue which displayed only low levels of expression. Further examination of the CYP1 family was carried out by immunoblot analysis. All breast tumours studied were found to express CYP1B1, and not CYP1A1 or CYP1A2. Moreover, CYP1B1 was identified in a number of kidney tumours but not in corresponding normal kidney, indicating that CYP1B1 may be a tumour-specific form of CYP, RT-PCR, in combination with restriction digestion and DNA sequencing, was used to identify CYP mRNA species present in several tumour types. Although CYP1A1 mRNA was identified in breast carcinomas, CYP1B1 was found to be the most frequently expressed form of the CYP1 family in this tissue. CYP3A mRNA was also displayed by several breast tumours, and demonstrated by sequencing to be CYP3A5. A similar situation to breast tumours was observed in tumours of the gastro-intestinal and urinary tracts, with CYP1B1 being the most frequently expressed form of the CYP1 family, and only a small number of samples displaying evidence of CYP1A mRNA. The effects of the expression of xenobiotic metabolising enzymes in tumours may be complex, and depend upon the relative amounts of active protein present, but it is likely that they will exert an influence on both the development of carcinogenesis and the anti-cancer drug resistance of tumours.

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Faridwajidi, Mustafa Fadzil. "Transgenic Drosophila as an in vivo model of human drug metabolism." Thesis, University of Newcastle Upon Tyne, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.254027.

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Lenz, Eva-Maria. "Multinuclear NMR and HPLC-NMR spectroscopic studies on xenobiotic metabolism." Thesis, Birkbeck (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.267785.

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Tugnait, Meera. "Multinuclear magnetic resonance studies on the metabolism model of fluoroaromatic xenobiotics." Thesis, Birkbeck (University of London), 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.296519.

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Cockburn, Elinor M. "The relevance of prostanoid metabolism in the development of drug-induced nephrotoxicity." Thesis, University of Aberdeen, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.481095.

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The enzymes prostaglandin synthetase (PGS) and lipoxygenase can cooxidise a variety of xenobiotics to reactive intermediates during the metabolism of arachidonic acid (AA). PGS exhibited a gradient of activity within the kidney which was greatest in the papilla and least in the cortex. Rabbit and rat renal microsomes metabolised the model compound, tetramethylphenylenediamine (TMPD), in the presence of AA by pathways which were predominantly PGS and lipoxygenase-dependent, respectively. Therefore, both enxymes may play a role in the development of site-specific nephrotoxicity within the kidney. The model papillotoxin 2-bromoethanamine (2-BEA) which exhibits target selective toxicity for the renal papilla, was found to be significantly more toxic to medullary interstitial cells than to proximal tubule cells in culture. Toxicity was enhanced significantly by AA whereas inhibitors of cyclooxygenase (indomethacin, aspirin), prostaglandin hydroperoxidase (propylthiouracyl) and lipoxygenase (nordihydrogauaretic acid) all significantly decreased 2-BEA toxicity. This suggests that toxicity is mediated either by the hydroperoxidase component of PGS or by lipoxygenase. Thromboxane A₂ (TxA₂) is thought to play a pivotal role in cyclosporin A (CsA) induced nephrotoxicity. Administration of a thromboxane synthetase inhibitor (TSI) normalised TxB₂ excretion but only partially protected against other factors involved. However, treatment with angiotensin converting enzyme inhibitor either alone or in combination with TSI did not affect CsA nephrotoxicity. Tubular toxicity, manifest as N-acetyl-β-D-glucosaminidase (NAG) enzymuria, glycosuria, vacuolation, calcification and chronic tubule damage, may contribute to the CsA-induced reduction in renal function. In addition to protecting against CsA-induced nephrotoxicity, the administration of TSI to CsA-treated rats also partially reversed pre-existing renal damage.

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Merrell, Matthew David. "Xenosensor Regulation of Enzymes and Transporters in Drug Exposure and Disease." Diss., The University of Arizona, 2011. http://hdl.handle.net/10150/194051.

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A large and varied array of xenobiotics (foreign chemicals) enters into our bodies every day. In order to prevent toxicity resulting from xenobiotic accumulation, the body has developed a complex and integrated network of enzymes and transporters to promote and control the metabolism and excretion of drugs and other compounds. Drug metabolizing enzymes are classified as oxidative (Phase I) or conjugative (Phase II), and generally result in increased hydrophilicity of their substrates. Drug transporters actively route xenobiotics into (Phase 0) or out of (Phase III) the cells. The expression of the proteins involved in drug metabolism and transport are coordinately regulated by xenosensing transcription factors, including the constitutive androstane receptor, the pregnane X receptor, the aryl hydrocarbon receptor, and Nrf2. Through the activation of these xenosensors, chemical exposure itself induces the processes which help to remove the xenobiotics from the body. The liver is the major organ of drug metabolism in the body. Chronic hepatic diseases impact the activity of xenosensors and the expression of their enzyme and transporter gene targets. Nonalcoholic fatty liver disease (NAFLD) is the most prevalent liver disease in the United States, affecting 20-30% of the populations. This profoundly underdiagnosed disease has significant effects on hepatic gene expression and may increase the risk of adverse drug reactions and xenobiotic toxicity in affected patients. This manuscript presents original research which contributes to our understanding of xenosensor function in the contexts of chemical exposure and liver disease. Manuscripts in this dissertation investigate 1) the induction profile and mechanisms of the experimental therapeutic agent oltipraz, 2) the xenosensor-regulated mechanisms of induction of the drug transporter ABCC3, 3) the impact of NAFLD on the expression of major drug metabolizing enzymes, and 4) the utility of altered drug disposition as a biomarker for NAFLD progression. The findings of these studies highlight the clinical importance of xenosensor activation and the potential pharmacological and toxicological consequences of hepatic disease.

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Books on the topic "Drugs Xenobiotics"

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Anzenbacher, Pavel, and Ulrich M. Zanger, eds. Metabolism of Drugs and Other Xenobiotics. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2012. http://dx.doi.org/10.1002/9783527630905.

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Ioannides, Costas, ed. Enzyme Systems that Metabolise Drugs and Other Xenobiotics. Chichester, UK: John Wiley & Sons, Ltd, 2001. http://dx.doi.org/10.1002/0470846305.

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Ioannides, Costas, ed. Enzyme Systems that Metabolise Drugs and Other Xenobiotics. Chichester, UK: John Wiley & Sons, Ltd, 2001. http://dx.doi.org/10.1002/0470846305.

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Disposition of toxic drugs and chemicals in man. 6th ed. Foster City, Calif: Biomedical Publications, 2002.

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Baselt, Randall C. Disposition of toxic drugs and chemicals in man. 5th ed. Foster City, Calif: Chemical Toxicology Institute, 2000.

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Lau, Grace S. N. Metabolic activation of drugs and other xenobiotics in hepatocellular carcinoma. Hong Kong: Chinese University Press, 1997.

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International ISSX Meeting (7th 2004 Vancouver, B.C.). Abstracts from the 7th International ISSX Meetinng [sic]: August 29 - September 2, 2004, Vancouver, Canada. New York: Marcel Dekker, 2004.

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North, American ISSX Meeting (7th 1996 San Diego Calif ). Seventh North American ISSX Meeting, San Diego, California USA, October 20-24, 1996. Bethesda, Md: International Society for the Study of Xenobiotics, 1996.

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International ISSX Meeting (2nd 1988 Kōbe-shi, Japan). Xenobiotic metabolism and disposition: Proceedings of the 2nd International ISSX Meeting, Kobe, Japan, May 16-20, 1988. London: Taylor & Francis, 1989.

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North, American ISSX Meeting (5th 1993 Tucson Arizona). Fifth North American ISSX Meeting, Tucson, Arizona USA, October 17-21, 1993. Bethesda, Md: International Society for the Study of Xenobiotics, 1993.

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Book chapters on the topic "Drugs Xenobiotics"

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Meyer, Markus R., and Hans H. Maurer. "Drugs of Abuse (Including Designer Drugs)." In Metabolism of Drugs and Other Xenobiotics, 429–63. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2012. http://dx.doi.org/10.1002/9783527630905.ch16.

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Riedmaier, Stephan, and Ulrich M. Zanger. "Cardiovascular Drugs." In Metabolism of Drugs and Other Xenobiotics, 331–63. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2012. http://dx.doi.org/10.1002/9783527630905.ch12.

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Schwab, Matthias, Elke Schaeffeler, and Hiltrud Brauch. "Anticancer Drugs." In Metabolism of Drugs and Other Xenobiotics, 365–78. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2012. http://dx.doi.org/10.1002/9783527630905.ch13.

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Baumann, Pierre, and Christoph Hiemke. "Central Nervous System Drugs." In Metabolism of Drugs and Other Xenobiotics, 301–29. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2012. http://dx.doi.org/10.1002/9783527630905.ch11.

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Roch-Ramel, Françoise, and Marc E. De Broe. "Renal handling of drugs and xenobiotics." In Clinical Nephrotoxins, 21–46. Dordrecht: Springer Netherlands, 2003. http://dx.doi.org/10.1007/1-4020-2586-6_2.

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Broe, Marc E. De, and Françoise Roch-Ramel. "Renal handling of drugs and xenobiotics." In Clinical Nephrotoxins, 13–30. Dordrecht: Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-015-9088-4_2.

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De Broe, Marc E., and FranÇoise Roch-Ramel. "Renal handling of drugs and xenobiotics." In Clinical Nephrotoxins, 43–71. Boston, MA: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-84843-3_3.

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Somogyi, Andrew A., and Janet K. Coller. "Drugs against Acute and Chronic Pain." In Metabolism of Drugs and Other Xenobiotics, 403–28. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2012. http://dx.doi.org/10.1002/9783527630905.ch15.

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Huerta-Fontela, Maria, Maria Teresa Galceran, and Francesc Ventura. "Illicit Drugs in the Urban Water Cycle." In Xenobiotics in the Urban Water Cycle, 51–71. Dordrecht: Springer Netherlands, 2009. http://dx.doi.org/10.1007/978-90-481-3509-7_3.

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Berliner, Lawrence J., and Hirotada Fujii. "Free Radical Intermediates of Drugs and Xenobiotics." In Supramolecular Structure and Function 7, 119–29. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1363-6_9.

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Conference papers on the topic "Drugs Xenobiotics"

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Solon, Eric. "Autoradiography, imaging mass spectrometry and other preclinical imaging techniques to study tissue distribution of xenobiotics in animal models." In Visualizing and Quantifying Drug Distribution in Tissue III, edited by Conor L. Evans and Kin Foong Chan. SPIE, 2019. http://dx.doi.org/10.1117/12.2508522.

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Ahmed, Sumaya, and Nasser Rizk. "The Expression of Bile Acid Receptor TGR5 in Adipose Tissue in Diet-Induced Obese Mice." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0212.

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Bile acids are significant physiological factors for digestion, solubilization, absorption, toxic metabolites and xenobiotics. In addition, bile acids are responsible of signal transduction as well as metabolic regulation that activate several receptors such as farnesoid X receptor (FXR) and the membrane G-protein receptor 5 (TGR5). Activation of TGR5 by bile acids is associated with prevention of obesity as well as ameliorating the resistance to insulin via increasing energy expenditure. The objective of this research is to investigate TGR5 gene expression level in different fat depots including visceral or epididymal adipose tissue (eWAT), brown adipose tissue and inguinal adipose tissue (iWAT) and to study the response of TGR5 gene expression to the antiobesity treatment (SFN). Three groups of male CD1 mice were used in this study; lean group fed with SCD, DIO mice on HFD and DIO obese mice treated with anti-obesity treatment. Body weight (BW) and phenotype data were evaluated by weekly including blood samples for analysis of glucose, insulin, leptin, triglycerides (TG). Total RNA was extracted from different fat depots and RT-PCR profiler array technology was used to in order to assess the mRNA expression of TGR5 and leptin. There was significant downregulation of TGR5 gene expression level in obese (DIO) mice and remarkable upregulation of TGR5 gene expression after successful weight loss in DIO mice treated with SFN in time dependent manner at 1 weeks and 4 weeks of ip applications. In conclusion, obesity is associated with decrease in expression of TGR5 in different fat depots and treatment with anti-obesity drug (Sulforaphane) causes stepwise upregulation of TGR5 gene expression in epididymal white adipose tissue parallel stepwise decrease in body weight. Increase of expression of TGR5 in DIO mice in eWAT is accompanied by improvement in glucose homeostasis and insulin action.

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