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Books on the topic 'Cytochrome P450 enzyme system'

Author: Grafiati

Published: 4 June 2021

Last updated: 2 February 2022

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1

Paul R. Ortiz de Montellano, Ian R. Phillips, and Elizabeth A. Shephard. Cytochrome P450 protocols. 3rd ed. New York: Humana, 2013.

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2

Ahlström, Marie. Cytochrome P450, metabolism and inhibition: Computational and experimental studies. Göteborg: Göteborg University, 2007.

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3

International Conference on Cytochrome P-450 (15th 2007 Bled, Slovenia). Proceedings of the 15th International Conference on Cytochromes P450: Biochemistry, biophysics, and functional genomics : Bled, Slovenia, June 17-21, 2007. Bologna, Italy: Medimond International Proceedings, 2007.

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4

Cozza, Kelly L. Concise guide to the cytochrome P450 system: Drug interaction principles for medical practice. Washington, DC: American Psychiatric Pub., 2001.

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5

Zhang, Yanhua. Effects of steroid hormones on cytochrome P450 enzyme activity in women. Ottawa: National Library of Canada, 2002.

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6

Wilson, Joanna Yvonne. Cytochrome P450 1A1 and aromatase (CYP19) in cetaceans: Enzyme expression and relationship to contaminant exposure. Cambridge, Mass: Massachusetts Institute of Technology, 2003.

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7

Cozza, Kelly L. Quick guide to the Cytochrome P450 system: Overview of drug interaction principles. Washington, DC: American Psychiatric Pub., 2002.

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8

International, Conference on Biochemistry and Biophysics of Cytochrome P.-450 (6th 1988 :. Vienna Austria). Cytochrome P-450: Biochemistry and biophysics : proceedings of the 6th International Conference on Biochemisty and Biophysics of Cytochrome P-450 held in Vienna at the University of Economics, July 3-8, 1988. London: Taylor & Francis, 1989.

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9

Worrall, Stephen Frederick. An investigation into the association between cytochrome P450 and glutathione S-transferase detoxification enzyme polymorphisms and human oral squamous cell carcinoma. Birmingham: University of Birmingham, 1998.

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10

1946-, Bachmanova G. I., ed. Cytochrome P-450 and active oxygen. London: Taylor & Francis, 1990.

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11

International, Conference on Advances in Prostaglandin Leukotriene and Other Bioactive Lipid Research (12th 2002 Istanbul Turkey). Advances in prostaglandin, leukotriene, and other bioactive lipid research: Basic science and clinical applications. New York: Kluwer Academic/Plenum Publishers, 2003.

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12

Zeliha, Yazıcı, ed. Advances in prostaglandin, leukotriene, and other bioactive lipid research: Basic science and clinical applications. New York: Kluwer Academic/Plenum Publishers, 2003.

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13

International Conference on Advances in Prostaglandin, Leukotriene, and Other Bioactive Lipid Research (12th 2002 Istanbul, Turkey). Advances in prostaglandin, leukotriene, and other bioactive lipid research: Basic science and clinical applications. New York: Kluwer Academic/Plenum Publishers, 2003.

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14

1951-, Phillips Ian R., and Shephard Elizabeth A. 1950-, eds. Cytochrome P450 protocols. Totowa, N.J: Humana Press, 1998.

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15

Ortiz de Montellano, Paul R., ed. Cytochrome P450: Structure, mechanism, and biochemistry. 3rd ed. New York: Kluwer Academic/Plenum Publishers, 2004.

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16

S, Lee Jae, Obach R. Scott, and Fisher Michael B, eds. Drug metabolizing enzymes: Cytochrome P450 and other enzymes in drug discovery and development. Lausanne, Switzerland: FontisMedia SA, 2003.

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17

Neil B., M.d. Sandson. Drug Interactions Casebook: The Cytochrome P450 System and Beyond. American Psychiatric Publishing, 2003.

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18

Ruckpaul, Klaus. Cytochrome P-450 Dependent Biotransformation of Endogenous Substrates (Frontiers in Biotransformation). Vch Pub, 1991.

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19

MD, Kelly L. Cozza, and Scott C. Armstrong MD. Concise Guide to the Cytochrome P450 System: Drug Interaction Guidelines for Medical Practice. 4th ed. American Psychiatric Association, 2001.

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20

Relationships between structure and function of Cytochrome P-450: Experiments, calculations, models. Berlin: Akademie Verlag, 1992.

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21

Cozza, Kelly L., C. M. D. Armstrong Scott, and R. M. D. Oesterheld Jessica. Concise Guide to Drug Interaction Principles for Medical Practice: Cytochrome P450s, Ugts, P-Glycoproteins (Concise Guides). 2nd ed. American Psychiatric Publishing, Inc., 2003.

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22

A, Bachmann Kenneth, ed. Lexi-Comp's drug interactions handbook: The new standard for drug and herbal interactions featuring a complete guide to cytochrome P450 enzyme substrates, inducers, and inhibitors. 2nd ed. Hudson, Ohio: Lexi-Comp, 2004.

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23

A, Bachmann Kenneth, ed. Lexi-Comp's drug interactions handbook: The new standard for drug and herbal interactions : featuring a complete guide to cytochrome P450 enzyme substrates, inducers, and inhibitors. Hudson, Ohio: Lexi-Comp, 2003.

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24

B, Matchar David, United States. Agency for Healthcare Research and Quality., and Duke University Evidence-based Practice Center., eds. Testing for cytochrome P450 polymorphisms in adults with non-psychotic depression treated with selective serotonin reuptake inhibitors (SSRIs). Rockville, MD: Agency for Healthcare Research and Quality, 2007.

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25

Testing for cytochrome P450 polymorphisms in adults with non-psychotic depression treated with selective serotonin reuptake inhibitors (SSRIs). Rockville, MD: AHRQ, 2007.

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26

O’Neal, M. Angela. Pain in the Back. Edited by Angela O’Neal. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190609917.003.0006.

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This case explores how bone health can be affected by antiepileptic drugs (AEDs), and why this is an important issue in women with epilepsy (WWE). AEDs affect bone health through activation of the cytochrome P450 system in the liver, leading to increased metabolism of vitamin D. The enzyme-inducing AEDs include phenytoin, carbamazepine, phenobarbital, and primidone. Risk factors for osteoporosis include female gender, low body mass, inadequate vitamin D intake, and smoking. The specific AEDs used and the length of treatment confer additional risks. Furthermore, in WWE, risks are magnified related to falls, either from seizures or related to medication toxicity. Screening with bone density and measures to promote bone health are extremely important in these at-risk women.

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27

van Dorp, Eveline L. A., Douglas Eleveld, Erik Olofsen, and Jaap Vuyk. Drug distribution and elimination in anaesthetic practice. Edited by Michel M. R. F. Struys. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0012.

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An understanding of pharmacokinetics is vital for the practice of anaesthesia. Drugs are, after administration, distributed throughout the body to the effect site (mostly the brain) to exert their effects. This can be influenced by differences in protein binding, systemic blood flow, and concomitant medication. Elimination of drugs from the body is through two main routes: either unchanged through the kidneys or through metabolism by the liver (and consecutive excretion through the kidneys). This process depends on the amount of hepatic blood flow and the amount of hepatic extraction. This in turn depends on the amount of protein binding and the intrinsic hepatic clearance. The cytochrome P450 enzyme family also plays an important role in drug elimination. Individual differences in enzyme activity can lead to differences in drug effect and clearances. Changes in enzyme activity by enzyme induction and inhibition can also be of influence on drug clearance. Compartmental, non-compartmental, and physiologically based models, and various statistical approaches to estimate these models, may be used to analyze the distribution and elimination of anaesthetic agents.

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28

Emel, Arinç, Schenkman John B, Hodgson Ernest 1932-, and NATO Advanced Study Institute on Molecular Aspects of Drug Metabolizing Enzymes (1993 : Kus̜adası, Turkey), eds. Molecular aspects of oxidative drug metabolizing enzymes: Their significance in environmental toxicology, chemical carcinogenesis, and health. Berlin: Springer-Verlag, 1995.

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29

Schenkman, John B. Molecular Aspects of Oxidative Drug Metabolizing Enzymes: Their Significance in Environmental Toxicology, Chemical Carcinogenesis and Health (Nato a S I Series Series H, Cell Biology). Springer-Verlag Telos, 1995.

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30

Deegan, Patrick. Porphyria. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0179.

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This chapter discusses six diseases caused by inborn errors of metabolism affecting the biosynthesis of haem. Haem is a tetracyclic metal-binding compound involved in oxygen transport (in haemoglobin and myoglobin) and redox reactions (e.g. in the cytochrome P450 system). Each of these conditions is caused by a single gene defect in one of the enzymes involved in the biosynthesis of haem. Inheritance is usually autosomal dominant with incomplete penetrance. The enzyme defect results in disease, not as a result of deficiency of the reaction product, but as a result of accumulation of precursors. Early, soluble precursors, 5-aminolaevulinic acid, and porphobilinogen (not porphyrins as such) are neurotoxic and, when present in great excess, as occurs when flux through the haem synthetic pathway is increased in response to particular medications or hormones, lead to acute neurovisceral crises. Later cyclical precursors (porphyrins) in the pathway are also water soluble and excreted in urine, but are susceptible to activation by electromagnetic radiation in the visible spectrum and are converted to free-radical metabolites that cause pain, inflammation, and tissue damage in the skin. The final haem precursors (also porphyrins) are hydrophobic and excreted in the bile and faeces and are also activated by light to toxic metabolites.

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31

Cascorbi, Ingolf. Polymorphic cytochrome P450 2D6 as the responsible enzyme of activation. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0079.

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The landmark paper discussed in this chapter is ‘Bioactivation of the narcotic drug codeine in human liver is mediated by the polymorphic monooxygenase catalyzing debrisoquine 4-hydroxylation (cytochrome P-450 dbl/bufI)’, published by Dayer et al. in 1988. Codeine is an old but frequently prescribed drug used for the treatment of mild-to-moderate pain. However, its use is nowadays restricted after observations of partly fatal respiratory repression in children. Codeine itself exhibits no analgesic effect, but is partly activated by O-demethylation to morphine by cytochrome P450 2D6 (CYP2D6). The identification of the polymorphic CYP2D6 as the enzyme responsible for activation was achieved by Dayer et al. in 1998 and was an important milestone contributing to the widely observed inter-individual differences of drug action and side effects of codeine. Translating the pharmacogenetics of codeine into clinical practice is currently underway in clinical trials, to identify ineffective analgesics and, in particular, avoid severe adverse events.

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32

P450 Chem Carcinogen (Gann Monograph on Cancer Research). Plenum Press, 1985.

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33

Olkkola, Klaus T., Hugo E. M. Vereecke, and Martin Luginbühl. Drug interactions in anaesthetic practice. Edited by Michel M. R. F. Struys. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0021.

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When two or more drugs are administered simultaneously, the pharmacological response may be greater or less than the sum of the effects of the individual drugs. One drug may antagonize or potentiate the effects of the other and there may be also qualitative differences in response. Although some drug interactions increase the toxicity or result in loss of therapeutic effect, others are beneficial. Indeed, modern anaesthetic techniques depend on beneficial drug interactions. A sound combination of drugs helps clinicians to increase both the efficacy and safety of drug treatment. Drugs may interact on a pharmaceutical, pharmacodynamic, or pharmacokinetic basis. Many pharmacodynamic interactions are predictable and can be avoided by the use of common sense. However, it is much more difficult to predict the likelihood of pharmacokinetic and pharmaceutical interactions despite good prior knowledge of pharmacokinetics and chemical properties of individual drugs. Pharmaceutical drug interactions usually occur before the drug is given to the patient and they are caused by chemical (such as acid–base, salt formation, oxidation–reduction, hydrolysis, or epimerization) or physical (such as adsorption/absorption or emulsion breaking) reactions. When drugs have a pharmacokinetic interaction, one drug alters the absorption, distribution, or the elimination of the other drug. Many pharmacokinetic drug interactions are due to inhibition or induction of cytochrome P450 enzymes. Pharmacodynamic drug interactions are caused by drugs having an effect on the same receptors or the same physiological system. This chapter gives anaesthetists an overview of clinically relevant perioperative drug interactions.

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34

Irizar, Amaia. The inter-relationship between the cytochrome P450-dependent mixed-function oxidase system and disease. 1995.

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35

Lexi-Comp's drug interactions handbook: The new standard for drug and herbal interactions featuring a complete guide to cytochrome P450 enzyme substrates, inducers, and inhibitors. Hudson, OH: Lexi-Comp, 2004.

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36

Drug Metabolism Enzymes. Marcel Dekker, 2003.

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37

Ruckpaul, Klaus. Medicinal Implications in Cytochrome P-450 Catalyzed Biotransformations (Frontiers in Biotransformation, Vol 8). Vch Pub, 1993.

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38

Advances in Prostaglandin, Leukotriene and Other Bioactive Lipid Research: Basic Science and Clinical Applications (Advances in Experimental Medicine and Biology). Springer, 2003.

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39

Fabbri, Chiara, and Alessandro Serretti. The treatment of bipolar disorder in the era of personalized medicine: myth or promise? Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198748625.003.0031.

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Bipolar disorder (BD) is a chronic disease associated with high personal and socio-economic burden. Genetics accounts for 20–95% of variability in central nervous system drug disposition and pharmacodynamics, thus genetic markers are considered a promising way to develop tailored treatments and improve the prognosis of the disease. Among mood stabilizers, lithium response was the most investigated phenotype and the most replicated genes are involved in synaptic plasticity (BDNF), serotonergic (SLC6A4) and dopaminergic (DRD1) neurotransmission, and second messenger cascades (GSK3B). Relevant pharmacogenetic findings regarding other mood stabilizers are hyperammonaemia (CPS1 gene) and hepatic dysfunction (POLG gene) induced by valproate and immune-mediated cutaneous hypersensitivity reactions (HLA-B*1502) induced by lamotrigine or carbamazepine. Polymorphisms in cytochrome (CYP) P450 genes are expected to provide useful information particularly in case of polypharmacy. Despite few pharmacogenetic tests are currently recommended, the development of pharmacogenetics in other fields of medicine provides an encouraging perspective.

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