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Review Article

Biotransformation and bioactivation reactions – 2016 literature highlights

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Pages 285-317 | Received 05 Apr 2017, Accepted 30 Apr 2017, Published online: 31 May 2017

References

  • Agrahari, V., et al., 2016. A comprehensive insight on ocular pharmacokinetics. Drug Delivery and Translational Research, 6 (6), 735–754.
  • Bushee, J.L., Dunne, C.E., and Argikar, U.A., 2015. An in vitro approach to investigate ocular metabolism of a topical, selective β1-adrenergic blocking agent, betaxolol. Xenobiotica, 45, 396–405.
  • Cirello, A.L., et al., 2016. In vitro ocular metabolism and bioactivation of ketoconazole in rat, rabbit and human. Drug Metabolism Pharmacokinetics, pii: S1347–S4367.
  • Dalvie, D., et al., 2009. Assessment of three human in vitro systems in the generation of major human excretory and circulating metabolites. Chemical Research in Toxicology, 22 (2), 357–368.
  • Duvvuri, S., Majumdar, S., and Mitra, A.K., 2004. Role of metabolism in ocular drug delivery. Current Drug Metabolism, 5 (6), 507–515.
  • Lee, V.H., Chien, D.S., and Sasaki, H., 1988. Ocular ketone reductase distribution and its role in the metabolism of ocularly applied levobunolol in the pigmented rabbit. Journal of Pharmacology and Experimental Therapeutics, 246 (3), 871–878.
  • Nakano, M., et al., 2014. Ocular cytochrome P450s and transporters: roles in disease and endobiotic and xenobiotic disposition. Drug Metabolism Reviews, 46 (3), 247–260.
  • Woodward, D.F., et al., 1987. Dihydrolevobunolol is a potent ocular beta-adrenoceptor antagonist. Journal of Ocular Pharmacology, 3 (1), 11–15.

References

  • De Lazzari, E., et al., 2008. Hepatotoxicity of nevirapine in virologically suppressed patients according to gender and CD4 cell counts. HIV Medicine, 9 (4), 221–226.
  • Erickson, D.A., et al., 1999. Characterization of the in vitro biotransformation of the HIV-1 reverse transcriptase inhibitor nevirapine by human hepatic cytochromes P-450. Drug Metabolism and Disposition: The Biological Fate of Chemicals, 27 (12), 1488–1495.
  • Martin, A.M., et al., 2005. Predisposition to nevirapine hypersensitivity associated with HLA-DRB1*0101 and abrogated by low CD4 T-cell counts. AIDS, 19 (1), 97–99.
  • Meng, X., et al., 2013. Detection of drug bioactivation in vivo: mechanism of nevirapine-albumin conjugate formation in patients. Chemical Research in Toxicology, 26, 575−583.
  • Popovic, M., et al., 2006. Study of the sequence of events involved in nevirapine-induced skin rash in Brown Norway rats. Chemical Research in Toxicology, 19 (9), 1205–1214.
  • Riska, P., et al., 1999. Disposition and biotransformation of the antiretroviral drug nevirapine in humans. Drug Metabolism and Disposition: The Biological Fate of Chemicals, 27 (8), 895–901.
  • Sharma, A.M., et al., 2012. Bioactivation of nevirapine to a reactive quinone methide: implications for liver injury. Chemical Research in Toxicology, 25, 1708−1719.
  • Srivastava, A., et al., 2010. Quantifying the metabolic activation of nevirapine in patients by integrated applications of NMR and mass spectrometries. Drug Metabolism and Disposition: The Biological Fate of Chemicals, 38 (1), 122–132.
  • Stern, J.O., et al., 2003. A comprehensive hepatic safety analysis of nevirapine in different populations of HIV infected patients. Journal of Acquired Immune Deficiency Syndromes, 34, S21–S33.

References

  • Scian, M., and Atkins, W.M., 2015. The busulfan metabolite EdAG irreversibly glutathionylates glutaredoxins. Archives of Biochemistry and Biophysics, 583, 96–104.
  • Hassan, M., and Ehrsson, H., 1987. Metabolism of 14C-busulfan in isolated perfused rat liver. European Journal of Drug Metabolism and Pharmacokinetics, 12 (1), 71–76.

References

  • Chen, M.X., et al., 2016. 9-Glutathiony1-6,7-dihydro-1-hydroxymethy1-5H-pyrrolizine is the major pyrrolic glutathione conjugate of retronecine-type pyrrolizidine alkaloids in liver microsomes and in rats. Chemical Research in Toxicology, 29, 180–189.
  • EFSA. 2016. Dietary exposure assessment to pyrrolizidine alkaloids in the European population. EFSA Journal, 14, 4572.
  • Fu, P., 2017. Pyrrolizidine alkaloids: metabolic activation pathways leading to liver tumor initiation. Chemical Research in Toxicology, 30, 81–89.
  • Li, W.W., et al., 2016. Lysine adduction by reactive metabolite(s) of monocrotaline. Chemical Research in Toxicology, 29, 333–341.
  • Lin, G., et al., 2011. Hepatic sinusoidal obstruction syndrome associated with consumption of Gynura segetum. Journal of Hepatology, 54, 666–673.
  • Mattocks, A.R., and White, I.N.H., 1970. Estimation of metabolites of pyrrolizidine alkaloids in animal tissues. Analytical Biochemistry, 38, 529–535.
  • Rietjens, I.M.C.M., et al., 2005. Molecular mechanisms of toxicity of important food-borne phytotoxins. Molecular Nutrition and Food Research, 49, 131–158.
  • Merz, K.-H., and Schrenk, D., 2016. Interim relative potency factors for the toxicological risk assessment of pyrrolizidine alkaloids in food and herbal medicines. Toxicology Letters, 263, 44–57.
  • Ruan, J.Q., et al., 2015. Blood pyrrole-protein adducts-A biomarker of pyrrolizidine alkaloid-induced liver injury in humans. Journal of Environmental Science and Health Part C Environmental Carcinogenisis and Ecotoxicology Reviews, 33, 404–421.
  • Wang, Y.P., et al., 2005. Metabolic activation of the tumorigenic pyrrolizidine alkaloid, retrorsine, leading to DNA adduct formation in vivo. International Journal of Environmental Research and Public Health, 2, 74–79.
  • Xia, Q.S., et al., 2016. Pyrrolizidine alkaloid-protein adducts: potential non-invasive biomarkers of pyrrolizidine alkaloid-induced liver toxicity and exposure. Chemical Research in Toxicology, 29, 1282–1292.
  • Xia, Q.S., et al., 2013. Pyrrolizidine alkaloid-derived DNA adducts as a common biological biomarker of pyrrolizidine alkaloid-induced tumorigenicity. Chemical Research in Toxicology, 26, 1384–1396.
  • Yan, C.C., and Huxtable, R.J., 1995. Relationship between glutathione concentration and metabolism of the pyrrolizidine alkaloid, monocrotaline, in the isolated, perfused liver. Toxicology and Applied Pharmacology, 130, 132–139.
  • Zhao, Y.W., et al., 2014. Reaction of dehydropyrrolizidine alkaloids with valine and hemoglobin. Chemical Research in Toxicology, 27, 1720–1731.

References

  • EFSA. 2005. Opinion of the scientific panel on food additives, flavourings, processing aids and materials in contact with food on a request from the commission related to semicarbazide in food. The EFSA Journal, 219, 1–36.
  • Fundador, E., and Rusling, J., 2007. Detection of labeled abasic sites in damaged DNA by capillary electrophoresis with laser-induced fluorescence. Analytical and Bioanalytical Chemistry, 387, 1883–1890.
  • Hayatsu, H., Takeishi, K.I., and Ukita, T., 1966. The modification of nucleosides and nucleotides. 3. A selective modification of cytidine with semicarbazide. Biochimica Et Biophysica Acta, 123, 445–457.
  • Hirakawa, K., et al., 2003. Carcinogenic semicarbazide induces sequence-specific DNA damage through the generation of reactive oxygen species and the derived organic radicals. Mutation Research, 536 (1–2), 91–101.
  • Li, J., et al., 2013. Combination of pentafluorophenylhydrazine derivatization and isotope dilution LC-MS/MS techniques for the quantification of apurinic/apyrimidinic sites in cellular DNA. Analytical and Bioanalytical Chemistry, 405, 4059–4066.
  • Melton, D., et al., 2014. Covalent adduct formation between the antihypertensive drug hydralazine and abasic sites in double- and single-stranded DNA. Chemical Research in Toxicology, 27, 2113–2118.
  • Wang, Y., Chan, H.W., and Chan, W., 2016. Facile Formation of a DNA Adduct of Semicarbazide on Reaction with Apurinic/Apyrimidinic Sites in DNA. Chemical Research in Toxicology, 29, 834–840.

References

  • EFSA 2014. Endogenous formaldehyde turnover in humans compared with exogenous contribution from food sources. EFSA Journal, 12, 3350.
  • Jiang, T., et al., 2007. N-formylation of lysine in histone proteins as a secondary modification arising from oxidative DNA damage. Proceedings of the National Academy of Sciences of the United States of America USA, 104, 60–65.
  • Liu, J., and Chan, W., 2015. Quantification of thiazolidine-4-carboxylic acid in toxicant-exposed cells by isotope-dilution liquid chromatography-mass spectrometry reveals an intrinsic antagonistic response to oxidative stress-induced toxicity. Chemical Research in Toxicology, 28, 394–400.
  • Liu, J., Chan, K.K.J., and Chan, W., 2016. Identification of protein thiazolidination as a novel molecular signature for oxidative stress and formaldehyde exposure. Chemical Research in Toxicology, 29, 1865–1871.
  • Palmieri, B., and Sblendorio, V., 2007. Oxidative stress tests: overview on reliability and use. Part I. European Review for Medical and Pharmacological Sciences, 11, 309–342.

References

  • Boer, J., et al., 2016. Roles of UGT, P450, and gut microbiota in the metabolism of epacadostat in humans. Drug Metabolism and Disposition: The Biological Fate of Chemicals, 44, 1668–1674.
  • Haiser, H.J., and Turnbaugh, P.J., 2013. Developing a metagenomic view of xenobiotic metabolism. Pharmacological Research, 69, 21–31.
  • Spanogiannopoulos, P., et al., 2016. The microbial pharmacists within us: a metagenomic view of xenobiotic metabolism. Nature Reviews Microbiology, 14, 273–287.
  • Sousa, T., et al., 2008. The gastrointestinal microbiota as a site for the biotransformation of drugs. International Journal of Pharmaceutics, 363, 1–25.

References

  • Asakura, M., et al., 2015. Dipeptidyl peptidase-4 greatly contributes to the hydrolysis of vildagliptin in human liver. Drug Metabolism and Disposition: The Biological Fate of Chemicals, 43, 477–484.
  • Foti, R.S., and Dalvie, D.K., 2016. Cytochrome P450 and non-cytochrome P450 oxidative metabolism: contributions to the pharmacokinetics, safety, and efficacy of xenobiotics. Drug Metabolism and Disposition: The Biological Fate of Chemicals, 44, 1229–1245.
  • He, H., et al., 2009a. Absorption, metabolism, and excretion of [14C]vildagliptin, a novel dipeptidyl peptidase 4 inhibitor, in humans. Drug Metabolism Disposition, 37, 536–544.
  • He, H., et al., 2009b. Disposition of vildagliptin, a novel dipeptidyl peptidase 4 inhibitor, in rats and dogs. Drug Metabolism Disposition, 37, 545–554.
  • Otieno, M.A., et al., 2017. Mechanisms for hepatobiliary toxicity in rats treated with an antagonist of melanin concentrating hormone receptor 1 (MCHR1). Toxicological Sciences: An Official Journal of the Society of Toxicology, 155, 379–388.
  • Shi, J., et al., 2016. Metabolism and bioactivation of fluorochloridone, a novel selective herbicide, in vivo and in vitro. Environmental Science &Amp; Technology, 50, 9652–9660.
  • Villhauer, E.B., et al., 2003. 1-[[(3-hydroxy-1-adamantyl)amino]acetyl]-2-cyano-(S)-pyrrolidine: a potent, selective, and orally bioavailable dipeptidyl peptidase IV inhibitor with antihyperglycemic properties. Journal of Medicinal Chemistry, 46, 2774–2789.
  • Xie, C., et al., 2013. Metabolism and bioactivation of famitinib, a novel inhibitor of receptor tyrosine kinase, in cancer patients. British Journal of Pharmacology, 168, 1687–1706.

References

  • Albaugh, D.R., et al., 2012. Time-dependent inhibition and estimation of CYP3A clinical pharmacokinetic drug-drug interactions using plated human cell systems. Drug Metabolism and Disposition: The Biological Fate of Chemicals, 40, 1336–1344.
  • Grimm, S.W., et al., 2009. The conduct of in vitro studies to address time-dependent inhibition of drug-metabolizing enzymes: a perspective of the pharmaceutical research and manufacturers of America. Drug Metabolism and Disposition, 37, 1355–1370.
  • Huang, J.C.A., et al., 2014. Evaluation of drug-drug interactions of VX-509 (decernotinib), an oral selective janus kinase 3 inhibitor, in healthy volunteers, in: The European League Against Rheumatism, Paris. 73, Sup 2, THU0135. DOI 10.1136/annrheumdis-2014-eular.1184.
  • Parkinson, A., et al., 2010. System-dependent outcomes during the evaluation of drug candidates as inhibitors of cytochrome P450 (CYP) and uridine diphosphate glucuronosyltransferase (UGT) enzymes: human hepatocytes versus liver microsomes versus recombinant enzymes. Drug Metabolism and Pharmacokinetics, 25, 16–27.
  • Williams, J.A., et al., 2004. Drug-drug interactions for UDP-glucuronosyltransferase substrates: a pharmacokinetic explanation for typically observed low exposure (AUCI/AUC) ratios. Drug Metabolism and Disposition: The Biological Fate of Chemicals, 32, 1201–1208.
  • Zetterberg, C., et al., 2016. VX-509 (Decernotinib)-mediated CYP3A time-dependent inhibition: an aldehyde oxidase metabolite as a perpetrator of drug-drug interactions. Drug. Drug Metabolism and Disposition: The Biological Fate of Chemicals, 44, 1286–1295.

References

  • Alexander, J., et al., 1991. Formation of a glutathione conjugate and a semistable transportable glucuronide conjugate of N2-oxidized species of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) in rat liver. Carcinogenesis, 12, 2239–2245.
  • Fallon, J.K., et al., 2013. Targeted quantitative proteomics for the analysis of 14 UGT1As and -2Bs in human liver using nanoUPLC-MS/MS with selected reaction monitoring. Journal of Proteome Research, 12, 4402–4413.
  • Cai, T., et al., 2016. Bioactivation of heterocyclic aromatic amines by UDP glucuronosyltransferases. Chemical Research Toxicology, 29, 879–891.
  • Girard, H., et al., 2008. UGT1A1 and UGT1A9 functional variants, meat intake, and colon cancer, among Caucasians and African-Americans. Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis, 644, 56–63.
  • Ishii, Y., Takeda, S., and Yamada, H., 2010. Modulation of UDP-glucuronosyltransferase activity by protein-protein association. Drug Metabolism Reviews, 42, 145–158.
  • Lépine, J., et al., 2004. Specificity and regioselectivity of the conjugation of estradiol, estrone, and their catecholestrogen and methoxyestrogen metabolites by human uridine diphospho-glucuronosyltransferases expressed in endometrium. The Journal of Clinical Endocrinology and Metabolism, 89, 5222–5232.
  • Miners, J.O., et al., 2011. Characterization of niflumic acid as a selective inhibitor of human liver microsomal UDP-glucuronosyltransferase 1A9: application to the reaction phenotyping of acetaminophen glucuronidation. Drug Metabolism and Disposition: The Biological Fate of Chemicals, 39, 644–652.
  • Styczynski, P., et al., 1993. The direct glucuronidation of 2-amino-1-methyl-6-phenylimidazo[4,5-b] pyridine (PhIP) by human and rabbit liver microsomes. Chemical Research in Toxicology, 6, 846–851.
  • Tang, Y., et al., 2012. UDP-Glucuronosyltransferase-mediated metabolic activation of the tobacco carcinogen 2-amino-9H-pyrido[2,3-b]indole. The Journal of Biological Chemistry, 287, 14960–14972.
  • Walsky, R.L., et al., 2012. Optimized assays for human UDP-glucuronosyltransferase (UGT) activities: altered alamethicin concentration and utility to screen for UGT inhibitors. Drug Metabolism and Disposition: The Biological Fate of Chemicals, 40, 1051–1065.

References

  • Avonto, C., et al., 2015. A fluorescence high throughput screening method for the detection of reactive electrophiles as potential skin sensitizers. Toxicology and Applied Pharmacology, 289, 177–184.
  • Christensson, J.B., et al., 2008. Limonene hydroperoxide analogues differ in allergenic activity. Contact Dermatitis, 59, 344–352.
  • Hausen, B.M.R.J., and Harkenthal, M., 1999. Degradation products of monoterpenes are the sensitizing agents in tea tree oil. American Journal of Contact Dermatitis : Official Journal of the American Contact Dermatitis Society, 10, 68–77.
  • Karlberg, A.T., et al., 2008. Allergic contact dermatitis––formation, structural requirements, and reactivity of skin sensitizers. Chemical Research in Toxicology, 21, 53–69.
  • Karlberg, A.T., and Dooms-Goossens, A., 1997. Contact allergy to oxidized d-limonene among dermatitis patients. Contact Dermatitis, 36, 201–206.
  • Rudbäck, J., et al., 2012. α-Terpinene, an antioxidant in tea tree oil, autoxidizes rapidly to skin allergens on air exposure. Chemical Research in Toxicology, 25, 713–721.

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