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Relevant bibliographies by topics / Liver; Toxicology

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Academic literature on the topic 'Liver; Toxicology'

Author: Grafiati

Published: 4 June 2021

Last updated: 9 February 2022

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Journal articles on the topic "Liver; Toxicology"

1

Taguchi, Keiko, and Thomas W. Kensler. "Nrf2 in liver toxicology." Archives of Pharmacal Research 43, no. 3 (2019): 337–49. http://dx.doi.org/10.1007/s12272-019-01192-3.

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Valerio, Luis G., and Rakesh Dixit. "Special Issue on Liver Toxicology." Toxicology Mechanisms and Methods 18, no. 8 (2008): 613. http://dx.doi.org/10.1080/15376510802439945.

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ERKEKOĞLU, Pınar, and Belma KOÇER GÜMÜŞEL. "In Vitro Liver Models in Toxicology." Journal of Literature Pharmacy Sciences 8, no. 1 (2019): 1–17. http://dx.doi.org/10.5336/pharmsci.2018-61664.

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Mcfarlane, M. "Toxicology of the liver (2nd edn)." Journal of Applied Toxicology 19, no. 1 (1999): 73. http://dx.doi.org/10.1002/(sici)1099-1263(199901/02)19:1<73::aid-jat542>3.0.co;2-4.

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Ballet, François. "Preventing Drug-Induced Liver Injury: How Useful Are Animal Models?" Digestive Diseases 33, no. 4 (2015): 477–85. http://dx.doi.org/10.1159/000374093.

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Drug-induced liver injury (DILI) is the most common organ toxicity encountered in regulatory animal toxicology studies required prior to the clinical development of new drug candidates. Very few reports have evaluated the value of these studies for predicting DILI in humans. Indeed, compounds inducing liver toxicity in regulatory toxicology studies are not always correlated with a risk of DILI in humans. Conversely, compounds associated with the occurrence of DILI in phase 3 studies or after market release are often tested negative in regulatory toxicology studies. Idiosyncratic DILI is a rare

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Guillouzo, Andre. "Liver Cell Models in in Vitro Toxicology." Environmental Health Perspectives 106 (April 1998): 511. http://dx.doi.org/10.2307/3433803.

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Guillouzo, A. "Liver cell models in in vitro toxicology." Environmental Health Perspectives 106, suppl 2 (1998): 511–32. http://dx.doi.org/10.1289/ehp.98106511.

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Marx, J. "TOXICOLOGY: Protecting Liver From Painkiller's Lethal Dose." Science 298, no. 5592 (2002): 341a—342. http://dx.doi.org/10.1126/science.298.5592.341a.

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Liu, Jing, Yang Fan, Hang Yu, et al. "Allopurinol Protects Against Cholestatic Liver Injury in Mice Not Through Depletion of Uric Acid." Toxicological Sciences 181, no. 2 (2021): 295–305. http://dx.doi.org/10.1093/toxsci/kfab034.

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Abstract Cholestasis is one of the most severe manifestations of liver injury and has limited therapeutic options. Allopurinol (AP), an inhibitor of uric acid (UA) synthesis, was reported to prevent liver damage in several liver diseases. However, whether AP protects against intrahepatic cholestatic liver injury and what is the role of UA in the pathogenesis of cholestasis remain unknown. In this study, we reported that AP attenuated liver injury in a mouse model of intrahepatic cholestasis induced by alpha-naphthylisothiocyanate (ANIT). AP showed no significant effect on glutathione depletion

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Brimblecombe, R. W., G. B. Leslie, and T. F. Walker. "Toxicology of Cimetidine." Human Toxicology 4, no. 1 (1985): 13–25. http://dx.doi.org/10.1177/096032718500400103.

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1 Cimetidine has been shown to have low acute toxicity in dogs and rodents. Repeated-dose studies of up to 24 months' duration in rodents at doses up to 950 mg day kg-1 showed few adverse effects. Liver weight was consistently increased at the highest dose and testis, prostate and seminal vesicle weights were reduced in a dose- and time-related fashion. Cimetidine was not carcinogenic in the rat. 2 In tests of up to 1 year's duration in dogs two animals receiving 504 mg day kg-1 had to be killed before the end of the study. They had degenerative changes in the liver and renal tubular nephrosis

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Dissertations / Theses on the topic "Liver; Toxicology"

1

Hamilton, Geraldine Alexandra. "Characterisation and evaluation of liver spheroids as a model for long-term culture of hepatocytes." Thesis, University of Hertfordshire, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.245460.

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Badger, Andrew Ashley 1970. "Alterations in chemically-induced liver injury by immunomodulators." Diss., The University of Arizona, 1998. http://hdl.handle.net/10150/282642.

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Studies presented in this dissertation determined biochemical mechanisms underlying the modulation of chemical-induced liver injury by retinol and GdC₃ The first objective was to determine the role of inflammatory cells in the retinol potentiation of CCl₄-induced liver injury. Plasma alanine aminotranferase activities and histological analysis of liver sections both illustrated significant potentiation of CCl₄ hepatotoxicity by a single dose of retinol. The mechanism for this potentiation involves priming of Kupffer cells (KC) (i.e. by enhancing their response to toxic stimuli) as established

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3

Terneus, Marcus V. "A mechanistic study of the protective effects of S-Adenosyl-L-Methionine against hepatotoxicity of acetaminophen." Huntington, WV : [Marshall University Libraries], 2006. http://www.marshall.edu/etd/descript.asp?ref=698.

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Goetz, Amber Kristina. "Gene Expression Profiling in Testis and Liver of Mice to Identify Modes of Action of Conazole Toxicities." NCSU, 2003. http://www.lib.ncsu.edu/theses/available/etd-11142003-170100/.

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Conazoles are a class of azole fungicides used in both pharmaceutical and agricultural applications. This study focused on 4 conazoles that exhibit a range of carcinogenic and reproductive effects, in order to identify common and unique modes of action. Conazoles target cytochrome P450s (CYPs), and the inhibition and induction of various CYP activities may be part of the toxic modes of action in liver and testis. We used gene expression profiling to characterize a broader range of conazole effects and to identify additional modes of action. Adult male CD-1 mice were dosed daily by gavage for 1

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Salamat, Julia. "The Role of CYP2A5 in Cadmium-Induced Liver Injury." Digital Commons @ East Tennessee State University, 2018. https://dc.etsu.edu/etd/3498.

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Cadmium is present in food and groundwater. Tobacco smoking and occupational exposure are also major sources for cadmium. Cadmium is primarily accumulated in liver, a major organ metabolizing exogenous chemicals. Chemical metabolism may cause detoxification, but it can also cause bio-activation resulting in liver damage. Cytochrome P450s (CYP) are major liver metabolism enzymes, and cadmium chloride (CdCl2) can induce CYP2A5 in mice. We examined the effect of CYP2A5 on CdCl2-induced liver injury using CYP2A5-knockout (cyp2a5-/-) mice. The cyp2a5-/- mice and their control WT mice were injected

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Sharpe, Amy-Joan Lorna 1965. "Substrate specificity of rat liver aldehyde dehydrogenase with chloroacetaldehydes." Thesis, The University of Arizona, 1991. http://hdl.handle.net/10150/277906.

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Chlorinated acetaldehydes have recently been the focus of research due to their role as reactive intermediates and their possible occurrence in chlorinated drinking water. The metabolism of these compounds, however, has not been extensively studied. In this study, the in vitro substrate specificity of cytosolic and mitochondrial rat liver aldehyde dehydrogenase toward these compounds was investigated. Both crude and semi-purified preparations of the enzymes were used. Monochloroacetaldehyde was found to be extensively metabolized by this enzyme system. It was metabolized to a greater extent th

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Stevens, Jeffrey Charles 1963. "Selective inactivation of four rat liver microsomal androstenedione hydroxylases by chloramphenicol analogs." Thesis, The University of Arizona, 1988. http://hdl.handle.net/10150/276700.

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The steroid androstenedione has been shown to be a valuable tool for the study of selective inactivation of rat liver cytochrome P-450 isozymes. The validity of this method was investigated using microsomes, purified cytochromes P-450, cytochrome P-450 antibodies, and the mechanism-based inactivator chloramphenicol. Enzyme inactivation and antibody inhibition studies show that microsomes from phenobarbital- and non-phenobarbital-treated rats are needed to accurately monitor the inactivation of the major phenobarbital-inducible P-450 isozyme (PB-B) and of the major constitutive androstenedione

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Gustafson, Richard Allan 1958. "Effect of reduced glutathione on the metabolism of chloroaldehydes by rat liver aldehyde dehydrogenase." Thesis, The University of Arizona, 1992. http://hdl.handle.net/10150/278192.

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The identification of chlorinated organic compounds in drinking supplies has resulted in an interest in the metabolism and toxicity of chlorinated aldehydes. Another possible factor in the metabolism of chloroaldehydes is the endogenaous tripeptide glutathione. The formation of glutathioneconjugates with chloroaldehydes may increase or decrease their rate of reaction with the aldehyde dehydrogenase enzyme. This study found that the rat liver aldehyde dehydrogenase isozymes lost activity with time regardless of storage conditions. In vitro assays of enzyme activity confirmed substrate specifici

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Brown, Alan Perry. "Generation and expression of halothane derived protein adducts in the guinea pig liver." Diss., The University of Arizona, 1993. http://hdl.handle.net/10150/186218.

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The volatile anesthetic halothane can be bioactivated in the liver to the reactive intermediate, trifluoroacetyl chloride, which is capable of covalently modifying liver protein. The product of this reaction is trifluoroacetyl-N-ε-amino lysine, which can act as a foreign epitope in altering both protein immunogenicity and antigenicity. Protein adduct formation appears to be responsible for the development of both an acute and an immune-mediated hepatotoxicity. The goal of this research project was to detect, quantify, and characterize the formation of protein adducts in the guinea pig liver, f

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Li, Xilin. "Role of Diet and Xenobiotics in the Progression of Nonalcoholic Fatty Liver Disease." Thesis, Indiana University, 2018. http://pqdtopen.proquest.com/#viewpdf?dispub=10830274.

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<p> Non-alcoholic fatty liver disease (NAFLD) has become the leading cause of chronic liver disease. The spectrum of NAFLD ranges from simple steatosis, to non-alcoholic steatohepatitis (NASH), fibrosis, cirrhosis, and potentially hepatocellular carcinoma. Dietary factors and chemical exposure have been associated with the disease progression. In addition, the presence of NAFLD changes the metabolism of drugs and chemicals, which may in turn increase the susceptibility of the liver to xenobiotic induced toxicity. To examine the potential interplay of chemicals on diet-induced NAFLD, three stud

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Books on the topic "Liver; Toxicology"

1

IARC Working Group on the Evaluation of Carcinogenic Risks to Humans (1994 Lyon, France). Schistosomes, liver flukes and Helicobacter pylori. The Agency, 1994.

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2

Farrell, Geoffrey C. Drug-induced liver disease. Churchill Livingstone, 1994.

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3

1931-, Chambers P. L., ed. Recent developments in toxicology: Trends, methods, and problems : proceedings of the European Society of Toxicology Meeting held in Leipzig, September 12-14, 1990. Springer-Verlag, 1991.

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4

G, Poli, ed. Free radicals in the pathogenesis of liver injury: Proceedings of the Second Congress on Free Radicals in Liver Injury, 9-11 June 1988, Turin, Italy. Pergamon Press, 1989.

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1931-, Chambers P. L., Henschler Dietrich, and Oesch Franz 1938-, eds. Mouse liver tumors: Relevance to human cancer risk : Symposium of the European Society of Toxicology, held in Rome, February 2-5, 1986. Springer-Verlag, 1987.

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6

International Symposium on Cirrhosis, Hepatic Encephalopathy, and Ammonium Toxicity, Molecular Basis and Clinical Aspects (1989 Valencia, Spain). Cirrhosis, hepatic encephalopathy, and ammonium toxicity. Plenum Press, 1990.

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Symposium on Cytoprotection. (9th 1991 Kyoto, Japan). Cytoprotection and cytobiology: Proceedings of the Ninth Symposium on Cytoprotection, Kyoto, March 2, 1991. Edited by Kawai Keiichi 1932- and Yunoki Kazuo. Excerpta Medica, 1992.

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8

P, Spoelstra, ed. Drug-induced hepatic injury: A comprehensive survey of the literature on adverse drug reactions up to January 1985. Elsevier Science Publishers, 1985.

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9

Drug-induced hepatic injury. 2nd ed. Elsevier, 1992.

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10

Gupta, Aniruddha Sen. Our toxic world a guide to hazardous substances in our everyday lives. SAGE Publications, 2010.

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Book chapters on the topic "Liver; Toxicology"

1

McGill, Mitchell R., C. David Williams, and Hartmut Jaeschke. "Liver Toxicology." In Mammalian Toxicology. John Wiley & Sons, Inc., 2015. http://dx.doi.org/10.1002/9781118683484.ch20.

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2

Kenna, J. Gerry, Mikael Persson, Scott Q. Siler, et al. "Liver." In Drug Discovery Toxicology. John Wiley & Sons, Inc, 2016. http://dx.doi.org/10.1002/9781119053248.ch8.

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3

Monckton, Chase P., and Salman R. Khetani. "Engineered Human Liver Cocultures for Investigating Drug-Induced Liver Injury." In Methods in Pharmacology and Toxicology. Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7677-5_11.

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4

Swenberg, J. A., and T. R. Fennell. "DNA Damage and Repair in Mouse Liver." In Archives of Toxicology. Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71617-1_15.

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Neumann, H. G. "Variables Influencing DNA-Binding in Mouse Liver." In Archives of Toxicology. Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71617-1_17.

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6

Balint, G. A., G. Karácsony, Á. Pap, and V. Varró. "The Effect of Prostacyclin on the Liver." In Archives of Toxicology. Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-69928-3_78.

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Evelo, C. T. A., J. Atema, J. H. J. Copius-Peereboom, P. H. S. Fijneman, J. C. L. M. Pertijs, and R. P. Bos. "Liver Damage after Coal-tar Treatment does not Prevent Induction of Glutathione S-Transferases in Rat Liver." In Archives of Toxicology. Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74117-3_13.

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8

Burcham, Philip C. "Target-Organ Toxicity: Liver and Kidney." In An Introduction to Toxicology. Springer London, 2013. http://dx.doi.org/10.1007/978-1-4471-5553-9_6.

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9

Hollander, C. F., C. F. A. van Bezooijen, and H. A. Solleveld. "Anatomy, Function and Aging in the Mouse Liver." In Archives of Toxicology. Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71617-1_22.

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Metzler, M., and G. H. Degen. "Sex Hormones and Neoplasia: Liver Tumors in Rodents." In Archives of Toxicology. Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71617-1_23.

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Conference papers on the topic "Liver; Toxicology"

1

Affifi, Nagia N., Ola A. Heikal, Rasha S. Hanafi, Salma N. Tammam, and Olga Tarasenko. "APPLICATION OF BIODEGRADABLE NANOPARTICLES IN LIVER TARGETING OF TACROLIMUS." In BIOLOGY, NANOTECHNOLOGY, TOXICOLOGY, AND APPLICATIONS: Proceedings of the 5th BioNanoTox and Applications International Research Conference. AIP, 2011. http://dx.doi.org/10.1063/1.3587467.

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