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Journal articles on the topic 'Liver; Toxicology'

Author: Grafiati

Published: 4 June 2021

Last updated: 9 February 2022

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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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Liu, Xiaoyan, Yanqiu Liu, Yang Qu, Mengchun Cheng, and Hongbin Xiao. "Metabolomic profiling of emodin-induced cytotoxicity in human liver cells and mechanistic study." Toxicology Research 4, no. 4 (2015): 948–55. http://dx.doi.org/10.1039/c4tx00246f.

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12

Lickteig, Andrew J., Youcai Zhang, Curtis D. Klaassen, and Iván L. Csanaky. "Effects of Absence of Constitutive Androstane Receptor (CAR) on Bile Acid Homeostasis in Male and Female Mice." Toxicological Sciences 171, no. 1 (2019): 132–45. http://dx.doi.org/10.1093/toxsci/kfz143.

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AbstractAccumulation of bile acids (BAs) in hepatocytes has a role in liver disease and also in drug-induced liver injury. The constitutive androstane receptor (CAR) has been shown to protect against BA-induced liver injury. The polymorphism of CAR has recently been shown to modify the pharmacokinetics and pharmacodynamics of various drugs. Thus, it was hypothesized that polymorphism of CAR may also influence BA homeostasis. Using CAR-null and WT mice, this study modeled the potential consequences of CAR polymorphism on BA homeostasis. Our previous study showed that chemical activation of CAR

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13

Friedman, Leonard, John Scalera, James E. Keys, et al. "Some Biochemical and Histological Effects of 2-Chloroethanol in Rats." Journal of the American College of Toxicology 1, no. 3 (1992): 37–56. http://dx.doi.org/10.3109/10915818209018017.

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The effects of 2-chioroethanol (2-CE) on rat tissue following in vitro and in vivo exposure were studied. At concentrations as low as 2.5 mg/ml, protein synthesis in liver slices was inhibited; at concentrations of 25 mg/ml and above, RNA synthesis and respiration were also impaired. Single oral doses of 2-CE to young adult rats at levels of 15-40 mg/kg body weight depressed liver nonprotein sulfhydryl (GSH) concentration and liver protein but not RNA synthesis. Liver lipid was increased by 7 hr after a single oral dose of 30 mg/kg. The time courses and dose-response relationship for GSH deple

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14

Rao, K. V. K., M. V. Hosur, C. Fernandes, and S. V. Bhide. "Den Induced Liver Carcinogenesis in Rats: Growth Inhibitory Polypeptides Isolated from Normal Livers and Liver Tumours." Journal of Toxicology: Toxin Reviews 8, no. 1-2 (1989): 217–26. http://dx.doi.org/10.3109/15569548909059751.

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15

Berry, C. L. "Liver Lesions in an Autopsy Population." Human Toxicology 6, no. 3 (1987): 209–14. http://dx.doi.org/10.1177/096032718700600306.

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Examination of the liver in 1500 consecutive autopsies performed in the coronial system in south-east London revealed a wide range of lesions. Around 5% of livers contained a solitary lesion, clinically non-evident lesions included cirrhosis, adenomas and metastatic carcinoma. Hamartomas are relatively common.

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16

Imparato, Giorgia, Brunella Corrado, Vincenza De Gregorio, Francesco Urciuolo, and Paolo Netti. "Gut-liver on chip for in vitro toxicology study." Toxicology Letters 280 (October 2017): S133. http://dx.doi.org/10.1016/j.toxlet.2017.07.371.

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17

Irelan, J. T., D. G. Nguyen, C. C. Grundy, et al. "Bioprinted human liver tissues for toxicology and disease modeling." Toxicology Letters 258 (September 2016): S149. http://dx.doi.org/10.1016/j.toxlet.2016.06.1574.

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18

Smith, P. F., A. J. Gandolfi, C. L. Krumdieck, et al. "Dynamic organ culture of precision liver slices for toxicology." Life Sciences 36, no. 14 (1985): 1367–75. http://dx.doi.org/10.1016/0024-3205(85)90042-6.

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19

Anand, Sathanandam S., and Harihara M. Mehendale. "Liver regeneration: a critical toxicodynamic response in predictive toxicology." Environmental Toxicology and Pharmacology 18, no. 2 (2004): 149–60. http://dx.doi.org/10.1016/j.etap.2004.02.011.

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20

Johnson, Kamin J., Scott S. Auerbach, and Eduardo Costa. "A Rat Liver Transcriptomic Point of Departure Predicts a Prospective Liver or Non-liver Apical Point of Departure." Toxicological Sciences 176, no. 1 (2020): 86–102. http://dx.doi.org/10.1093/toxsci/kfaa062.

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Abstract Identifying a toxicity point of departure (POD) is a required step in human health risk characterization of crop protection molecules, and this POD has historically been derived from apical endpoints across a battery of animal-based toxicology studies. Using rat transcriptome and apical data for 79 molecules obtained from Open TG-GATES (Toxicogenomics Project-Genomics Assisted Toxicity Evaluation System) (632 datasets), the hypothesis was tested that a short-term exposure, transcriptome-based liver biological effect POD (BEPOD) could estimate a longer-term exposure “systemic” apical e

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21

McGreal, Steven R., Karim Rumi, Michael J. Soares, Benjamin L. Woolbright, Hartmut Jaeschke, and Udayan Apte. "Disruption of Estrogen Receptor Alpha in Rats Results in Faster Initiation of Compensatory Regeneration Despite Higher Liver Injury After Carbon Tetrachloride Treatment." International Journal of Toxicology 36, no. 3 (2017): 199–206. http://dx.doi.org/10.1177/1091581817706067.

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Estrogen receptor alpha (ESR1) is 1 of the 2 intracellular receptors for estrogen and is expressed by hepatocytes in the liver. The role of ESR1 in the regulation of toxicant-induced liver injury and compensatory regeneration is not completely clear. We investigated the role of ESR1 in liver regeneration after carbon tetrachloride (CCl4)-induced liver injury using wild type (WT) and ESR1 knockout (ESR1-KO) rats. Adult female WT and ESR1-KO rats were treated with 1 mL/kg CCl4 and euthanized over a time course of 0 to 48 hours. Liver injury measured by serum alanine amino transaminase, and histo

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22

Furuya, Shinji, Joseph A. Cichocki, Kranti Konganti, et al. "Histopathological and Molecular Signatures of a Mouse Model of Acute-on-Chronic Alcoholic Liver Injury Demonstrate Concordance With Human Alcoholic Hepatitis." Toxicological Sciences 170, no. 2 (2018): 427–37. http://dx.doi.org/10.1093/toxsci/kfy292.

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Abstract Human alcoholic hepatitis (AH) carries a high mortality rate. AH is an acute-on-chronic form of liver injury characterized by hepatic steatosis, ballooned hepatocytes, neutrophil infiltration, and pericellular fibrosis. We aimed to study the pathogenesis of AH in an animal model which combines chronic hepatic fibrosis with intragastric alcohol administration. Adult male C57BL6/J mice were treated with CCl4 (0.2 ml/kg, 2×weekly by intraperitoneal injections for 6 weeks) to induce chronic liver fibrosis. Then, ethyl alcohol (up to 25 g/kg/day for 3 weeks) was administered continuously t

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23

Hastings, Kenneth L., Martin D. Green, Bin Gao, Patricia E. Ganey, Robert A. Roth, and Gary R. Burleson. "Beyond Metabolism: Role of the Immune System in Hepatic Toxicity." International Journal of Toxicology 39, no. 2 (2020): 151–64. http://dx.doi.org/10.1177/1091581819898399.

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The liver is primarily thought of as a metabolic organ; however, the liver is also an important mediator of immunological functions. Key perspectives on this emerging topic were presented in a symposium at the 2018 annual meeting of the American College of Toxicology entitled “Beyond metabolism: Role of the immune system in hepatic toxicity.” Viral hepatitis is an important disease of the liver for which insufficient preventive vaccines exist. Host immune responses inadequately clear these viruses and often potentiate immunological inflammation that damages the liver. In addition, the liver is

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24

Wang, Tao, Maria Papoutsi, Marion Wiesmann, et al. "Investigation of Correlation Among Safety Biomarkers in Serum, Histopathological Examination, and Toxicogenomics." International Journal of Toxicology 30, no. 3 (2011): 300–312. http://dx.doi.org/10.1177/1091581811401920.

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This article addresses the issue of miscorrelation between hepatic injury biomarkers and histopathological findings in the drug development context. Our studies indicate that the use of toxicogenomics can aid in the drug development decision-making process associated with such miscorrelated data. BLZ945 was developed as a Colony-Stimulating Factor 1 Receptor (CSF-1R) inhibitor. Treatment of BLZ945 in rats and monkeys increased serum alanine aminotransferase (ALT) and aspartate transaminase (AST). However, liver hypertrophy was the only histopathological liver finding in rats, and there was no

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25

Kornalik, F. "Mouse liver tumors." Toxicon 27, no. 3 (1989): 399. http://dx.doi.org/10.1016/0041-0101(89)90193-1.

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26

Denlinger, Robert H. "Toxicologic Pathology of the Liver." Toxicologic Pathology 23, no. 6 (1995): 747–49. http://dx.doi.org/10.1177/019262339502300614.

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27

Popp, James A. "Toxicologic Pathology of the Liver." Toxicologic Pathology 24, no. 1 (1996): 3. http://dx.doi.org/10.1177/019262339602400102.

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28

Elmore, Susan A., Vivian S. Chen, Schantel Hayes-Bouknight, et al. "Proceedings of the 2016 National Toxicology Program Satellite Symposium." Toxicologic Pathology 45, no. 1 (2016): 11–51. http://dx.doi.org/10.1177/0192623316672074.

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The 2016 annual National Toxicology Program Satellite Symposium, entitled “Pathology Potpourri” was held in San Diego, CA, at the Society of Toxicologic Pathology’s (STP) 35th annual meeting. The goal of this symposium was to present and discuss challenging diagnostic pathology and/or nomenclature issues. This article presents summaries of the speakers’ talks, along with select images that were used by the audience for voting and discussion. Some lesions and topics covered during the symposium included malignant glioma and histiocytic sarcoma in the rodent brain; a new statistical method desig

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29

Lang, Leslie H. "Gastroenterologists Named to Scientific Advisory Committee for Liver Toxicology Study." Gastroenterology 130, no. 1 (2006): 4–5. http://dx.doi.org/10.1053/j.gastro.2005.12.013.

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30

Morley, Stephen R., and Jennifer Bolton. "Variation in postmortem liver sampling: implications for postmortem toxicology interpretation." Journal of Clinical Pathology 65, no. 12 (2012): 1136–37. http://dx.doi.org/10.1136/jclinpath-2012-200980.

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31

Andrews, Elise, and Ann K. Daly. "Flucloxacillin-induced liver injury." Toxicology 254, no. 3 (2008): 158–63. http://dx.doi.org/10.1016/j.tox.2008.08.009.

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32

Crizer, David M., Sreenivasa C. Ramaiahgari, Stephen S. Ferguson, et al. "Benchmark Concentrations for Untargeted Metabolomics Versus Transcriptomics for Liver Injury Compounds in In Vitro Liver Models." Toxicological Sciences 181, no. 2 (2021): 175–86. http://dx.doi.org/10.1093/toxsci/kfab036.

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Abstract Interpretation of untargeted metabolomics data from both in vivo and physiologically relevant in vitro model systems continues to be a significant challenge for toxicology research. Potency-based modeling of toxicological responses has served as a pillar of interpretive context and translation of testing data. In this study, we leverage the resolving power of concentration-response modeling through benchmark concentration (BMC) analysis to interpret untargeted metabolomics data from differentiated cultures of HepaRG cells exposed to a panel of reference compounds and integrate data in

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33

You, Dahea, Lascelles E. Lyn-Cook, Daniel M. Gatti, et al. "Nitrosative Stress and Lipid Homeostasis as a Mechanism for Zileuton Hepatotoxicity and Resistance in Genetically Sensitive Mice." Toxicological Sciences 175, no. 2 (2020): 220–35. http://dx.doi.org/10.1093/toxsci/kfaa037.

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Abstract Zileuton is an orally active inhibitor of leukotriene synthesis for maintenance treatment of asthma, for which clinical usage has been associated with idiosyncratic liver injury. Mechanistic understanding of zileuton toxicity is hampered by the rarity of the cases and lack of an animal model. A promising model for mechanistic study of rare liver injury is the Diversity Outbred (J:DO) mouse population, with genetic variation similar to that found in humans. In this study, female DO mice were administered zileuton or vehicle daily for 7 days (i.g.). Serum liver enzymes were elevated in

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34

Jaeschke, Hartmut, Jephte Y. Akakpo, David S. Umbaugh, and Anup Ramachandran. "Novel Therapeutic Approaches Against Acetaminophen-induced Liver Injury and Acute Liver Failure." Toxicological Sciences 174, no. 2 (2020): 159–67. http://dx.doi.org/10.1093/toxsci/kfaa002.

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Abstract Liver injury and acute liver failure caused by acetaminophen (APAP, N-acetyl-p-aminophenol, paracetamol) overdose is a significant clinical problem in most western countries. The only clinically approved antidote is N-acetylcysteine (NAC), which promotes the recovery of hepatic GSH. If administered during the metabolism phase, GSH scavenges the reactive metabolite N-acetyl-p-benzoquinone imine. More recently, it was shown that NAC can also reconstitute mitochondrial GSH levels and scavenge reactive oxygen/peroxynitrite and can support mitochondrial bioenergetics. However, NAC has side

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35

Takitani, Kimitaka, Hiroshi Miyazaki, Atsushi Yoden, and Hiroshi Tamai. "Children’s toxicology from bench to bed - Liver Injury (2): Mechanism of antioxidant therapy for nonalcoholic fatty liver disease." Journal of Toxicological Sciences 34, Special_ (2009): SP223—SP228. http://dx.doi.org/10.2131/jts.34.sp223.

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36

Murayama, Kei, and Akira Ohtake. "Children’s toxicology from bench to bed - Liver Injury (4): Mitochondrial respiratory chain disorder and liver disease in children." Journal of Toxicological Sciences 34, Special_ (2009): SP237—SP243. http://dx.doi.org/10.2131/jts.34.sp237.

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37

Elmore, Susan A., Mark F. Cesta, Torrie A. Crabbs, et al. "Proceedings of the 2019 National Toxicology Program Satellite Symposium." Toxicologic Pathology 47, no. 8 (2019): 913–53. http://dx.doi.org/10.1177/0192623319876929.

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The 2019 annual National Toxicology Program Satellite Symposium, entitled “Pathology Potpourri,” was held in Raleigh, North Carolina, at the Society of Toxicologic Pathology’s 38th annual meeting. The goal of this symposium was to present and discuss challenging diagnostic pathology and/or nomenclature issues. This article presents summaries of the speakers’ talks along with select images that were used by the audience for voting and discussion. Various lesions and topics covered during the symposium included aging mouse lesions from various strains, as well as the following lesions from vario

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38

Shavila, J., L. J. King, and D. V. Parke. "Spontaneous development of fatty liver in ferrets in a toxicology study." Toxicology 112, no. 2 (1996): 105–16. http://dx.doi.org/10.1016/0300-483x(96)03351-3.

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39

Maritim, Alice C., Brian H. Moore, Ruth A. Sanders, and John B. Watkins. "Effects of Melatonin on Oxidative Stress in Streptozotocin-Induced Diabetic Rats." International Journal of Toxicology 18, no. 3 (1999): 161–66. http://dx.doi.org/10.1080/109158199225440.

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Oxidative stress plays an important role in diabetes and other oxygen-related diseases. Melatonin, a pineal hormone thought to be a scavenger of oxygen radicals and a potentially advantageous therapeutic agent in diseases having oxidative stress, was administered (10 mg/kg ip, in gum tragacanth to prolong its absorption, once a day for 4 successive days) to normal and 30-day streptozotocin-induced diabetic Sprague-Dawley rats, after which markers of oxidative stress were assessed in the liver, kidney, intestine, and spleen. Alanine and aspartate aminotransferase activities in serum, which were

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40

Cutler, David. "Liver cirrhosis finding." Trends in Pharmacological Sciences 22, no. 9 (2001): 449. http://dx.doi.org/10.1016/s0165-6147(00)01838-1.

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41

Smith, Brenda, Josh Rowe, Paul B. Watkins, et al. "Mechanistic Investigations Support Liver Safety of Ubrogepant." Toxicological Sciences 177, no. 1 (2020): 84–93. http://dx.doi.org/10.1093/toxsci/kfaa093.

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Abstract Small-molecule calcitonin gene-related peptide (CGRP) receptor antagonists have demonstrated therapeutic efficacy for the treatment of migraine. However, previously investigated CGRP receptor antagonists, telcagepant and MK-3207, were discontinued during clinical development because of concerns about drug-induced liver injury. A subsequent effort to identify novel CGRP receptor antagonists less likely to cause hepatotoxicity led to the development of ubrogepant. The selection of ubrogepant, following a series of mechanistic studies conducted with MK-3207 and telcagepant, was focused o

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42

Brauer, Manfred. "Magnetic Resonance Imaging and Spectroscopy: New Noninvasive In Vivo Approaches in Toxicology Research." Alternatives to Laboratory Animals 21, no. 4 (1993): 411–25. http://dx.doi.org/10.1177/026119299302100403.

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Magnetic Resonance Imaging (MRI) and Spectroscopy (MRS) give anatomical and biochemical information about a human patient or animal in a non-invasive manner. This unique quality permits the study of toxicological responses of an organ within an intact animal and in a manner in which many fewer animals are needed than by conventional methods of investigation. The use of MRI and MRS in the study of hepatotoxicants, particularly bromobenzene and ethanol, is reviewed. Bromobenzene causes localised hepatic oedema and bioenergetic deterioration; these changes were followed with time by 1H MRI and 31

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43

Su, Guangyue, Haifeng Wang, Jiao Bai, Gang Chen, and Yuehu Pei. "A Metabonomics Approach to Drug Toxicology in Liver Disease and its Application in Traditional Chinese Medicine." Current Drug Metabolism 20, no. 4 (2019): 292–300. http://dx.doi.org/10.2174/1389200220666181231124439.

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Background: The progression of liver disease causes metabolic transformation in vivo and thus affects corresponding endogenous small molecular compounds. Metabonomics is a powerful technology which is able to assess global low-molecular-weight endogenous metabolites in a biological system. This review is intended to provide an overview of a metabonomics approach to the drug toxicology of diseases of the liver. Methods: The regulation of, and relationship between, endogenous metabolites and diseases of the liver is discussed in detail. Furthermore, the metabolic pathways involved in drug interv

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44

Kessova, Irina, and Arthur I. Cederbaum. "CYP2E1: Biochemistry, Toxicology, Regulation and Function in Ethanol-Induced Liver Injury." Current Molecular Medicine 3, no. 6 (2003): 509–18. http://dx.doi.org/10.2174/1566524033479609.

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45

Grove, Jane I., and Guruprasad P. Aithal. "Human leukocyte antigen genetic risk factors of drug-induced liver toxicology." Expert Opinion on Drug Metabolism & Toxicology 11, no. 3 (2014): 395–409. http://dx.doi.org/10.1517/17425255.2015.992414.

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46

Myllynen, P., P. Pienimäki, H. Raunio, and K. Vähäkangas. "Microsomal metabolism of carbamazepine and oxcarbazepine in liver and placenta." Human & Experimental Toxicology 17, no. 12 (1998): 668–76. http://dx.doi.org/10.1177/096032719801701204.

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Metabolism of both carbamazepine (CBZ) and oxcarbaze-pine (OCBZ) were catalyzed by human liver microsomes and microsomes from livers of CBZ-induced or non-induced C57BL/6 mice. Human placental microsomes metabolized only OCBZ. Mouse liver microsomes metabolized CBZ to carbamazepine-10,11-epoxide (CBZ-E), 10- hydroxy-10,11-dihydro-carbamazepine (10-OH-CBZ), 3- hydroxy-carbamazepine (3-OH-CBZ), 10,11-trans-dihydroxy-10,11-dihydro-carbamazepine (10,11-D) and to an unidentified metabolite. CBZ-pretreatment of mice increased both ethoxyresorufin O-deethylase activity in the liver and the amount of

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47

Orrenius, Sten. "Role of Cell Death in Toxicology: Does It Matter How Cells Die?" Annual Review of Pharmacology and Toxicology 59, no. 1 (2019): 1–14. http://dx.doi.org/10.1146/annurev-pharmtox-010818-021725.

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My research activity started with studies on drug metabolism in rat liver microsomes in the early 1960s. The CO-binding pigment (cytochrome P450) had been discovered a few years earlier and was subsequently found to be involved in steroid hydroxylation in adrenal cortex microsomes. Our early studies suggested that it also participated in the oxidative demethylation of drugs catalyzed by liver microsomes, and that prior treatment of the animals with phenobarbital caused increased levels of the hemoprotein in the liver, and similarly enhanced rates of drug metabolism. Subsequent studies of cytoc

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48

Borzelleca, Joseph F., Elizabeth C. Clarke, and L. W. Condie. "Short-Term Toxicity (1 and 10 Days) of Cadmium Chloride in Male and Female Rats: Gavage and Drinking Water." Journal of the American College of Toxicology 8, no. 2 (1989): 377–404. http://dx.doi.org/10.3109/10915818909019561.

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Male and female Sprague-Dawley-derived rats received CdCl2 by gavage at doses of 25, 51, 107, and 225 mg CdCl2 per kg body weight per day for 1 or 10 consecutive days or in drinking solutions at concentrations of 13–323 mg CdCl2 per liter for 10 consecutive days. There were appropriate controls. In the 1 day study in males only, an apparent treatment-related but not statistically significant decrease in body weight was reported; spleen weights and ratios were significantly lower and lung weights and ratios were significantly higher (in the highest dose only). Dose-dependent mortality was obser

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49

Watkins, John B., Phillip A. Gardner, John D. Feczko, and Kathleen M. Klueber. "Streptozotocin and Insulin-Dependent Diabetes Induce Changes in Hepatic Cytoarchitecture in Mice." International Journal of Toxicology 19, no. 6 (2000): 401–5. http://dx.doi.org/10.1080/109158100750058758.

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Streptozotocin (STZ) causes both direct organ toxicity and diabetes, and both actions can affect the structure and function of many organs. Because biliary excretory function changes with time after STZ injection, it was hypothesized that morphological changes would occur in livers from mice made diabetic with STZ. Blood glucose concentrations were elevated above that in control mice from day 3 onward. Liver tissue collected on days 1, 3, 5, 7, 14, 21, 28, 35, and 42 following a single administration of STZ (200 mg/kg IV) was prepared for electron microscopy using standard procedures. Liver sa

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Netter, K. J. "Mouse liver neoplasia — Current perspectives." Toxicology 37, no. 3-4 (1985): 330. http://dx.doi.org/10.1016/0300-483x(85)90099-x.

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