Academic literature on the topic 'Hepatic Toxicity and CCl4'

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Journal articles on the topic "Hepatic Toxicity and CCl4"

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Mohammed, Usman, Abdulrashid Mohammed, Daniel Hassan Mhya, Simon Mafulul Gabriel, and Daniel Dahiru. "Protective Efficiency of Pterocarpus erinaceus Leaves Extract in Carbon-tetrachloride-induced Hepatic and Hematological Injuries in Rats." Journal of Applied Life Sciences International 26, no. 3 (2023): 41–52. http://dx.doi.org/10.9734/jalsi/2023/v26i3606.

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Aims: Chemical toxicity is one of the major leading causes of tissues injuries, which impair the tissue’s ability to maintain normal physiological functions. Pterocarpus erinaceus is a medicinal plant use as traditional remedy for the treatment of several disorders associated with tissues injuries. This study therefore aimed at investigating tissues protective efficiency of Pterocarpus erinaceus leaves extract in carbon-tetrachloride-induced hepatic and hematological injuries in rats.
 Materials and Methods: Leaves of Pterocarpus erinaceous after collection were air-dried and pulverized.
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Shah, Muhammad Dawood, Senty Vun-Sang, and Mohammad Iqbal. "Phenolic Content, Antioxidant and Hepatoprotective Activities of Sabah Hoya coronaria Blume." Journal of Tropical Biology & Conservation (JTBC) 20 (October 15, 2023): 203–17. http://dx.doi.org/10.51200/jtbc.v20i.4656.

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A common challenge that regularly results from oxidative stress is hepatic damage. This condition is characterised by a gradual progression from steatosis to chronic hepatitis, fibrosis, cirrhosis, and hepatocellular carcinoma. The study proposed to assess the antioxidant activity and efficacy of Hoya coronaria aqueous extract in preventing CCl4-induced hepatic damage in rats. The DPPH technique was used in the study to assess the extract's antioxidant properties. The rats received dosages of 125 and 250 mg/kg body weight of H. coronaria extract for 14 days, followed by CCl4 exposure. After tw
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El-Bialy, Badr E., Neveen G. El-Boraey, Ragaa A. Hamouda, and Mohamed M. Abdel-Daim. "Comparative Protective Effects of Spirulina and Spirulina Supplemented with Thiamineagainst Sub-acute Carbon Tetrachloride Toxicity in Rats." Biomedical and Pharmacology Journal 12, no. 2 (2019): 511–26. http://dx.doi.org/10.13005/bpj/1670.

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Carbon tetrachloride (CCl4) is used extensively as an industrial solvent and considered the best-characterized experimental animal model of xenobiotic-induced hepatic toxicity via reactive oxygen species (ROS) generation. This study was designed to evaluate the protective effects of Spirulina platensis (SP) versus Spirulina platensis supplemented with thiamine (SPt) against subacute CCl4 toxicity in rats. Rats were divided into six equal groups; Control vehicle (0.5 ml/rat 1:1 olive oil in water), SP (800 mg/kg b.wt.), SPt (800 mg/kg b.wt.), CCl4 (1ml/kg b.wt.), SP + CCl4 and SPt + CCl4. All t
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Touiss, Ilham, Sabir Ouahhoud, Mohamed Harnafi, et al. "Toxicological Evaluation and Hepatoprotective Efficacy of Rosmarinic Acid-Rich Extract from Ocimum basilicum L." Evidence-Based Complementary and Alternative Medicine 2021 (January 31, 2021): 1–10. http://dx.doi.org/10.1155/2021/6676998.

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Exposure to carbon tetrachloride (CCl4) induces acute and chronic liver injuries as well as oxidative stress in rats. The present study was designed to evaluate the in vivo toxicity of rosmarinic acid-rich extract from Ocimum basilicum (RAE). The acute and subchronic oral toxicity of RAE was evaluated in Albinos mice. Hepatotoxicity was induced by the administration of CCl4-induced hepatic injury in rats. The hepatoprotective effect of RAE on aspartate aminotransferase, alanine transaminase, alkaline phosphatase, lactate dehydrogenase, bilirubin, total protein, albumin, triglycerides, total ch
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Jadeja, Ravirajsinh N., Menaka C. Thounaojam, Ansarullah, et al. "Toxicological evaluation and hepatoprotective potential of Clerodendron glandulosum.Coleb leaf extract." Human & Experimental Toxicology 30, no. 1 (2010): 63–70. http://dx.doi.org/10.1177/0960327110368420.

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This inventory evaluates toxicological effects and hepatoprotective potential of Clerodendron glandulosum.Coleb (CG) aqueous extract. Acute and subchronic toxicity tests were performed using Swiss albino mice as per the guideline of Organisation for Economic Cooperation and Development (OECD). Also, hepatoprotective potential of CG extract was examined in experimental model of carbon tetrachloride (CCl 4)-induced hepatotoxicity. Acute and subchronic toxicity tests revealed that CG extract is non-toxic and its median lethal dose (LD50) value is >5000 mg/kg bodyweight. Also, rats pretreated w
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Roomi, MW, T. Kalinovsky, NW Roomi, V. Ivanov, M. Rath, and A. Niedzwiecki. "A nutrient mixture suppresses carbon tetrachloride–induced acute hepatic toxicity in ICR mice." Human & Experimental Toxicology 27, no. 7 (2008): 559–66. http://dx.doi.org/10.1177/0960327108096851.

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We examined the effect of a nutrient mixture (NM) that contains lysine, proline, ascorbic acid, and green tea extract in mice treated with carbon tetrachloride (CCl4), a model of liver injury in which free radical, oxidative stress, and cytokine production are closely linked. Seven-week-old male Imprinting Control Region (ICR) mice were divided into four groups (A–D) of five animals each. Groups A and C mice were fed a regular diet for 2 weeks, whereas groups B and D mice were supplemented with 0.5% NM (w/w) during that period. Groups A and B received corn oil i.p., whereas groups C and D rece
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Alzahrani, Sabah Ali, Gamal M. Bekhet, Rebai Ben Ammar, et al. "The Inhibitory Effect of Geraniol on CCL4-induced Hepatorenal Toxicity in Pregnant Mice through the PI3K/AKT Signaling Pathway." Saudi Journal of Medicine & Medical Sciences 12, no. 1 (2024): 17–26. http://dx.doi.org/10.4103/sjmms.sjmms_225_23.

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Abstract Background: Hepatotoxicity caused by CCL4 is well known. Geraniol (GNL) has high antioxidant effect that can induces liver regeneration. However, the protective effect of GNL effect on CCL4-induced hepatorenal toxicity in pregnant mice has not yet been studied. Objective: To investigate whether GNL could protect against oxidative stress induced by CCL4 via the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway, which is regulated by phosphatidylinositol 3 kinase/protein kinase B (PI3K/AKT), and has been found to have protective effects on renal and hepatic tissues. Materials a
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A. Aziz, Tavga, Zheen A. Ahmed, Kasim M. Juma'a, Munaf H. Abdulrazzaq, Saad A. Hussain, and Saad A. Hussain. "Study of the Protective Effects of Benfotiamine Against CCl4-Induced Hepatotoxicity in Rats." Iraqi Journal of Pharmaceutical Sciences ( P-ISSN: 1683 - 3597 , E-ISSN : 2521 - 3512) 18, Suppl. (2017): 47–53. http://dx.doi.org/10.31351/vol18isssuppl.pp47-53.

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Liver is considered as the first target for the toxic effects of toxins and other xenobiotics, and this can be attributed to its role as a site which receive all absorbed xenobiotics from the gastrointestinal tract and its role as a major site for biotransformation of xenobiotics. The present study was designed to evaluate the possible hepatoprotective effect of benfotiamine against CCl4-induced hepatotoxicity in rats. The study was conducted on 48 male albino rats; the animals were allocated into 8 groups (6 rats in each group) and treated as follow: 4 groups treated with oral doses of either
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Bellassoued, Khaled, Ferdaws Ghrab, Houda Hamed, et al. "Protective effect of essential oil of Cinnamomum verum bark on hepatic and renal toxicity induced by carbon tetrachloride in rats." Applied Physiology, Nutrition, and Metabolism 44, no. 6 (2019): 606–18. http://dx.doi.org/10.1139/apnm-2018-0246.

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The inner bark of cinnamon (Cinnamomum verum) is widely used as a spice. Cinnamon plants are also a valuable source of essential oil used for medicinal purposes. The present study aimed to investigate the composition and in vitro antioxidant activity of essential oil of C. verum bark (CvEO) and its protective effects in vivo on CCl4-induced hepatic and renal toxicity in rats. Groups of animals were pretreated for 7 days with CvEO (70 or 100 mg/kg body weight) or received no treatment and on day 7 a single dose of CCl4 was used to induce oxidative stress. Twenty-four hours after CCl4 administra
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Ebaid, Hossam, Jameel Al-Tamimi, Iftekhar Hassan, et al. "Effect of Selenium Nanoparticles on Carbon Tetrachloride-Induced Hepatotoxicity in the Swiss Albino Rats." Applied Sciences 11, no. 7 (2021): 3044. http://dx.doi.org/10.3390/app11073044.

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Background: This study investigated selenium nanoparticles’ protective effects (SE-NPs) against carbon tetrachloride (CCl4)-induced hepatic injury in rats. Methods: Rats were divided into four groups (n = 8). Group 1 rats received the vehicle solution only. Group 2 received a single intraperitoneal injection of 1 mL/kg CCl4 in liquid paraffin (1:1 v/v). Group 3 was treated with SE-NPs (2.5 mg/kg) twice a week for three weeks before receiving CCl4 challenge. Oxidative stress, liver function, liver histopathology and serum lipid levels were evaluated. Results: Plasma concentrations of aspartate
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Dissertations / Theses on the topic "Hepatic Toxicity and CCl4"

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Wild, Stacie Lynn. "Pyrrolizidine alkaloids: Hepatic metabolism and extrahepatic toxicity." Diss., The University of Arizona, 1994. http://hdl.handle.net/10150/186599.

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Pyrrolizidine alkaloids are proposed to be metabolized in the liver to reactive pyrrole species, or dehydroalkaloids. These reactive pyrroles are hypothesized to be responsible for pyrrolizidine alkaloid toxicity. This dissertation research has established that dehydroalkaloids are, in fact, metabolites of pyrrolizidine alkaloids. It was first determined that dehydromonocrotaline is produced during hepatic microsomal metabolism of monocrotaline and that it has the ability to bind in vitro with a synthetic thiol-containing resin, Thiopropyl Sepharose 6B. Similarly, synthetic dehydromonocrotalin
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Powell, Christine Louise Rusyn Ivan. "Improving linkage of hepatic toxicity and pathology endpoints with toxicogenomics." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2007. http://dc.lib.unc.edu/u?/etd,997.

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Thesis (Ph. D.)--University of North Carolina at Chapel Hill, 2007.<br>Title from electronic title page (viewed Dec. 18, 2007). "... in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Curriculum in Toxicology." Discipline: Toxicology; Department/School: Medicine.
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Weyers, Carli. "Evaluating metabolism-induced toxicity using a non-hepatic cell line." Thesis, Rhodes University, 2018. http://hdl.handle.net/10962/61950.

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Sauer, John-Michael. "All- trans-retinol modulation of chemically-induced pulmonary and hepatic toxicity." Diss., The University of Arizona, 1996. http://hdl.handle.net/10150/187501.

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It has been previously reported that acute hypervitaminosis A in rats dramatically increases the hepatotoxicity of a number of chemicals. This potentiation appears to be mediated by the enhanced release of reactive oxygen species from retinol-primed Kupffer cells. However, in the lung it has been shown that retinol can protect against many of the inflammatory effects caused by bleomycin. Whether or not retinol pretreatment can modulate chemical-induced injury of compounds that cause both liver and lung toxicity is unknown. Therefore, the studies presented here were designed to test the hypothe
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Scott, Maya Millicent. "Canine hepatic slices as a model for studying drug toxicity and metabolism." Diss., Texas A&M University, 2005. http://hdl.handle.net/1969.1/3731.

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Tissue slices can be made from organs, such as liver, kidney, brain, and heart, and from various species including humans, dogs, non-human primates, rats and mice. It has been demonstrated that human and rat liver slices are viable for up to 2 days, and liver slices have been extensively used as an in vitro method to study hepatic drug metabolism and toxicity in humans. The objective of this study was to determine the utility of canine hepatic slices as an in vitro model for studying drug metabolism and hepatotoxicity in dogs. Canine hepatic slices were incubated in media containing various dr
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de, Barros Pereira I. M. "Investigation of biomarkers of hepatic and renal toxicity in the Han Wistar rat." Thesis, University College London (University of London), 2014. http://discovery.ucl.ac.uk/1435551/.

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The aim of this project was to identify urinary markers of hepatic and renal toxicity in the male Hanover-Wistar rat; acute and chronic injury models were developed by administration of CCl4. Nephrotoxicity was induced by administration of HCBD. In an acute dose study, CCl4-induced nephrotoxicity occurred above 2.0 mL/kg CCl4. To avoid kidney injury, 2.0 mL/kg CCl4 was chosen as the optimal dose. 1H NMR revealed many changes to the urinary metabolome following CCl4-induced liver injury including an increase in the resonances of taurine, creatine and formate and a decrease in hippurate and crea
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Celliere, Géraldine. "Multi-scale modeling of hepatic drug toxicity and its consequences on ammonia detoxification." Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCC100.

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La détoxification de l'ammoniaque est une fonction clé du foie. Récemment, il a été montré que les réactions communément admises dans ce processus étaient insuffisantes pour comprendre toutes les données expérimentales. Nous avons donc développé des explications possibles sous forme de modèles compartimentaux. Grâce à des procédures statistiques, les modèles ont été évalués et comparés. Il est apparu que l'enzyme glutamate déshydrogénase a une importance capitale dans la détoxification de l'ammoniaque. Lorsque l'on modélise des tissues, le choix de la représentation de l'espace peut influencer
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Mesić, Ana. "Space of Disse on Chip Model for Study of Hepatic Toxicity and Inflammation." Electronic Thesis or Diss., université Paris-Saclay, 2025. http://www.theses.fr/2025UPAST044.

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Cette thèse de doctorat s'inscrit dans le cadre du projet ANR DILI on Chip, qui vise à développer un modèle hépatique in vitro sur une puce microfluidique afin d'étudier les lésions hépatiques induites par les médica-ments (Drug-Induced Liver Injury, DILI).Le développement actuel des médicaments repose sur des modèles obsolètes, tels que les cultures cellulaires 2D et les tests in vivo, qui sont coûteux, inefficaces et incapables de prédire avec précision la toxicité hépa-tique. La technologie des organes-sur-puce basée sur la microfluidique constitue une alternative plus précise et dynamique,
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Geenen, Suzanne Aleida Birgitta. "Systems biology approach to understanding hepatic glutathione metabolism and its biomarkers of depletion." Thesis, University of Manchester, 2013. https://www.research.manchester.ac.uk/portal/en/theses/systems-biology-approach-to-understanding-hepatic-glutathione-metabolism-and-its-biomarkers-of-depletion(760cb481-d46b-494b-8aba-e8759aec025a).html.

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Drug induced liver injury is a leading cause of human illness and a major cause of drug withdrawals from the market. A systems biology approach has the potential to aid toxicology research since toxicological responses are a consequence of multiple non-linear and interdependent biological responses. Here such an approach is developed.The glutathione pathway is a key hepatic defence mechanism and deactivates reactive metabolites before they have the chance to damage cellular proteins. However, glutathione availability is limited and can vary between individuals. As hepatic glutathione levels ca
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Cardoso, Elsa Maria Pereira. "Lymphocytes in the liver and hepatic iron toxicity : human and animal models of iron overload." Doctoral thesis, Porto : Edição do Autor, 2000. http://hdl.handle.net/10216/64561.

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Books on the topic "Hepatic Toxicity and CCl4"

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Felipo, Vicente, and Santiago Grisolia, eds. Hepatic Encephalopathy, Hyperammonemia, and Ammonia Toxicity. Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-1989-8.

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Grisolía, Santiago, Vicente Felipo, and María-Dolores Miñana, eds. Cirrhosis, Hepatic Encephalopathy, and Ammonium Toxicity. Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5826-8.

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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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Vicente, Felipo, and Grisolía Santiago 1923-, eds. Hepatic encephalopathy, hyperammonemia, and ammonia toxicity. Plenum Press, 1994.

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Redegeld, Franciscus Antonius Maria. Hepatic and renal toxicity of xenobiotics: The role of metabolism and transport. s.n.], 1989.

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Felipo, Vicente, Santiago Grisolía, and Maria-Dolores Miñana. Cirrhosis, Hepatic Encephalopathy, and Ammonium Toxicity. Springer London, Limited, 2013.

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Hepatic Encephalopathy, Hyperammonemia, and Ammonia Toxicity. Island Press, 1995.

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Felipo, Vicente, and Santiago Grisolía. Hepatic Encephalopathy, Hyperammonemia, and Ammonia Toxicity. Springer London, Limited, 2012.

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Felipo, Vicente, and Santiago Grisolía. Hepatic Encephalopathy, Hyperammonemia, and Ammonia Toxicity. Springer, 2012.

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Felipo, Vicente, Santiago Grisolía, and Maria-Dolores Miñana. Cirrhosis, Hepatic Encephalopathy, and Ammonium Toxicity. Springer, 2012.

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Book chapters on the topic "Hepatic Toxicity and CCl4"

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Xu, Jinghai James, and Keith Hoffmaster. "Hepatic Toxicity." In ADMET for Medicinal Chemists. John Wiley & Sons, Inc., 2010. http://dx.doi.org/10.1002/9780470915110.ch8.

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Rainsford, K. D. "Hepatic Toxicity." In Ibuprofen: Pharmacology, Therapeutics and Side Effects. Springer Basel, 2012. http://dx.doi.org/10.1007/978-3-0348-0496-7_10.

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Thurman, Ronald G., Frederick C. Kauffman, and Jeffrey Baron. "Biotransformation and Zonal Toxicity." In Regulation of Hepatic Metabolism. Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5041-5_13.

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Cooper, Arthur J. L., James C. K. Lai, and Alan S. Gelbard. "Ammonia in Liver and Extrahepatic Tissues: An Overview of Metabolism and Toxicity in Mammals." In Hepatic Encephalopathy. Humana Press, 1989. http://dx.doi.org/10.1007/978-1-4612-4506-3_2.

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Dancygier, Henryk, and Christian P. Strassburg. "Hepatic Drug Metabolism and Drug Toxicity." In Clinical Hepatology. Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-04519-6_38.

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Coe, John E., Kamal G. Ishak, and M. J. Ross. "Hepatic Toxicity of Estrogen in Armenian and Chinese Hamsters." In Hormonal Carcinogenesis III. Springer New York, 2001. http://dx.doi.org/10.1007/978-1-4612-2092-3_52.

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Viña, Juan R., Federico V. Pallardo, Tadayasu Furukawa, and Jose Viña. "Oral glutathione increases hepatic glutathione and prevents acetaminophen toxicity." In Amino Acids. Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-011-2262-7_87.

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Felipo, Vicente, Eugenio Grau, Maria-Dolores Miñana, and Santiago Grisolia. "Activation of NMDA Receptor Mediates the Toxicity of Ammonia and the Effects of Ammonia on the Microtubule-Associated Protein MAP-2." In Cirrhosis, Hyperammonemia, and Hepatic Encephalopathy. Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2484-7_8.

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Pan, Guoyu. "Roles of Hepatic Drug Transporters in Drug Disposition and Liver Toxicity." In Advances in Experimental Medicine and Biology. Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-7647-4_6.

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Tharwat, Alaa, Thomas Gabel, and Aboul Ella Hassanien. "Classification of Toxicity Effects of Biotransformed Hepatic Drugs Using Optimized Support Vector Machine." In Proceedings of the International Conference on Advanced Intelligent Systems and Informatics 2017. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-64861-3_15.

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Conference papers on the topic "Hepatic Toxicity and CCl4"

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Fatima, S., N. Sheikh, and A. Tayyeb. "Investigation of hepatic and renal toxicity induced by omeprazole in CCl4 injury mouse model." In 35. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0038-1677070.

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Jung, YS, J. Albin, YH Kim та ін. "Orphan nuclear receptor ERRg regulates hepatic TGF-β2 expression and fibrogenic response in CCl4-induced acute liver injury". У Viszeralmedizin 2021 Gemeinsame Jahrestagung Deutsche Gesellschaft für Gastroenterologie, Verdauungs- und Stoffwechselkrankheiten (DGVS), Sektion Endoskopie der DGVS, Deutsche Gesellschaft für Allgemein und Viszeralchirurgie (DGAV). Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1733620.

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Jung, YS, J. Albin, YH Kim та ін. "Orphan nuclear receptor ERRg regulates hepatic TGF-β2 expression and fibrogenic response in CCl4-induced acute liver injury". У Viszeralmedizin 2021 Gemeinsame Jahrestagung Deutsche Gesellschaft für Gastroenterologie, Verdauungs- und Stoffwechselkrankheiten (DGVS), Sektion Endoskopie der DGVS, Deutsche Gesellschaft für Allgemein und Viszeralchirurgie (DGAV). Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1733620.

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Zhao Yong-Mei, Chen Ai-Xia, and Du Xi-Chun. "Effects of the battery liquid on chromosomal aberration, Hepatic and Nephric toxicity in Mice." In 2011 International Symposium on Water Resource and Environmental Protection (ISWREP). IEEE, 2011. http://dx.doi.org/10.1109/iswrep.2011.5893487.

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Malia, R. G., H. J. Kennedy, D. R. Triger, and F. E. Preston. "PROTECTIVE EFFECT OF VITAMIN K AGAINST ACETAMINOPHEN (PARACETAMOL) TOXICITY IN THE HAMSTER." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644341.

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We have previously reported that paracetamol may interfere with the metabolism of vitamin K via the vitamin K 2, 3-epoxide cycle. (Thrombosis and Haemostasis, 54,205,1985). In this study we have examined the effects of large doses of vitamin K on experimentally induced paracetamol hepatic necrosis in a hamster model. Paracetamol (1.2g/Kg) when given by gavage to 24 hamsters (Group I) resulted in 10 deaths (42%) at 24 hours. Simultaneous administration of lmg vitamin K intraperitoneally (Group II) reduced mortality to 3/24 (12%); mortality was 2/24 (8%) if vitamin K was given 4 hours after the
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Harvey, Shalon L., Jessica L. Beers, and Klarissa D. Jackson. "Evaluation of the Time- and Dose-Dependent Toxicity of Sunitinib Using a 3-D Human Hepatic Spheroid Model." In ASPET 2023 Annual Meeting Abstracts. American Society for Pharmacology and Experimental Therapeutics, 2023. http://dx.doi.org/10.1124/jpet.122.241590.

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Parisi, S., M. C. Ditto, M. Scarati, M. Priora, and F. Enrico. "AB0499 Evaluation of the effectiveness of metaxodine in the hepatic toxicity due to methotrexate in patients with rheumatoid arthritis." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.6253.

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"Hepatoprotective Effect of Typhonium flagelliforme against Thioacetamide Induced Liver Cirrhosis in Rats." In 4th International Conference on Biological & Health Sciences (CIC-BIOHS’2022). Cihan University, 2022. http://dx.doi.org/10.24086/biohs2022/paper.643.

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Typhonium flagelliforme (T. flagelliforme) was utilized in outdated medication for handling numerous syndromes. This study aimed to investigate hepatoprotection effects of T. flagelliforme against thioacetamide (TAA) hepatotoxicity in rodents.Thirty rodents arbitrarily separated five clusters. Collection 1 was intraperitoneally injected distilled water thrice /week and fed (p.o) daily with 10% Tween 20 to eight weeks. Collection 2-5 i.p. injected with 200 mg/kg TAA three times thrice per week for 8 weeks and fed 10% Tween 20, 50 mg/kg silymarin, 250 and 500 mg/kg of T. flagelliforme extract da
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Al-dosari, Aldana, Nadin Younes, and Gheyath Nasrallah. "Ecotoxicological assessment of two surfactant on the emryonic development." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2021. http://dx.doi.org/10.29117/quarfe.2021.0149.

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In this study, zebrafish (Danio rerio) embryos was served as a model for marine fauna to determine if there is any potential of organ-specific toxicity (neuromuscular, hepatic, cytotoxic, and cardiac) caused by Silicone-Q-22 and Ploy-Q-47. as both surfactants are considered eco-friendly corrosion inhibitors. The calculated LC50 of Silicon-Q-22 and Poly-Q-47 was 22.36 and 8.28 mg/L, respectively. At NOEC both surfactants had resulted in teratogenic defects and cardiotoxicity, but only poly Q-47 resulted in neurotoxicity.
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Goldstein, J., G. Singh, J. Fort, and A. Bello. "SAT0092 Success-1 in osteoarthritis (oa) trial: celecoxib demonstrates significantly lower hepatic toxicity than diclofenac in the treatment of osteoarthritis." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.467.

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Reports on the topic "Hepatic Toxicity and CCl4"

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Lawanprasert, Somsong, Chaiyo Chaichantipyuth, Supatra Srichairat, Nuansri Niwattisaiwong, and Laddawal Phivthong-ngam. Subchronic exposure of Pueraria mirifica in normal - and high cholesterol diet fed rats : influence on hepatic cytochrome P450, lipid profile and toxicity. Chulalongkorn University, 2004. https://doi.org/10.58837/chula.res.2004.28.

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Pueraria mirifica airy shaw and suvatabandhu, know locally as Kwao Keur, is a plant in family Leguminosae. In this study, effects of P.mirifica on hepatic cytochrome P450 (CYP), serum lipid profile and subchronic toxicity were investigated in male Wistar rats. Rats were randomly divided into four treatment groups as following: normal diet-fed group; normal diet-fed supplemented with P.mirifica group; high cholesterol diet-fed group; high cholesterol diet-fed supplemented with P.mirifica group. Each group comprised 10 rats. P.mirifica was administered orally at a dosage of 100 mg/kg/day for 90
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