Relevant bibliographies by topics / Acetaminophen Toxicology

Academic literature on the topic 'Acetaminophen Toxicology'

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Published: 4 June 2021
Last updated: 29 January 2023

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Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters

Journal articles on the topic "Acetaminophen Toxicology":

1

David Josephy, P. "The Molecular Toxicology of Acetaminophen." Drug Metabolism Reviews 37, no. 4 (January 2005): 581–94. http://dx.doi.org/10.1080/03602530500205200.

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Nabavi, Nima, Mohammad Moshiri, Shahrad Tajoddini, and Bita Dadpour. "A Basis for the Decision to Rule in or out Acetaminophen Toxicity: Assessment of the Serum Level Within 4 Hours Post Overdose." Iranian Journal of Toxicology 15, no. 4 (October 1, 2021): 265–70. http://dx.doi.org/10.32598/ijt.15.4.820.1.

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Background: Acetaminophen is a popular antipyretic and analgesic medication worldwide; however, its therapeutic window is narrow, which may lead to overdose or toxicity. This study was conducted to assess the correlation between the serum acetaminophen levels before and 4 hours after the acute toxicity with this drug. The objective of this study was to test the validity of the serum level to arrive at a clinical decision on the toxicity with acetaminophen. Methods: This cross-sectional study was performed on patients hospitalized and treated with a diagnosis of acute acetaminophen overdose during one year (Sept. 2018 to Sept. 2019) at the Toxicology Department of Imam Reza Hospital, Mashhad, Iran. Patients were analyzed for demographics, time of ingestion, their first and second serum acetaminophen concentrations. Results: A total of 204 patients (106 male & 98 female) were included in this study. The average dose of acetaminophen ingestion by these patients was 14.5±3.50 g and all patients were treated successfully with N-Acetyl-Cysteine (NAC). The variables of age (P=0.293), serum acetaminophen levels at 1-2 h (P=0.679), and at 2-3 h (P=0.126) did not have significant relationships with the serum acetaminophen level on the fourth hour. However, the serum acetaminophen levels tested between 3-4 h and acetaminophen intoxication dosage had significant relationships with the acetaminophen level on the fourth hour. Conclusion: In patients with acute acetaminophen toxicity, the data on the serum levels obtained before a 4-hour timepoint from the ingestion were not useful to decide on the need for the rescue treatment with N-acetyl-cysteine.
3

Stern, Stephan T., Mary K. Bruno, Gayle E. Hennig, Robert A. Horton, Jeanette C. Roberts, and Steven D. Cohen. "Contribution of acetaminophen-cysteine to acetaminophen nephrotoxicity in CD-1 mice: I. Enhancement of acetaminophen nephrotoxicity by acetaminophen-cysteine." Toxicology and Applied Pharmacology 202, no. 2 (January 2005): 151–59. http://dx.doi.org/10.1016/j.taap.2004.06.030.

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Bentur, Yedidia, Yael Lurie, Ada Tamir, Daniel C. Keyes, and Fuad Basis. "Reliability of history of acetaminophen ingestion in intentional drug overdose patients." Human & Experimental Toxicology 30, no. 1 (March 30, 2010): 44–50. http://dx.doi.org/10.1177/0960327110366784.

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The objective of this study was to determine the reliability of denial of acetaminophen ingestion in intentional drug overdose patients. All intentional drug overdose patients admitted to an emergency department who were able to provide a history were included. A detailed history was obtained on names, timing and number of medications ingested, and serum acetaminophen was assayed. Multidrug ingestion was defined as the reporting of ≥2 medications. Patients were considered ‘reliable’ if they reported acetaminophen ingestion and had detectable acetaminophen levels or the other way around. Validity parameters of acetaminophen history were assessed by sensitivity, specificity and positive and negative predictive values. A total of 154 patients were included. History was significantly more reliable in patients who denied ingestion of acetaminophen (n = 107) compared with patients who reported it (n = 47; 95.3% vs 65.9%, respectively; p < 0.0001, 95% CI of the difference 17.5%—41.2%). No suicidal patient who denied both acetaminophen and multidrug ingestions had a detectable acetaminophen level (negative predictive value 1, 95% CI 0.93—1.0). It is suggested that denial of both acetaminophen and multidrug ingestions by intentional drug overdose patients after a thorough history taking can be considered reliable for acetaminophen history. In facilities with limited resources, these patients may not require routine acetaminophen screening.
5

Hodell, M., P. D'Eon, R. Hessler, S. Inbar, A. Leck, U. Patel, and G. Whiteley. "143 TOXICOLOGY PANEL FOR ETHANOL, SALICYLATE, and ACETAMINOPHEN." Therapeutic Drug Monitoring 19, no. 5 (October 1997): 583. http://dx.doi.org/10.1097/00007691-199710000-00153.

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Gussow, Leon. "Toxicology Rounds: A New Development in Acetaminophen Toxicity." Emergency Medicine News 33, no. 4 (April 2011): 10. http://dx.doi.org/10.1097/01.eem.0000396895.17374.a6.

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Mofenson, H. C., T. R. Caraccio, H. Nawaz, and G. Steckler. "Acetaminophen Induced Pancreatitis." Journal of Toxicology: Clinical Toxicology 29, no. 2 (January 1991): 223–30. http://dx.doi.org/10.3109/15563659109038615.

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Karadas, S., M. Aslan, H. Gonullu, C. Kati, L. Duran, S. Olmez, ME Kucukoglu, and H. Demir. "Acetaminophen intoxication is associated with decreased serum paraoxonase and arylesterase activities and increased lipid hydroperoxide levels." Human & Experimental Toxicology 33, no. 11 (February 5, 2014): 1134–40. http://dx.doi.org/10.1177/0960327113511477.

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Background: Acetaminophen is at present one of the most commonly used analgesics and antipyretics. Recent evidence has suggested that oxidative stress is involved in the mechanism of acetaminophen intoxication. Paraoxonase-1 (PON1) plays an important role as an endogenous free-radical scavenging molecule. The aim of this study was to evaluate the influence of serum PON1 activity and oxidative stress in patients with acetaminophen intoxication. Methods: A total of 20 patients with acetaminophen intoxication and 25 healthy controls were enrolled. Serum total antioxidant capacity (TAC), lipid hydroperoxide (LOOH) levels, and paraoxonase and arylesterase activities were measured spectrophotometrically. Results: The serum TAC levels and the paraoxonase and arylesterase activities were significantly lower in patients with acetaminophen intoxication compared with controls (all, p < 0.001), while the serum LOOH levels were significantly higher ( p < 0.001). Conclusions: Our results suggest that decreased PON1 activity seems to be associated with increased oxidative stress in patients with acetaminophen intoxication. Measuring serum PON1 activity may be useful in assessing the development of toxicity risk in acetaminophen toxicity. It would be useful to recommend vitamins with antioxidant effects such as vitamins C and E along with medical treatments.
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Rousar, Tomas, Erika Nydlova, Otto Kucera, Petr Cesla, Martina Vrbova, and Zuzana Cervinkova. "Acetaminophen–glutathione conjugate: A possible role in acetaminophen toxicity." Toxicology Letters 221 (August 2013): S88. http://dx.doi.org/10.1016/j.toxlet.2013.05.109.

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Chandrasekaran, Victor Raj Mohan, Se-Ping Chien, Dur-Zong Hsu, and Ming-Yie Liu. "Anti-hepatotoxic effects of 3,4-methylenedioxyphenol and N-acetylcysteine in acutely acetaminophen-overdosed mice." Human & Experimental Toxicology 30, no. 10 (January 14, 2011): 1609–15. http://dx.doi.org/10.1177/0960327110394226.

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3,4-Methylenedioxyphenol (sesamol) is effective against acetaminophen-induced liver injury in rats. Whether sesamol’s anti-hepatotoxic effect is comparable to that of N-acetylcysteine has never been studied. We investigated the anti-hepatotoxic effects of sesamol and N-acetylcysteine on acetaminophen-induced hepatotoxicity in mice. Equimolar doses (1 mmol/kg) of sesamol and N-acetylcysteine significantly inhibited acetaminophen (300 mg/kg)-increased serum aspartate transaminase and alanine transaminase levels 6 h post-administration. Sesamol and N-acetylcysteine maintained hepatic glutathione levels and inhibited lipid peroxidation. Moreover, the combination of sesamol and N-acetylcysteine antagonistically inhibited sesamol’s protection against acetaminophen-induced liver injury. We conclude that the protective effect of sesamol against acetaminophen-induced liver damage is comparable to that of N-acetylcysteine by maintaining glutathione levels and inhibiting lipid peroxidation in mice.
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Journal articles

Dissertations / Theses on the topic "Acetaminophen Toxicology":

1

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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Haire, Kambria. "Elucidation of the Role of Poly(ADP-Ribose) Polymerase in Drug-Induced Toxicity." Scholar Commons, 2015. http://scholarcommons.usf.edu/etd/5959.

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Drug toxicity may cause liver injury, resulting in damage to cells and tissues. This damage can lead to cytotoxic events that may result in an activation of poly (ADP-ribose) polymerase (PARP). A study was conducted to determine if cocaine and acetaminophen toxicity lead to DNA damage and to the activation of the repair protein, PARP in the liver using the hepatotoxicants: cocaine and acetaminophen (APAP). A dose-response analysis for cocaine concluded that a dose as low as 20 mg/kg resulted in elevated ALT levels. A higher dose of 60 mg/kg was tested for analyses but resulted in severe hemorrhaging. The dose-response analyses for APAP resulted in no elevated liver enzyme levels for a 75 mg/kg and 150 mg/kg dose. A dose of 50 mg/kg for cocaine, and a dose of 300 mg/kg for APAP were used to analyze temporal trends for both toxicants. Both cocaine and APAP produced incremental increases in ALT at the 2 hour, 6 hour, 18 hour, and 24 hour time points, respectively. PARP activity analysis for cocaine measured the highest activity at the 2hr and 6hr time points. PARP analysis for acetaminophen measured gradual increases until the 18 hour time point where the highest level of PARP activity was measured. A PARP inhibition analysis was conducted with cocaine and (APAP) to understand the impact of a PARP inhibitor, 1,5-dihydroxyisoquinoline (DIQ), on PARP activity in the liver. A 50 mg/kg dose of cocaine or a 300 mg/kg dose of APAP was administered, followed by a 10 mg/kg dose of DIQ at 1) the time of initial toxicant dose (0 hour), or 2) 1 hour after initial toxicant dose (1hr). The PARP inhibition analysis for cocaine and APAP was conducted at 6 and 18 hours post initial dose, respectively, when the highest levels of PARP were observed. Inhibition analyses determined that ALT declined significantly when DIQ was administered immediately following the initial toxicant dose for both toxicants. DIQ administered 1 hr after initial toxicant dose resulted in slightly higher ALT than the 0 hr time point. Decreases in PARP activity were observed at the 0 hr time point, with slightly higher PARP levels observed at the 1 hr time point. Decreased PARP activity was observed following DIQ treatment with both, a concurrent drug treatment and treatment following drug administration. Cocaine and APAP treatment did not cause DNA fragmentation. A liver glutathione (GSH) analysis conducted for cocaine and APAP did not correlate with DIQ alteration of PARP activity. The mechanism of DIQ effects on drug-induced hepatotoxicity appears to be GSH independent. DIQ was effective in reducing drug-induced hepatotoxicity and preserving organ function.
3

Benitex, Yulianingsih. "The effects of phenetyl isothiocyanate and benzyl isothiocyanate on acetaminophen metabolism and toxicity in freshly isolated rat hepatocytes in cell suspension /." View abstract, 1999. http://library.ctstateu.edu/ccsu%5Ftheses/1563.html.

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Thesis (M.S.)--Central Connecticut State University, 1999.
Thesis advisor: Carol A. Jones. " ... in partial fulfillment of the requirements for the degree of Master of Science in Chemistry." Includes bibliographical references (leaves 42-51).
4

Abdulkareem, Mohammed Hasan. "The Interaction Between Dichloroacetate, Trichloroacetate and Acetaminophen: Effects on Oxidative Stress Induction in AML 12 Cells." University of Toledo Health Science Campus / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=mco1469703005.

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Woods, Sally. "Comparison of metformin, rosiglitazone, and acetaminophen in the prevention of olanzapine toxicity in mice." University of Cincinnati / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1305892985.

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Ward, Jeanine. "MicroRNA Markers of Acetaminophen Toxicity: A Master's Thesis." eScholarship@UMMS, 2012. https://escholarship.umassmed.edu/gsbs_diss/625.

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Background To investigate plasma microRNA (miRNA) profiles indicative of hepatotoxicity in the setting of lethal acetaminophen (APAP) toxicity in mice. Methods Using plasma from APAP poisoned mice, either lethally (500 mg/kg) or sublethally (150 mg/kg) dosed, we screened commercially available murine microRNA libraries (SABiosciences, Qiagen Sciences, MD) to evaluate for unique miRNA profiles between these two dosing parameters. Results We distinguished numerous, unique plasma miRNAs both up- and down-regulated in lethally compared to sublethally dosed mice. Of note, many of the greatest up- and down-regulated miRNAs, included, but were not limited to, 574-5p, 466g, 466f-3p, 375, 29c, and 148a. There was a statistically significant increase in alanine aminotransferase levels in the lethal compared to sublethal APAP dosing groups at the 12 h time point ( P < 0.001). There was 90% mortality in the lethally compared to sublethally dosed mice at the 48 h time point ( P = 0.011). Conclusion We identified unique plasma miRNAs both up- and down-regulated in lethally dosed APAP poisoned mice.
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Nicholls-Grzemski, Felicity April. "The effect of short-term pretreatment with peroxisome proliferators on the acute toxicity of various toxicants, including paracetamol /." Title page, table of contents and abstract only, 1998. http://web4.library.adelaide.edu.au/theses/09PH/09phn6158.pdf.

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Adeleye, Adeola Patience. "Perfluorinated compounds, bishenol a and acetaminophen in selected waste water treatment plants in and around Cape Town, South Africa." Thesis, Cape Peninsula University of Technology, 2016. http://hdl.handle.net/20.500.11838/2331.

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Thesis (MTech (Chemistry))--Cape Peninsula University of Technology, 2016.
The release of wastewater to the aquatic environment is most likely to introduce some trace levels of organic contaminants, some of which may be toxic, carcinogenic, or endocrine disruptors, as well as, persistent in the environment. Additionally, increasing contamination of surface waters by wastewater effluents has made water treatment processes more challenging and expensive. The presence of these pollutants in the receiving water body may have negative effects on aquatic species and often pose potential human health risks through the reuse of treated wastewater for drinking purposes and other household use. In countries like South Africa, Namibia, USA, Singapore and Australia, water agencies are intensifying wastewater reclamation/wastewater reuse as part of their water resource agenda: in order to meet the demands of the growing populations. Nowadays, water reuse is generally considered as a viable method of water supply management. This study focused on the identification of the occurrence, quantification of emerging contaminants and evaluation of removal efficiency in wastewater treatment processes of three classes of emerging contaminants (ECs) in wastewater: 1) six types of perfluorinated compounds (PFCs), namely; perfluorooctanoic acid (PFOA), Perfluorooctane sulphonate (PFOS), perfluoroheptanoic acid (PFHpA), perfluorononanoic acid (PFNA), perfluorodecanoic acid (PFDA), and perfluoroundecanoic acid (PFUDA); 2) bisphenol A (BPA); and 3) Acetaminophen (ACP). These contaminants were identified and quantified in four wastewater treatment plants in the Western Cape. These treatment plants include three WWTPs in Cape Town, namely: Bellville WWTP, Scottsdene WWTP and Zandvliet WWTP and one WWTP in the central Karoo (Beaufort West wastewater reclamation plant).
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Minsart, Charlotte. "Involvement of High Mobility Group Box 1 protein in acetaminophen-induced liver injury: dissection of signaling pathways and potential therapeutic targeting." Doctoral thesis, Universite Libre de Bruxelles, 2021. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/319459.

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L’overdose au paracétamol est l’une des intoxications médicamenteuses la plus fréquente au monde, caractérisée par une atteinte hépatique dont l’issue peut être fatale. Les études réalisées sur ce phénomène ont montré que la phase initiale de la toxicité est induite par le métabolite actif du paracétamol, le N-acétyl-p-benzoquinone imine (NAPQI). Ce dernier, en l’absence de quantité suffisante de glutathion, s’accumulent dans la cellule et finit par se lier à d’autres protéines, principalement mitochondriales, formant alors des adduits. Cette liaison va altérer la fonction primaire des protéines et conduire, en cas d’overdose sévère, à la mort des hépatocytes. La mort cellulaire s’accompagne alors de la libération de composants cellulaire dont le rôle sera d’alerter le système immunitaire des lésions tissulaires. Ces composants prennent alors le nom d’«alarmines» ou de « damage-associated molecular patterns » (DAMPs). La protéine HMGB1 (High Mobility Group Box 1) fait partie de cette catégorie.Au cours de cette thèse nous nous sommes intéressés de plus près à la protéine HMGB1, à son origine ainsi qu’à son rôle dans l’amplification et la propagation des lésions hépatiques initialement induites par l’overdose au paracétamol. Nos travaux se sont d’abord portés sur l’étude de la protéine HMGB1 dans un modèle murin d’hépatite au paracétamol. Nos expériences nous permettent, d’une part, de confirmer que la libération d’HMGB1 est liée à la sévérité des lésions hépatiques et d’autre part, de démontrer que l’amplification et la propagation de ces lésions, dans les phases précoces de l’intoxication au paracétamol, peuvent se produire indépendamment des cellules immunitaires. Sur base de ces résultats, nous avons émis l’hypothèse de l’existence d’un dialogue entre la protéine HMGB1 et les hépatocytes plutôt que du dialogue, généralement décrit dans la littérature, entre la protéine HMGB1 et les cellules du système immunitaire Nos travaux se sont donc poursuivis, in vitro, sur une lignée cellulaire d’hépatocytes humains, les cellules HepaRG. Ces expériences nous ont permis, d’une part, de confirmer l’implication de la protéine HMGB1 dans l’hépatotoxicité au paracétamol et de mettre en évidence la capacité de cette protéine à provoquer, sans intermédiaire, la mort des cellules HepaRG. D’autre part, ces expériences nous permettent de suggérer la participation de la protéine HMGB1 dans la propagation et l’amplification de la mort des hépatocytes exposés au paracétamol par une voie de signalisation impliquant l’axe TLR4/TRIF/RIPK3. Finalement, l’inhibition de la protéine HMGB1 semblant être bénéfique, nous avons investigué la potentielle efficacité de l’administration d’une combinaison de N-acétylcystéine et de glycyrrhizine dans notre modèle murin. L’idée était de combiner une drogue qui agit sur l’accumulation du métabolite toxique et une seconde qui agit sur la phase de propagation du signal. Nos résultats, bien que préliminaires, ont démontré l’efficacité de cette combinaison à la fois sur la nécrose hépatique et sur la survie des souris. En conclusion, nos travaux confirment l’importance du rôle joué par la protéine HMGB1 dans l’hépatotoxicité induite par le paracétamol et nous permettent de mettre en évidence un nouveau mécanisme, impliquant la protéine HMGB1, qui pourrait contribuer à l’amplification et la propagation des lésions hépatiques induites par une overdose de paracétamol.
Doctorat en Sciences biomédicales et pharmaceutiques (Médecine)
info:eu-repo/semantics/nonPublished
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Boudreau, Jordache. "Electrochemical Generation of Reactive Species and their Application as Chemotherapeutics." Thesis, 2012. http://hdl.handle.net/10214/3588.

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A major limitation in developing a successful cancer treatment is the need for a distinction between normal and cancerous tissue. For solid tumors, this distinction can be made on a spatial basis, and successful treatments have been developed accordingly; however, many of these treatments cause pathologies in healthy tissue, much to the detriment of patient health. To address this issue for solid tumours, a conceptual approach would be to administer the chemotherapeutic drug locally, such that the intra-tumour concentration was high, while the systemic exposure to the drug remained low, thus, minimizing side effects. The present research focuses on providing proof-of-concept for the electrochemical generation of a toxicant from a prodrug, and subsequent use to elicit cytotoxicity in cancer cells, in attempts to electrochemically mimic monooxygenase-catalyzed bioactivation. Electro-oxidation of acetaminophen and cyclophosphamide substrates at graphite and Ti/RuO2 anodes was successful in generating their respective toxicants; however, the graphite anode was superior with respect to current efficiency and toxicant yield. Electrolyses conducted in batch and flow reactors produced effluents which reduced EMT-6 cell viability to the IC99 level. This thesis provides proof-of-concept for electrochemical prodrug activation as a viable area for further cancer research.

Books on the topic "Acetaminophen Toxicology":

1

Foisy, Michelle M. An Overview of Acetaminophen overdoses at the Ottawa General Hospital. [Ottawa: s.n., 1989.

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Bishākta sirāpa: Bhejāla pyārāsiṭāmala kāhinī. Ḍhākā: Bāṃlādeśa Seṇṭāra phara Ayāḍabhānsaḍ Sṭāḍija, 1994.

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J, Meredith T., World Health Organization, Commission of the European Communities., and International Program on Chemical Safety., eds. Antidotes for poisoning by paracetamol. Cambridge: Published by Cambridge University Press on behalf of the World Health Organization and of the European Commission, 1995.

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Book chapters on the topic "Acetaminophen Toxicology":

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Bateman, D. Nicholas. "Acetaminophen (Paracetamol)." In Critical Care Toxicology, 1–25. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-20790-2_108-1.

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Bateman, D. Nicholas. "Acetaminophen (Paracetamol)." In Critical Care Toxicology, 1–25. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-20790-2_108-2.

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Bateman, D. Nicholas. "Acetaminophen/Paracetamol." In Critical Care Toxicology, 1145–69. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-17900-1_108.

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Wormser, U., and D. Calp. "Induction of Hepatic Metallothionein Following Acetaminophen Administration." In Archives of Toxicology, 375–77. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73113-6_68.

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Bavia, Lorena, Izonete Cristina Guiloski, Milena Carvalho Carneiro, and Maritana Mela Prodocimo. "Different Mice Strains in Biomarker Responses to Toxic Agents: The Example of Acetaminophen." In Biomarkers in Toxicology, 1–23. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-87225-0_78-1.

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Warnet, J. M., M. O. Christen, M. Thevenin, D. Biard, A. Jacqueson, and J. R. Claude. "Study of Glutathione and Glutathione Related Enzymes in Acetaminophen-Poisoned Mice. Prevention by Anethole Trithione Pretreatment." In Archives of Toxicology, 322–25. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74117-3_61.

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Svendsen, O., H. B. Christensen, J. Rygaard, and P. Juul. "Comparative Study on the Toxicity of Acetaminophen and Mercuric Chloride in Normal and Athymic Mice and Rats." In Archives of Toxicology, 191–96. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74117-3_28.

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Ellouk-Achard, S., V. Levresse, C. Martin, C. Pham-Huy, H. Dutertre-Catella, M. Thevenin, J. M. Warnet, and J. R. Claude. "Ex Vivo and in Vitro Models in Acetaminophen Hepatotoxicity Studies. Relationship between Glutathione Depletion, Oxidative Stress and Disturbances in Calcium Homeostasis and Energy Metabolism." In Archives of Toxicology, 209–14. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79451-3_18.

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Shankar, Kartik, and Harihara M. Mehendale. "Acetaminophen." In Encyclopedia of Toxicology, 18–23. Elsevier, 2005. http://dx.doi.org/10.1016/b0-12-369400-0/00011-9.

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Sellon, Rance K. "Acetaminophen." In Small Animal Toxicology, 550–58. Elsevier, 2006. http://dx.doi.org/10.1016/b0-72-160639-3/50031-9.

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