Journal articles: 'Acetaminophen toxicity'

1

Cook, Matthew D., and Richard F. Clark. "Acetaminophen Toxicity." Pediatric Emergency Care 21, no. 10 (October 2005): 703–4. http://dx.doi.org/10.1097/01.pec.0000181412.33859.51.

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Mayhew, Maren. "Acetaminophen Toxicity." Journal for Nurse Practitioners 3, no. 3 (March 2007): 186–88. http://dx.doi.org/10.1016/j.nurpra.2007.01.025.

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Mitchell, Jerry R. "Acetaminophen Toxicity." New England Journal of Medicine 319, no. 24 (December 15, 1988): 1601–2. http://dx.doi.org/10.1056/nejm198812153192409.

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Mirochnitchenko, Oleg, Miriam Weisbrot-Lefkowitz, Kenneth Reuhl, Laishun Chen, Chung Yang, and Masayori Inouye. "Acetaminophen Toxicity." Journal of Biological Chemistry 274, no. 15 (April 9, 1999): 10349–55. http://dx.doi.org/10.1074/jbc.274.15.10349.

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Roach, Janey A., and Brett Stacey. "Acetaminophen Toxicity." Orthopaedic Nursing 16, no. 3 (May 1997): 49???55. http://dx.doi.org/10.1097/00006416-199705000-00013.

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Bartlett, Dana. "Acetaminophen Toxicity." Journal of Emergency Nursing 30, no. 3 (June 2004): 281–83. http://dx.doi.org/10.1016/j.jen.2004.01.023.

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Regal, Randolph E. "Acetaminophen Chronic Toxicity." Drug Intelligence & Clinical Pharmacy 20, no. 6 (June 1986): 507. http://dx.doi.org/10.1177/106002808602000620.

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Roberge, Raymond. "Chronic acetaminophen toxicity." Journal of Emergency Medicine 25, no. 4 (November 2003): 474. http://dx.doi.org/10.1016/j.jemermed.2003.08.006.

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Myers, Wade C., Terrance A. Otto, Elaine Harris, Daniel Diaco, and Anthony Moreno. "ACETAMINOPHEN OVERDOSE AS A SUICIDAL GESTURE: A SURVEY OF ADOLESCENTS' KNOWLEDGE OF ITS POTENTIAL FOR TOXICITY." Pediatrics 93, no. 6 (June 1, 1994): A36. http://dx.doi.org/10.1542/peds.93.6.a36.

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Acetaminophen is a popular nonprescription analgesic that is often taken in overdose by adolescents during suicidal gestures. The authors hypothesized that most adolescents are naive about the toxic and lethal potential of acetaminophen in overdose. A one-page, 12-item questionnaire was administered to 169 high school students to evaluate their perceptions and knowledge in this area. Whereas only 22% of the sample underestimated the dose of acetaminophen necessary to cause harm, 40.5% underestimated the potential lethality of acetaminophen in overdose. Moreover, 17% of the sample did not believe one could ingest enough acetaminophen to cause death. The lack of knowledge about acetaminophen's potential dangerousness, its widespread availability, and an absence of early symptoms of hepatotoxicity make this medication highly dangerous to those adolescents who take it in overdose during parasuicidal behavior.

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Poolsawat, S. S., C. A. Huerta, G. A. Miranda, and L. T. Nguyen. "Acetaminophen: fatty enhanced toxicity." Proceedings, annual meeting, Electron Microscopy Society of America 44 (August 1986): 332–33. http://dx.doi.org/10.1017/s0424820100143286.

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Drug toxicity accounts for 10%-30% of all medical in-patients admissions; some of the drug induced illnesses often occur following hospitalization. 5%-6% of medical in-patients deaths are initiated or induced by drug intake (1-4); about one-third of these cases are caused by non-prescription drugs. Acetaminophen, considered among the safest of all over-the-counter analgesics, has been reported to induce fatal hepatic necrosis both in man and animals (5-8). Frequently, adverse drug reactions arise from hypersensitivity to a drug and its side effects, or to drug interactions with food and food additives. This study is undertaken to observe the effect of acetaminophen on the liver when a fatty diet is simultaneously administered.Swiss Webster mice were individually gavaged with a 286 mg/Kg dosis of acetaminophen for 4 days; control animals received saline alone. Both groups received rat feed plus 20% fat and were euthanized on the 5th day. Liver tissues were either fixed in 2% gluteraldehyde; post-fixed in 1% osmnium tetroxide in 0.1M sodium cacodylate buffer and embedded in Araldite 502 for TEM; or processed for alkaline phosphatase activity (9).Hepatocyte derived from mice exposed to acetaminophen (Fig. 1) showed increased Golgi Apparatus (GA) and secretory granules (SG) activity. These phenomena appear to be responsible for the elevated alkaline phosphatase activity (Fig. 2) in response to acetaminophen detoxification exerted by the hepatocyte. However, when a fatty diet is incorporated into the study: the hepatocyte exhibited generalized cytoplasmic lysis and increased lipid droplets (Fig. 3), localized coagulative necrosis of the hepatocyte normally found in the caudal and right lobes of the liver (Fig. 4) and increased pynotic hepatocytes (Fig. 5) are noted

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Dunlevy, Timothy M., and Maryann P. Wall. "Pediatric Subacute Acetaminophen Toxicity." Otolaryngology–Head and Neck Surgery 116, no. 1 (January 1997): 134–36. http://dx.doi.org/10.1016/s0194-59989770366-8.

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Haun, S. E., J. E. Segeleon, and R. M. Ward. "Acetaminophen Toxicity in Children." PEDIATRICS 110, no. 1 (July 1, 2002): 197–98. http://dx.doi.org/10.1542/peds.110.1.197.

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SMITH, DEBORAH H. "Managing acute acetaminophen toxicity." Nursing 37, no. 1 (January 2007): 58–63. http://dx.doi.org/10.1097/00152193-200701000-00042.

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&NA;. "Managing acute acetaminophen toxicity." Nursing 37, no. 1 (January 2007): 64. http://dx.doi.org/10.1097/00152193-200701000-00043.

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Rowden, Adam K., Jeffrey Norvell, David L. Eldridge, and Mark A. Kirk. "Updates on Acetaminophen Toxicity." Medical Clinics of North America 89, no. 6 (November 2005): 1145–59. http://dx.doi.org/10.1016/j.mcna.2005.06.009.

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SHAW, GINA. "Acetaminophen and Liver Toxicity." Neurology Today 9, no. 17 (September 2009): 16. http://dx.doi.org/10.1097/01.nt.0000360732.96148.a8.

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Srikanth, Chittur V., Asit K. Chakraborti, and Anand K. Bachhawat. "Acetaminophen toxicity and resistance in the yeast Saccharomyces cerevisiae." Microbiology 151, no. 1 (January 1, 2005): 99–111. http://dx.doi.org/10.1099/mic.0.27374-0.

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Acetaminophen (paracetamol), one of the most widely used analgesics, is toxic under conditions of overdose or in certain disease conditions, but the mechanism of acetaminophen toxicity is still not entirely understood. To obtain fresh insights into acetaminophen toxicity, this phenomenon was investigated in yeast. Acetaminophen was found to be toxic to yeast cells, with erg mutants displaying hypersensitivity. Yeast cells grown in the presence of acetaminophen were found to accumulate intracellular acetaminophen, but no metabolic products of acetaminophen could be detected in these extracts. The toxicity response did not lead to an oxidative stress response, although it did involve Yap1p. The cytochrome P450 enzymes of yeast, Erg5p and Erg11p, did not appear to participate in this process, unlike the mammalian systems. Furthermore, we could not establish a central role for glutathione depletion or the cellular glutathione redox status in acetaminophen toxicity, suggesting differences from mammalian systems in the pathways causing toxicity. Investigations of the resistance mechanisms revealed that deletion of the glutathione-conjugate pumps Ycf1p (a target of Yap1p) and Bpt1p, surprisingly, led to acetaminophen resistance, while overexpression of the multidrug resistance pumps Snq2p and Flr1p (also targets of Yap1p) led to acetaminophen resistance. The Yap1p-dependent resistance to acetaminophen required a functional Pdr1p or Pdr3p protein, but not a functional Yrr1p. In contrast, resistance mediated by Pdr1p/Pdr3p did not require a functional Yap1p, and revealed a distinct hierarchy in the resistance to acetaminophen.

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Spielberg, Stephen P. "Acetaminophen toxicity in lymphocytes heterozygous for glutathione synthetase deficiency." Canadian Journal of Physiology and Pharmacology 63, no. 5 (May 1, 1985): 468–71. http://dx.doi.org/10.1139/y85-081.

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We have studied the effects of acetaminophen metabolites generated by a murine hepatic microsomal system on lymphocytes from two subjects heterozygous for glutathione synthetase deficiency. Heterozygous cells exhibited greater dose-related toxicity than controls. Following a 2-h incubation with acetaminophen and the microsomal system, cells were washed and incubated for 16 h in the presence or absence of N-acetylcysteine, the standard antidote for acetaminophen toxicity. In control cells, glutathione content was replenished to nearly base-line values and toxicity was prevented. N-Acetylcysteine thus prevented toxicity even after covalent binding of acetaminophen metabolites had occurred. Heterozygous cells failed to use N-acetylcysteine as efficiently to resynthesize glutathione, and the cells were not protected from acetaminophen toxicity. Heterozygotes may be at increased risk of toxicity from drugs whose metabolites are detoxified by glutathione conjugation.

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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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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.

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Moulding, Thomas S. "Acetaminophen, Isoniazid, and Hepatic Toxicity." Annals of Internal Medicine 114, no. 5 (March 1, 1991): 431. http://dx.doi.org/10.7326/0003-4819-114-5-431_2.

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22

Gyamlani, Geeta G., Chirag R. Parikh, and Suhail Raoof. "ACETAMINOPHEN TOXICITY: A CONTINUING CHALLENGE." Critical Care Medicine 27, Supplement (December 1999): A50. http://dx.doi.org/10.1097/00003246-199912001-00100.

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23

Gussow, Leon. "N-Acetylcysteine and Acetaminophen Toxicity." Emergency Medicine News 26, no. 3 (March 2004): 28. http://dx.doi.org/10.1097/00132981-200403000-00022.

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McClain, C. J., J. Holtzman, J. Allen, J. Kromhout, and S. Shedlofsky. "Clinical Features of Acetaminophen Toxicity." Journal of Clinical Gastroenterology 10, no. 1 (February 1988): 76–80. http://dx.doi.org/10.1097/00004836-198802000-00016.

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25

Saccomano, Scott J. "Acute acetaminophen toxicity in adults." Nursing Critical Care 14, no. 5 (September 2019): 10–17. http://dx.doi.org/10.1097/01.ccn.0000578816.14164.9f.

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MECHCATIE, ELIZABETH. "FDA Panel Confronts Acetaminophen Toxicity." Internal Medicine News 42, no. 14 (August 2009): 7. http://dx.doi.org/10.1016/s1097-8690(09)70516-5.

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MECHCATIE, ELIZABETH. "FDA Panel Addresses Acetaminophen Toxicity." Family Practice News 39, no. 14 (August 2009): 49. http://dx.doi.org/10.1016/s0300-7073(09)70617-6.

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Lucas, Gerard Nimal. "Paracetamol (Acetaminophen) toxicity in children." Sri Lanka Journal of Child Health 32, no. 3 (July 12, 2009): 61. http://dx.doi.org/10.4038/sljch.v32i3.703.

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Saccomano, Scott J. "Acute acetaminophen toxicity in adults." Nurse Practitioner 44, no. 11 (November 2019): 42–47. http://dx.doi.org/10.1097/01.npr.0000586020.15798.c6.

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30

Waseem, Muhammad, Scott Bomann, Joel Gernsheimer, and Heidi Pinkert. "Unusual presentation of acetaminophen toxicity." American Journal of Emergency Medicine 21, no. 1 (January 2003): 88–89. http://dx.doi.org/10.1053/ajem.2003.50022.

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Schwegman, Alex, Erin DeMartino, Katie Finley, and Kirstin Kooda. "AN ATYPICAL ACETAMINOPHEN TOXICITY PRESENTATION." Chest 156, no. 4 (October 2019): A2055. http://dx.doi.org/10.1016/j.chest.2019.08.2009.

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Gürsoy, Murat, Ibrahim C. Haznedaroğlu, Ismail Çelik, Nilgün Sayinalp, Osman I. Özcebe, Semra V. Dündar, and Chantal Guévremont. "Agranulocytosis, Plasmacytosis, and Thrombocytosis Followed by a Leukemoid Reaction Due to Acute Acetaminophen Toxicity." Annals of Pharmacotherapy 30, no. 7-8 (July 1996): 762–65. http://dx.doi.org/10.1177/106002809603000710.

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OBJECTIVE: To describe a patient who developed hepatotoxicity, reactive plasmacytosis with thrombocytosis and life-threatening agranulocytosis, followed by a leukemoid reaction, apparently caused by acute acetaminophen toxicity. SETTING: University-affiliated hospital. CASE SUMMARY: A 19-year-old white woman who took an overdose of acetaminophen developed hepatotoxicity and reactive plasmacytosis with thrombocytosis and life-threatening agranulocytosis, followed by a leukemoid reaction. Symptoms, signs, and laboratory findings regressed with symptomatic therapy during the follow-up period. CONCLUSIONS: We believe that acute acetaminophen toxicity was responsible for these hematologic abnormalities. This profile of hematologic adverse effects associated with acetaminophen toxicity has not been reported previously.

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White, Steven J., and Barry H. Rumack. "The Acetaminophen Toxicity Equations: “Solutions” for Acetaminophen Toxicity Based on the Rumack-Matthew Nomogram." Annals of Emergency Medicine 45, no. 5 (May 2005): 563–64. http://dx.doi.org/10.1016/j.annemergmed.2004.11.033.

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Kasmi, Irena, Sashenka Sallabanda, and Gentian Kasmi. "Fulminate Hepatic Failure in a 5 Year Old Female after Inappropriate Acetaminophen Treatment." Open Access Macedonian Journal of Medical Sciences 3, no. 3 (September 8, 2015): 443–46. http://dx.doi.org/10.3889/oamjms.2015.080.

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BACKGROUND: Acetaminophen is a drug widely used in children because of its safety and efficacy. Although the risk of its toxicity is lower in children such reactions occur in pediatric patients from intentional overdoses and less frequently attributable to unintended inappropriate dosing. The aim of reporting this case is to attract the attention to the risk of the acetaminophen toxicity when administered in high doses.CASE PRESENTATION: We report here a 5 year old girl who developed fulminate liver failure with renal impairment and acute pancreatitis, as a result of acetaminophen toxicity caused from unintentional repeated supratherapeutic ingestion, with a total administered dose of 4800 mg in three consecutive days, 1600 mg/day, approximately 90 mg/kg/day. The blood level of acetaminophen after 10 hours of the last administered dose was 32 mg/l. The patient presented with high fever, jaundice, lethargic, agitating with abdominal pain accompanied by encephalopathy. The liver function test revealed with high level of alanine aminotransferase 5794 UI/l and aspartate aminotransferase 6000 UI/l. Early initiation of oral N-acetylcysteine (NAC) after biochemical evidence of liver toxicity was beneficial with rapid improvement of liver enzymes, hepatic function and encephalopathy. During the course of the illness the child developed acute pancreatitis with hyperamylasemia 255 UI/L and hyperlypasemia 514 UI/ L. Patient totally recovered within 29 days.CONCLUSION: Healthcare providers should considered probable acetaminophen toxicity in any child who has received the drug and presented with liver failure. When there is a high index of suspicion of acetaminophen toxicity NAC should be initiated and continued until there are no signs of hepatic dysfunction.

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Reshi, Mohd Salim, Deepa Yadav, Chhavi Uthra, Sadhana Shrivastava, and Sangeeta Shukla. "Acetaminophen-induced renal toxicity: preventive effect of silver nanoparticles." Toxicology Research 9, no. 4 (June 17, 2020): 406–12. http://dx.doi.org/10.1093/toxres/tfaa040.

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Abstract Present study was planned to investigate the ameliorative effect of silver nanoparticles (AgNPs) on acetaminophen-induced nephrotoxicity. Our results demonstrate that therapy of AgNPs at three different doses (50, 100 and 150 μg/kg once only) prevented the acetaminophen (2 g/kg once only) induced acute renal toxicity. AgNPs treated animals also show less intensity in the histological alterations in kidneys and corroborating the results of analysis of serum urea and creatinine. In addition, AgNPs therapy prevented the acetaminophen-induced oxidative stress, which was confirmed by the alleviated lipid peroxidation, enhanced renal reduced glutathione content and restored enzymatic activities of superoxide dismutase, catalase and adenosine triphosphatase in kidney. Thus, our results demonstrate a possible protective potential of AgNPs on renal toxicity induced by acetaminophen. This study will definitely lead to the development of therapeutic drug against nephrotoxicity, after further clinical and preclinical studies.

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Dom, Aaron M., Rebecca Royzer, and Courtney Olson-Chen. "Malnourishment-Associated Acetaminophen Toxicity in Pregnancy." Obstetrics & Gynecology 137, no. 5 (April 6, 2021): 877–80. http://dx.doi.org/10.1097/aog.0000000000004351.

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37

Beltrán-Olazábal, Alejandra, Patricia Martínez-Galán, Rubén Castejón-Moreno, Miren Edurne García-Moreno, Cristina García-Muro, and Eduardo Esteban-Zubero. "Management of acetaminophen toxicity, a review." Iberoamerican Journal of Medicine 1, no. 1 (October 2, 2019): 22–28. http://dx.doi.org/10.53986/ibjm.2019.0003.

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Acetaminophen (APAP) is a widely used drug in our environment with few adverse effects. Because of this, several patients affected by APAP hepatotoxicity unknown that the APAP dose-intake was excessive. This damage is mainly produced via one of APAP metabolites: N-acetyl-para-benzo-quinone imine (NAPQI), which is very toxic. The drug’s ingested doses as well as the length of time from APAP ingestion to N-acetylcysteine (NAC) therapy are the most essential determining factors in both the development and severity of APAP hepatotoxicity. However, there are other factors related, including alcohol intake, herbs and medications, age and genetic factors, nutritional status, and chronic liver disease. The ingestion of a toxic dose of APAP causes different clinical manifestations that depend fundamentally on the time elapsed since the intake. The diagnosis process depends on the intake (acute single overdose of after repeated overdoses). The Rumack-Matthew nomogram is acceptable after an acute single overdose, being the “possible hepatic toxicity” point 200 μg/mL at 4 hours and 25 μg/mL at 16 hours). This normogram is no applicable in after repeated overdoses. NAC is the antidote for APAP intoxication, and could be administered orally or intravenous. Finally, a multidisciplinary approach with the support of Psychiatry, Intensive Care Unit as well as Gastroenterology and Digestive Department will be necessary, especially in the case of attempted autolysis and severe liver failure.

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Donovan, J. Ward. "Medical Fortune-telling: Predicting Acetaminophen Toxicity." Academic Emergency Medicine 6, no. 11 (November 1999): 1079–82. http://dx.doi.org/10.1111/j.1553-2712.1999.tb00106.x.

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39

Fixl, Alyssa N., Robert M. Woods, and Katelyn Dervay. "Intravenous N-Acetylcysteine for Acetaminophen Toxicity." AACN Advanced Critical Care 28, no. 4 (December 15, 2017): 305–10. http://dx.doi.org/10.4037/aacnacc2017869.

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Potfay, Rebecca, George Mueller, and Sammy Pedram. "Acetaminophen Myocardial Toxicity: An Underrecognized Entity." Chest 146, no. 4 (October 2014): 247A. http://dx.doi.org/10.1378/chest.1992998.

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Conner, Christopher S., Barry H. Rumack, Brenda R. Morand, and Michelle Depot. "Acetaminophen: Acute Overdose Toxicity in Children." Drug Intelligence & Clinical Pharmacy 19, no. 12 (December 1985): 911–12. http://dx.doi.org/10.1177/106002808501901207.

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Bartle, William R., Frances L. Paradiso, John E. Derry, and Donald J. Livingstone. "Delayed Acetaminophen Toxicity despite Acetylcysteine Use." DICP 23, no. 6 (June 1989): 509. http://dx.doi.org/10.1177/106002808902300617.

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James, Laura P., Pippa M. Simpson, Henry C. Farrar, Gregory L. Kearns, Gary S. Wasserman, Jeffrey L. Blumer, Michael D. Reed, Janice E. Sullivan, and Jack A. Hinson. "Cytokines and Toxicity in Acetaminophen Overdose." Journal of Clinical Pharmacology 45, no. 10 (October 2005): 1165–71. http://dx.doi.org/10.1177/0091270005280296.

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Isik, Bunyamin, Reyhan Bayrak, Ali Akcay, and Sadik Sogut. "Erdosteine Against Acetaminophen Induced Renal Toxicity." Molecular and Cellular Biochemistry 287, no. 1-2 (March 11, 2006): 185–91. http://dx.doi.org/10.1007/s11010-005-9110-6.

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Carreiro, Stephanie, James Marvel-Coen, Rosalind Lee, Brittany Chapman, and Victor Ambros. "Circulating microRNA Profiles in Acetaminophen Toxicity." Journal of Medical Toxicology 16, no. 2 (December 2, 2019): 177–87. http://dx.doi.org/10.1007/s13181-019-00739-6.

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Weeks, Benjamin S., Paul Gamache, Norman W. Klein, Jack A. Hinson, Mary Bruno, and Edward Khairallah. "Acetaminophen toxicity to cultured rat embryos." Teratogenesis, Carcinogenesis, and Mutagenesis 10, no. 5 (1990): 361–71. http://dx.doi.org/10.1002/tcm.1770100502.

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Owumi, Solomon E., James P. Andrus, Leonard A. Herzenberg, and Leonore A. Herzenberg. "Co-administration of N-Acetylcysteine and Acetaminophen Efficiently Blocks Acetaminophen Toxicity." Drug Development Research 76, no. 5 (August 2015): 251–58. http://dx.doi.org/10.1002/ddr.21262.

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Yao, Hsien-Tsung, Chien-Chun Li, and Chen-Hui Chang. "Epigallocatechin-3-Gallate Reduces Hepatic Oxidative Stress and Lowers CYP-Mediated Bioactivation and Toxicity of Acetaminophen in Rats." Nutrients 11, no. 8 (August 10, 2019): 1862. http://dx.doi.org/10.3390/nu11081862.

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Epigallocatechin-3-gallate (EGCG) is the most abundant polyphenol in green tea. To investigate the effects of dietary EGCG on oxidative stress and the metabolism and toxicity of acetaminophen in the liver, rats were fed diets with (0.54%) or without EGCG supplementation for four weeks and were then injected intraperitoneally with acetaminophen (1 g/kg). The results showed that EGCG lowered hepatic oxidative stress and cytochrome P450 (CYP) 1A2, 2E1, and 3A, and UDP-glucurosyltransferase activities prior to acetaminophen injection. After acetaminophen challenge, the elevations in plasma alanine aminotransferase activity and histological changes in the liver were ameliorated by EGCG treatment. EGCG reduced acetaminophen-induced apoptosis by lowering the Bax/Bcl2 ratio in the liver. EGCG mildly increased autophagy by increasing the LC3B II/I ratio. Lower hepatic acetaminophen–glutathione and acetaminophen–protein adducts contents were observed after EGCG treatment. EGCG increased glutathione peroxidase and NAD(P)H quinone 1 oxidoreductase activities and reduced organic anion-transporting polypeptides 1a1 expression in the liver after acetaminophen treatment. Our results indicate that EGCG may reduce oxidative stress and lower the metabolism and toxicity of acetaminophen. The reductions in CYP-mediated acetaminophen bioactivation and uptake transporter, as well as enhanced antioxidant enzyme activity, may limit the accumulation of toxic products in the liver and thus lower hepatotoxicity.

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Bhushan, Bharat, and Udayan Apte. "Acetaminophen Test Battery (ATB): A Comprehensive Method to Study Acetaminophen-Induced Acute Liver Injury." Gene Expression 20, no. 2 (November 11, 2020): 125–38. http://dx.doi.org/10.3727/105221620x15901763757677.

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Acetaminophen (APAP) overdose is the major cause of acute liver failure (ALF) in the Western world. Extensive research is ongoing to identify the mechanisms of APAP-induced ALF. APAP-induced acute liver injury is also one of the most commonly studied drug-induced liver injury models in the field of hepatotoxicity. APAP toxicity is triphasic and includes three mechanistically interlinked but temporally distinct phases of initiation, progression, and recovery/regeneration. Despite how commonly it is studied, the methods to study APAP toxicity differ significantly, often leading to confusing and contradictory data. There are number of reviews on mechanisms of APAP toxicity, but a detailed mechanism-based comprehensive method and list of assays that covers all phases of APAP hepatotoxicity are missing. The goal of this review is to provide a standard protocol and guidelines to study APAP toxicity in mice including a test battery that can help investigators to comprehensively analyze APAP toxicity in the specific context of their hypothesis. Further, we will identify the major roadblocks and common technical problems that can significantly affect the results. This acetaminophen test battery (ATB) will be an excellent guide for scientists studying this most common and clinically relevant drug-induced liver injury and will also be helpful as a roadmap for hypothesis development to study novel mechanisms.

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Rootring, Ellen, Cheryl L. Sargel, and Joseph D. Tobias. "Acute Hepatic Dysfunction Related to Chronic Acetaminophen Administration." Journal of Pediatric Pharmacology and Therapeutics 26, no. 5 (June 28, 2021): 497–501. http://dx.doi.org/10.5863/1551-6776-26.5.497.

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Abstract:

Toxicity related to acetaminophen is most encountered with the acute ingestion of large doses. However, toxicity may also result from chronic ingestion, even when recommended doses are administered over a prolonged period of time. We present the case of a 20-month-old female toddler who received therapeutic recommended doses of acetaminophen (oral or intravenous) following multiple surgical interventions for treatment of a tracheo-esophageal fistula following ingestion of a button battery. The potential role of chronic acetaminophen administration in the etiology of hepatoxicity is discussed and prevention strategies are presented.

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Journal articles on the topic 'Acetaminophen toxicity'

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