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Artículos de revistas sobre el tema "Acetaminophen Toxicology"

Autor: Grafiati
Publicado: 4 de junio de 2021
Última modificación: 29 de enero de 2023

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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 dur
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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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4

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. Validi
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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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6

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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7

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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8

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 hyd
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9

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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10

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
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11

Sahu, Kamal Kant, Ajay Kumar Mishra, Amos Lal, and Susan V. George. "Acetaminophen induced methemoglobinemia." Clinical Toxicology 58, no. 7 (October 17, 2019): 784–85. http://dx.doi.org/10.1080/15563650.2019.1677909.

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12

Rianprakaisang, Tony, Adam Blumenberg, and Robert G. Hendrickson. "Acetaminophen-associated methemoglobinemia." Clinical Toxicology 58, no. 7 (November 4, 2019): 785–86. http://dx.doi.org/10.1080/15563650.2019.1682153.

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13

Huitema, A. DR, M. Soesan, P. L. Meenhorst, C. HW Koks, and J. H. Beijnen. "A dose-dependent delayed hypersensitivity reaction to acetaminophen after repeated acetaminophen intoxications." Human & Experimental Toxicology 17, no. 7 (July 1998): 406–8. http://dx.doi.org/10.1177/096032719801700708.

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We report a case of a 29-year-old woman with a borderline personality disorder who presented with intentional substantial acetaminophen (paracetamol) overdosage on nine occasions during a period of 21 months. In most cases, the patient presented at the hospital within 4 h after ingestion and was treated with gastric lavage, activated charcoal, laxatives and intravenous N-acetylcysteine. During the sixth overdosage the patient developed a rash on her chest and shoulders which was considered an anaphylactoid reaction to N-acetylcysteine. Therefore she was treated with oral methionine subsequentl
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14

Sebe, Ahmet, Salim Satar, N. Rana Alpay, Mesude Murt, and Birol Güvenç. "Severe acetaminophen poisoning treated with a fractionated plasma separation and absorption system: A case report." Human & Experimental Toxicology 28, no. 11 (October 7, 2009): 729–32. http://dx.doi.org/10.1177/0960327109350800.

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Acetaminophen is an analgesic drug that is frequently used in suicide attempts. In this paper, we report on a 17-year-old girl who was admitted to an emergency department 15 hours after taking acetaminophen pills in a suicide attempt. Her serum acetaminophen level was 73 mg/L on admission; she had elevated liver enzymes suggesting hepatic necrosis. She was started on N-acetyl cystein (NAC), and treated successfully with a fractionated plasma separation and absorption system.
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15

Kozer, E., and M. McGuigan. "Treatment strategies for early presenting acetaminophen overdose: a survey of medical directors of poison centers in North America and Europe." Human & Experimental Toxicology 21, no. 3 (March 2002): 123–27. http://dx.doi.org/10.1191/0960327102ht235oa.

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Background: Acetaminophen is frequently used in self-poisoning in Western countries. Although treatment withN-acetylcysteine (NAC) reduces liver injury, no consensus exists on the preferred management of acetaminophen toxicity. Objectives: To describe the approach taken by toxicologists in North America and Europe toward the management of acetaminophen toxicity. Methods: Medical directors of poison centers in the US, Canada, and Europe were surveyed by means of a questionnaire presenting two clinical scenarios of acetaminophen overdose: a healthy adolescent with no risk factors who had an acut
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16

Ghannoum, Marc, Sara Kazim, Ami M. Grunbaum, Eric Villeneuve, and Sophie Gosselin. "Massive acetaminophen overdose: effect of hemodialysis on acetaminophen and acetylcysteine kinetics." Clinical Toxicology 54, no. 6 (April 27, 2016): 519–22. http://dx.doi.org/10.1080/15563650.2016.1175006.

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17

Hassan, Reham. "Acetaminophen induces programmed necrosis." Archives of Toxicology 93, no. 12 (November 14, 2019): 3641–42. http://dx.doi.org/10.1007/s00204-019-02625-0.

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18

Huitema, A. D. R., M. Soesan, P. L. Meenhorst, C. H. W. Koks, and J. H. Beijnen. "A dose-dependent delayed hypersensitivity reaction to acetaminophen after repeated acetaminophen intoxications." Human & Experimental Toxicology 17, no. 7 (July 1, 1998): 406–8. http://dx.doi.org/10.1191/096032798678908972.

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19

Yamada, Naoya, Takanori Komada, Nobuhiko Ohno, and Masafumi Takahashi. "Acetaminophen-induced hepatotoxicity: different mechanisms of acetaminophen-induced ferroptosis and mitochondrial damage." Archives of Toxicology 94, no. 6 (March 31, 2020): 2255–57. http://dx.doi.org/10.1007/s00204-020-02722-5.

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20

Xu, Jinghai J., Bart S. Hendriks, Jie Zhao, and David de Graaf. "Multiple effects of acetaminophen and p38 inhibitors: Towards pathway toxicology." FEBS Letters 582, no. 8 (February 20, 2008): 1276–82. http://dx.doi.org/10.1016/j.febslet.2008.01.063.

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21

Adekeye, AO, and AA Fafure. "Assessment of the cellular integrity and expression of melatonin receptor (MTNR1A) in the retina assaulted by ethanol and acetaminophen." Human & Experimental Toxicology 41 (January 2022): 096032712211490. http://dx.doi.org/10.1177/09603271221149010.

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Ethanol exposures have been reported to disrupt the development of the retina and optic nerve which can be considered as part of underlying mechanisms of visual pathway impairments. This study aims to investigate the cellular integrity of the retina and the expression of melatonin receptor (MTNR1A) in the retina when assaulted chronically and simultaneously by ethanol and acetaminophen. Animals were randomly grouped into five groups. Control (normal saline), Alcohol group (25% alcohol in 2% sucrose solution), Acetaminophen group, (100 mg/kg BW for 14 days), Acetaminophen + Alcohol group (25% a
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22

Lip, Gregory Y. H., and J. Allister Vale. "Does Acetaminophen Damage the Heart?" Journal of Toxicology: Clinical Toxicology 34, no. 2 (January 1996): 145–47. http://dx.doi.org/10.3109/15563659609013761.

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23

HOIVIK, DEBIE J., JOSÉ E. MANAUTOU, ANN TVEIT, DAYNA C. MANKOWSKI, EDWARD A. KHAIRALLAH, and STEVEN D. COHEN. "Evidence Suggesting the 58-kDa Acetaminophen Binding Protein Is a Preferential Target for Acetaminophen Electrophile." Toxicological Sciences 32, no. 1 (1996): 79–86. http://dx.doi.org/10.1093/toxsci/32.1.79.

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Hoivik, D. "Evidence Suggesting the 58-kDa Acetaminophen Binding Protein Is a Preferential Target for Acetaminophen Electrophile." Fundamental and Applied Toxicology 32, no. 1 (July 1996): 79–86. http://dx.doi.org/10.1006/faat.1996.0109.

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25

Dalhoff, Kim, Per Boye Hansen, Peter Ott, Steffen Loft, and Henrik E. Poulsen. "Acute Ethanol Administration Reduces the Antidote Effect of N-Acetylcysteine after Acetaminophen Overdose in Mice." Human & Experimental Toxicology 10, no. 6 (November 1991): 431–33. http://dx.doi.org/10.1177/096032719101000611.

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1 The combined antidote effect of N-acetylcysteine and ethanol on the toxicity of acetaminophen was investigated. 2 Fed male mice were given acetaminophen i.p. (600 mg kg-1) and after 5 min in addition ethanol i.p. (0.2 ml, 19% v/v), N-acetylcysteine i.p. (1.2 g kg -1, 0.2 ml), N-acetylcysteine + ethanol i.p. (same doses as given individually) or saline i.p. (0.4 ml). Survival rates were determined after 24, 48, 72 and 96 h. 3 In the N-acetylcysteine group the survival rate was 85%. This rate was significantly reduced to 43% in the N-acetylcysteine + ethanol group (P = 0.0001). In the groups g
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26

O'Brien, P. J., M. R. Slaughter, A. Swain, J. M. Birmingham, R. W. Greenhill, F. Elcock, and P. J. Bugelski. "Repeated acetaminophen dosing in rats: adaptation of hepatic antioxidant system." Human & Experimental Toxicology 19, no. 5 (May 2000): 277–83. http://dx.doi.org/10.1191/096032700678815918.

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Repeated dosing of acetaminophen (paracetamol) to rats is reported to decrease their sensitivity to its hepatotoxic effects, which are associated with oxidative stress and glutathione depletion. We determined if repeated acetaminophen dosing produced adaptive response of key antioxidant system enzymes. Male rats (Sprague-Dawley, 10 weeks) were given 800, 1200, or 1600 mg/kg/day acetaminophen by oral gavage for 4 days. Liver was assayed for oxidative stress and antioxidant markers: malondialdehyde (MDA), thiobar-bituric acid reactive substance (TBARS), total antioxidant status (TAS), glutathion
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27

Mehrpour, Omid, Farhad Saeedi, Ali Hadianfar, Bruno Mégarbane, and Christopher Hoyte. "Prognostic factors of acetaminophen exposure in the United States: An analysis of 39,000 patients." Human & Experimental Toxicology 40, no. 12_suppl (November 12, 2021): S814—S825. http://dx.doi.org/10.1177/09603271211061503.

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Acetaminophen is a frequently used over-the-counter or prescribed medication in the United States. Exposure to acetaminophen can lead to acute liver cytolysis, acute liver failure, acute kidney injury, encephalopathy, and coagulopathy. This retrospective cohort study (1/1/2012 to 12/31/2017) investigated the clinical outcomes of intentional and unintentional acetaminophen exposure using the National Poison Data System data. The frequency of outcomes, chronicity, gender, route of exposure, the reasons for exposure, and treatments as described. Binary logistic regression was used to estimate the
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28

Zyoud, Sa'ed H., Rahmat Awang, Syed Azhar Syed Sulaiman, and Samah W. Al-jabi. "High prevalence of hypokalemia after acute acetaminophen overdose: Impact of psychiatric illness." Human & Experimental Toxicology 29, no. 9 (February 9, 2010): 773–78. http://dx.doi.org/10.1177/0960327110361759.

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Background: Hypokalemia is not an isolated disease but an associated finding in a number of different diseases. It is also a commonly neglected condition among patients with acute acetaminophen overdose. Objectives: This study intended to determine the prevalence of hypokalemia and its clinical correlates in acute psychiatric illness among hypokalemic and normokalemic patients after acetaminophen overdose. Methods: This is a retrospective cohort study of hospital admissions for acute acetaminophen overdose conducted over a period of 5 years from 1 January 2004 to 31 December 2008. Demographic
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Shan, Shulin, Zhenyu Shen, and Fuyong Song. "Autophagy and acetaminophen-induced hepatotoxicity." Archives of Toxicology 92, no. 7 (June 6, 2018): 2153–61. http://dx.doi.org/10.1007/s00204-018-2237-5.

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30

Manautou, José E., Edward A. Khairallah, and Steven D. Cohen. "Evidence for common binding of acetaminophen and bromobenzene to the 58‐kda acetaminophen‐binding protein." Journal of Toxicology and Environmental Health 46, no. 3 (November 1995): 263–69. http://dx.doi.org/10.1080/15287399509532034.

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31

Stern, Stephan T., Mary K. Bruno, Robert A. Horton, Dennis W. Hill, Jeanette C. Roberts та Steven D. Cohen. "Contribution of acetaminophen-cysteine to acetaminophen nephrotoxicity II. Possible involvement of the γ-glutamyl cycle". Toxicology and Applied Pharmacology 202, № 2 (січень 2005): 160–71. http://dx.doi.org/10.1016/j.taap.2004.06.029.

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32

Seltzer, Justin A., Irvan Bubic, Garret A. Winkler, Nathan A. Friedman, Jessica Bagby, Christian A. Tomaszewski, Richard F. Clark, Allyson Kreshak, and Daniel R. Lasoff. "Sulfhemoglobinemia and methemoglobinemia following acetaminophen overdose." Toxicology Reports 9 (2022): 1725–27. http://dx.doi.org/10.1016/j.toxrep.2022.08.011.

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33

Hantson, Philippe, Marie Christiane Vekemans, Pierre François Laterre, Piet Vanormelingen, Paul Mahieu, and Michael Matthias Koerner. "Heart Donation After Fatal Acetaminophen Poisoning." Journal of Toxicology: Clinical Toxicology 35, no. 3 (January 1997): 325–26. http://dx.doi.org/10.3109/15563659709001221.

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Rumack, Barry H. "Acetaminophen Hepatotoxicity: The First 35 Years." Journal of Toxicology: Clinical Toxicology 40, no. 1 (January 2002): 3–20. http://dx.doi.org/10.1081/clt-120002882.

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35

Tenenbein, Milton. "Acetaminophen: The 150 mg/kg Myth." Journal of Toxicology: Clinical Toxicology 42, no. 2 (January 2004): 145–48. http://dx.doi.org/10.1081/clt-120030939.

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36

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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Potter, David W., and Jack A. Hinson. "Acetaminophen Peroxidation Reactions." Drug Metabolism Reviews 20, no. 2-4 (January 1989): 341–58. http://dx.doi.org/10.3109/03602538909103546.

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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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Sorodoc, Laurentiu, Catalina Lionte, Cristina Bologa, Ovidiu Petris, Victorita Sorodoc, and Carmen Buga. "Acute pancreatitis after nifedipine and acetaminophen poisoning — case report." Open Medicine 4, no. 4 (December 1, 2009): 527–31. http://dx.doi.org/10.2478/s11536-009-0057-y.

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AbstractThe incidence of drug-induced pancreatitis is rare. There have been several reports of acute pancreatitis as a complication in acute poisoning with drugs or toxins. We present a case of a young woman with acute pancreatitis secondary to an overdose of nifedipine and acetaminophen in a suicide attempt. We excluded other causes of acute pancreatitis by clinical history, serum toxicology, serology, and abdominal imaging. The most likely underlying pathophysiological mechanism was ischemic injury of the pancreas secondary to severe collapse induced by nifedipine and possible acetaminophen-
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Bond, G. Randall. "Acetaminophen protein adducts: A review." Clinical Toxicology 47, no. 1 (January 2009): 2–7. http://dx.doi.org/10.1080/15563650801941831.

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Chomchai, Summon, Chulithida Chomchai, and Taweepong Anusornsuwan. "Acetaminophen psi parameter: A useful tool to quantify hepatotoxicity risk in acute acetaminophen overdose." Clinical Toxicology 49, no. 7 (August 2011): 664–67. http://dx.doi.org/10.3109/15563650.2011.597031.

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BARTOLONE, JOHN B., STEVEN D. COHEN, and EDWARD A. KHAIRALLAH. "Immunohistochemical Localization of Acetaminophen-Bound Liver Proteins." Toxicological Sciences 13, no. 4 (1989): 859–62. http://dx.doi.org/10.1093/toxsci/13.4.859.

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BARTOLONE, J. "Immunohistochemical localization of acetaminophen-bound liver proteins." Fundamental and Applied Toxicology 13, no. 4 (November 1989): 859–62. http://dx.doi.org/10.1016/0272-0590(89)90339-4.

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Zyoud, Sa'ed H., Rahmat Awang, Syed Azhar Syed Sulaiman, Waleed M. Sweileh, and Samah W. Al-jabi. "Incidence of adverse drug reactions induced by N-acetylcysteine in patients with acetaminophen overdose." Human & Experimental Toxicology 29, no. 3 (January 13, 2010): 153–60. http://dx.doi.org/10.1177/0960327109359642.

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Background: Intravenous N-acetylcysteine (IV-NAC) is widely recognized as the antidote of choice for acetaminophen overdose. However, its use is not without adverse drug reactions (ADR) that might affect therapeutic outcome or lead to treatment delay. Objective: the aim of this study was to investigate the type and incidence of ADR induced by IV-NAC in patients treated for acetaminophen overdose. Methods: This is a retrospective study of patients admitted to the hospital for acute acetaminophen overdose over a period of 4 years (1 January 2005 to 31 December 2008). The primary outcome of inter
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45

Hart, S. G. E., W. P. Beierschmitt, D. S. Wyand, E. A. Khairallah, and S. D. Cohen. "Acetaminophen Nephrotoxicity in CD-1 Mice." Toxicology and Applied Pharmacology 126, no. 2 (June 1994): 267–75. http://dx.doi.org/10.1006/taap.1994.1116.

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46

Jørgensen, L., P. Thomsen, and H. E. Poulsen. "Disulfiram Prevents Acetaminophen Hepatotoxicity in Rats." Pharmacology & Toxicology 62, no. 5 (May 1988): 267–71. http://dx.doi.org/10.1111/j.1600-0773.1988.tb01885.x.

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Mehrpour, Omid, Shahin Shadnia, and Hossein Sanaei-Zadeh. "Late extensive intravenous administration of N-acetylcysteine can reverse hepatic failure in acetaminophen overdose." Human & Experimental Toxicology 30, no. 1 (March 23, 2010): 51–54. http://dx.doi.org/10.1177/0960327110366182.

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Acetaminophen is a commonly used analgesic and has been shown to be a main cause of drug-induced liver failure. N-acetylcysteine (NAC) should be employed as the antidote in case of acetaminophen poisoning within the first 8-10 hours. Oral administration of NAC is universally recommended and due to the adverse effects, the intravenous administration of the agent is reserved for patients with oral intolerance and severe complications. We here report an 18-year-old man with severe liver failure due to a huge ingestion of acetaminophen, who was taken into the Loghman Hakim Hospital Poison Center 7
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Donkor, Shadrack, Christopher Larbie, Gustav Komlaga, and Benjamin Obukowho Emikpe. "Evaluation of the Acute Hepatoprotective Potential of Hydroethanolic Extract of Duranta erecta L. Parts." Journal of Toxicology 2020 (December 9, 2020): 1–10. http://dx.doi.org/10.1155/2020/8815719.

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Liver disease is a major health problem and its treatment is costly in most developing countries with attendant adverse effects. This study aimed at determining the acute hepatoprotective efficacy of Duranta erecta hydroethanolic extracts of leaves, ripe and unripe fruits against CCl4-, and acetaminophen-induced hepatotoxicity in animals. Materials and Methods. CCl4 (1 mL/kg body weight in olive oil) and acetaminophen (500 mg/kg b.wt) were used to induce hepatotoxicity in the animals. Animals were treated with extracts at 250 mg/kg b.wt and standard drug, silymarin (100 mg/kg), for 7 days. Hep
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Wojdyla, Katarzyna, Krzysztof Wrzesinski, James Williamson, Stephen J. Fey, and Adelina Rogowska-Wrzesinska. "Acetaminophen-induced S-nitrosylation and S-sulfenylation signalling in 3D cultured hepatocarcinoma cell spheroids." Toxicology Research 5, no. 3 (2016): 905–20. http://dx.doi.org/10.1039/c5tx00469a.

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Polyakov, Alexey V., Andrey A. Svistunov, Svetlana N. Kondratenko, Irina V. Kovachevich, Lyudmila G. Repenkova, Marina I. Savelyeva, Evgenia V. Shikh, and Lidiya Y. Badriddinova. "Study of the pharmacokinetics of various drugs under conditions of antiorthostatic hypokinesia and the pharmacokinetics of acetaminophen under long-term spaceflight conditions." Drug Metabolism and Personalized Therapy 37, no. 2 (November 29, 2021): 163–75. http://dx.doi.org/10.1515/dmpt-2021-0159.

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Abstract Objectives To study the pharmacokinetics and relative bioavailability of drugs of different chemical structure and pharmacological action under conditions simulating the effects of some factors of spaceflight, as well as the peculiarities of the pharmacokinetics of acetaminophen under long-term spaceflight conditions. Methods The pharmacokinetics of verapamil (n=8), propranolol (n=8), etacizine (n=9), furosemide (n=6), and acetaminophen (n=7) in healthy volunteers after a single oral administration under normal conditions (background) and under antiorthostatic hypokinesia (ANOH), the
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