Literatura académica sobre el tema "Acetaminophen Toxicology"

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Artículos de revistas sobre el tema "Acetaminophen Toxicology"

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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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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. Validi
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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 hyd
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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
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Tesis sobre el tema "Acetaminophen Toxicology"

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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 hemorr
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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.<br>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).
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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
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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.<br>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 hea
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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 protéin
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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,
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Libros sobre el tema "Acetaminophen Toxicology"

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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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Capítulos de libros sobre el tema "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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