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Nam, Haemi. "Acetaminophen, Aggression, and Learning: An Investigation of Acetaminophen's Social Side Effects." The Ohio State University, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=osu1557155429796022.
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Poon, Yuk-king Karen. "The antagonistic effect of paracetamol on ethanol-induced gastric damage in rats /." [Hong Kong] : University of Hong Kong, 1989. http://sunzi.lib.hku.hk/hkuto/record.jsp?B12718592.
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Soliman, Gamal. "A study of acetaminophen analogues' toxicity." Thesis, University of Ottawa (Canada), 1985. http://hdl.handle.net/10393/4926.
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Reddyhoff, Dennis. "Mathematical modelling of acetaminophen induced hepatotoxicity." Thesis, Loughborough University, 2016. https://dspace.lboro.ac.uk/2134/23008.
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Acetaminophen, known as paracetamol in the UK and Tylenol in the United States, is a widespread and commonly used painkiller all over the world. Taken in large enough doses, however, it can cause fatal liver damage. In the U.S., 56000 people are admitted to hospital each year due to acetaminophen overdose and its related effects, at great cost to healthcare services. In this thesis we present a number of different models of acetaminophen metabolism and toxicity. Previously, models of acetaminophen toxicity have been complex and due to this complexity, do not lend themselves well to more advanced mathematical analysis such as the perturbation analysis presented later in this thesis. We begin with a simple model of acetaminophen metabolism, studying a single liver cell and performing numerical and sensitivity analysis to further understand the most important mechanisms and pathways of the model. Through this we identify key parameters that affect the total toxicity in our model. We then proceed to perform singular perturbation analysis, studying the behaviour of the model over different timescales, finding a number of key timescales for the depletion and subsequent recovery of various cofactors as well as critical dose above which we see toxicity occurring. Later in the thesis, this model is used to model metabolism in a spheroid cell culture, examining the difference spatial effects have on metabolism across a 3D cell culture. We then present a more complex model, examining the difference the addition of an adaptive response to acetaminophen overdose from the Nrf2 signalling pathway, has on our results. We aim to reproduce an unexplained result in the experimental data of our colleagues, and so analyse the steady states of our model when subjected to an infused dose, rather than a bolus one. We identify another critical dose which leads to GSH depletion in the infused dose case and find that Nrf2 adaptation decreases toxicity and model sensitivity. This model is then used as part of a whole-body PBPK model, exploring the effects that the distribution of the drug across the bloodstream and different organs has. We explore the affects of that a delay in up-regulation from the Nrf2 pathway has on the model, and find that with rescaled parameters we can qualitatively reproduce the results of our collaborators. Finally, we present the results of in vitro work that we have undertaken, the aim of which was to find new parameters for the model in human hepatocytes, rather than from rodent models, and find a new value for a parameter in our model from human cell lines.
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Mischkowski, Dominik. "The Social Side Effects of Acetaminophen." The Ohio State University, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=osu1438081282.
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Bashir, Shazma. "Mechanism of Paracetamol (acetaminophen) induced hypothermia." Thesis, University of East London, 2018. http://roar.uel.ac.uk/7308/.
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Paracetamol is a potent analgesic and antipyretic with limited side effects compared to the nonsteroidal anti-inflammatory drugs (NSAIDs) and opiates. Worldwide paracetamol is commonly used to treat pain and fever in both children and adults. Although, this drug has been in clinical use for more than a century, the mechanisms of action are not fully understood. Historically some of the actions of paracetamol were attributed to the inhibition of central cyclooxygenase (COX-1 and COX-2) enzymes however given the weak inhibitory effects on COX-1 and COX-2 enzymes, alternative targets have been suggested including a possible novel COX-3. The inhibition of COX-2 is accepted as the mechanism by which paracetamol reduces core temperature (Tc) in febrile animals. However, in non-febrile animals where COX-2 is not induced, paracetamol has also been shown to cause hypothermia by a mechanism that is not fully understood. Both the reduction of pyresis and induction of hypothermia can only occur when peripheral metabolic rate decreases and/or heat loss increases. In terms of antipyresis and hypothermia, the inhibition of lipolysis, fatty acid oxidation and mitochondria function are obvious alternative targets. Studies were undertaken to identify and characterise the putative COX-3 at protein and mRNA level using western blot analysis and reverse transcription polymerase chain reaction (RT-PCR) in mouse brain endothelial cells (b.End3) and whole brain tissues isolated from male C57BL/6 mice. Additional studies were also undertaken to assess if the hypothermic properties of paracetamol could be attributed to direct inhibition of thermogenic pathways in both 3T3-L1 adipocytes and primary brown adipocytes isolated from male Wistar rats. Adipocytes and isolated mitochondria were exposed to paracetamol and lipolysis, fatty acid oxidation (FAO), mitochondrial electron transport chain (ETC), assessed by measuring oxygen consumption rate (OCR). In these studies no expression of the COX-3 protein could be detected in brain endothelial cells and homogenates and no evidence of a COX-3 was detected at mRNA level. However, paracetamol caused a significant decrease (upto 70%; P < 0.01, from control) in both basal and stimulated lipolysis at 1, 3 and 24 hours without affecting cell viability. Paracetamol (10 mM) and its metabolite N-acetyl-p-benzoquinone imine (NAPQI) at 50 μM also significantly (P < 0.01, from control), reduced endogenous and exogenous FAO by 50% and 70% respectively. NAPQI (50 μM) had limited effect on mitochondrial uncoupling. Finally, paracetamol and other antipyretic compounds also significantly reduced ETC activity (upto 90%; P < 0.01, from control). Both the maintenance of normal body temperature (Tb) and the induction of pyresis require increased mitochondrial ETC activity normally initiated centrally and driven peripherally by reduction of substrates such as fatty acids and glucose. The failure to identify the COX-3 protein and the direct inhibition of lipolysis, FAO and ETC activity indicate that antipyretic actions of paracetamol could partly be attributed to it actions on peripheral energy generation systems and provide new drug targets for reducing fever and chemically inducing hypothermia.
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Xu, Zheng. "Developmental Toxicity of Dextromethorphan and Acetaminophen in Zebrafish Embryos/Larvae: Relevance of SULT-mediated Dextromethorphan/Acetaminophen Sulfation." Toledo, Ohio : University of Toledo, 2010. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=toledo1271433014.
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Thesis (M.S.)--University of Toledo, 2010.Typescript. "Submitted to the Graduate Faculty as a partial fulfillment of the requirement for the Master of Science in Pharmacology and Toxicology." "A thesis entitled"--at head of title. Title from title page of PDF document. Bibliography: p. 68-81.
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Harnagea, Theophilus Eugenia. "Acetaminophen stimulates proliferation of breast cancer cells." Morgantown, W. Va. : [West Virginia University Libraries], 1999. http://etd.wvu.edu/templates/showETD.cfm?recnum=773.
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Thesis (Ph. D.)--West Virginia University, 1999.Title from document title page. Document formatted into pages; contains ix, 137 p. : ill. Vita. Includes abstract. Includes bibliographical references (p. 115-134).
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Pandey, Rajiv 1967. "Crystal size manipulation of acetaminophen via recrystallization." Thesis, The University of Arizona, 1993. http://hdl.handle.net/10150/278344.
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The crystal size distribution (CSD) of any material determines its end use. Consequently, comminution processes are used to transform material from one size distribution to another. Often, recrystallization from solution is one of the processes used. Recently, a novel recrystallization process named the GAS process was developed to mill compounds that were thermally labile and insoluble in supercritical fluids. CSD could be manipulated using this process. To further illustrate the applicability of this process, size manipulation studies of acetaminophen (a widely available drug) were performed. The aim of this work was to produce crystals in the mass mean size range from 5mum to 50mum, and identify the conditions for producing the desired size distribution. A modified GAS process and a liquid anti-solvent (LAS) process were also investigated. Together with acetaminophen-butanol, other systems studied were aspirin-methanol and benzoic acid-methanol.
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Ito, Yoshiya, Nancy Machen, Edward Abril, and Robert McCuskey. "Effects of acetaminophen on hepatic microcirculation in mice." BioMed Central, 2004. http://hdl.handle.net/10150/610123.
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Mercer, Melissa Ann. "Pharmacokinetics and Safety of Acetaminophen in Adult Horses." Thesis, Virginia Tech, 2018. http://hdl.handle.net/10919/85379.
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Due to the detrimental side effects of NSAID administration, such as gastrointestinal ulceration and renal papillary necrosis, there is a profound need for clinical pain relief in horses with long term orthopedic disease whereby gastrointestinal side effects are obviated. Acetaminophen is one of the most commonly used analgesic drugs in humans, and is readily available as an inexpensive generic over-the-counter preparation. Acetaminophen has a number of mechanisms of action that differ from NSAIDs, including actions on the serotonergic, opioid, endocannabinoid and lipoxygenase pathways. These alternate pathways may provide greater efficacy against chronic or neuropathic pain in equine patients. Acetaminophen was preferred by physicians over COX-2 and nonselective NSAIDs, even when those drugs were coupled with proton-pump inhibitors to reduce gastrointestinal side effects; due to cost considerations and the occurrence of adverse side effects from those drugs. In horses, acetaminophen has been reported to be efficacious as an adjunct treatment for laminitis in one pony, and was an effective analgesic agent when combined with NSAIDs in a model of inducible foot pain. However, no studies have been performed to validate a dose-response curve in horses. A study recently completed by our group demonstrated rapid absorption following oral administration of acetaminophen. Reported human therapeutic plasma concentrations were achieved within 30 minutes of administration, with no clinical or clinicopathologic evidence of adverse side effects after two weeks of repeated dosing. Dose simulation trials indicate that a change in dosage schedule may be required in order to provide adequate plasma concentrations.Master of Science
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Sands, Shannon, and Joel Nielsen. "Consumer Knowledge of Acetaminophen Safety, Dosing, and Identification." The University of Arizona, 2012. http://hdl.handle.net/10150/623666.
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Class of 2012 AbstractSpecific Aims: The objective of this study is to evaluate consumers’ knowledge about over the counter (OTC) products containing acetaminophen (APAP). Methods: Doctor of pharmacy student researchers set up a booth at consenting community pharmacies and invited consumers to participate in a 10-15 minute knowledge assessment. The booth contained a table displaying several OTC medication bottles/packages. Adult participants: a) answered baseline questions verbally about their APAP knowledge and associated risks; b) identified OTC products at the booth that contain APAP; and c) calculated and demonstrated dosing of APAP. The researchers asked follow-up questions and assessed the accuracy of the dosing. Participants received APAP educational brochures upon completion. Main Results: Eighty percent of subjects reported not knowing what the abbreviation “APAP” means, and almost half of those who said that they knew what it means were incorrect. Very few participants were able to correctly identify the products containing APAP even with the product packaging information, with the percentage of incorrect responses as to whether a product contains APAP or not varying from 4.9% to 31.6%. More than 40% of the pediatric doses were incorrectly dosed for both of the pediatric formulations, even with the majority of subjects being parents. Conclusions: Consumers are not able to identify which over-the-counter products contain APAP even with the product packaging before them, and they do not know what the abbreviation “APAP” means. Better packaging and product ingredient information should be developed, and the abbreviation “APAP” should be avoided. Pediatric APAP products should be re-evaluated regarding safety and dosing.
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Sands, Shannon, Joel Nielsen, and Terri Warholak. "Consumer Knowledge of Acetaminophen Safety, Dosing, and Identification." The University of Arizona, 2012. http://hdl.handle.net/10150/614521.
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Class of 2012 AbstractSpecific Aims: The objective of this study is to evaluate consumers’ knowledge about over the counter (OTC) products containing acetaminophen (APAP). Methods: Doctor of pharmacy student researchers set up a booth at consenting community pharmacies and invited consumers to participate in a 10-15 minute knowledge assessment. The booth contained a table displaying several OTC medication bottles/packages. Adult participants: a) answered baseline questions verbally about their APAP knowledge and associated risks; b) identified OTC products at the booth that contain APAP; and c) calculated and demonstrated dosing of APAP. The researchers asked follow-up questions and assessed the accuracy of the dosing. Participants received APAP educational brochures upon completion. Main Results: Eighty percent of subjects reported not knowing what the abbreviation “APAP” means, and almost half of those who said that they knew what it means were incorrect. Very few participants were able to correctly identify the products containing APAP even with the product packaging information, with the percentage of incorrect responses as to whether a product contains APAP or not varying from 4.9% to 31.6%. More than 40% of the pediatric doses were incorrectly dosed for both of the pediatric formulations, even with the majority of subjects being parents. Conclusions: Consumers are not able to identify which over-the-counter products contain APAP even with the product packaging before them, and they do not know what the abbreviation “APAP” means. Better packaging and product ingredient information should be developed, and the abbreviation “APAP” should be avoided. Pediatric APAP products should be re-evaluated regarding safety and dosing.
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Eakins, R. M. "The hepatic adaptive response to repeat acetaminophen exposure." Thesis, University of Liverpool, 2016. http://livrepository.liverpool.ac.uk/3001381/.
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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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潘玉琼 and Yuk-king Karen Poon. "The antagonistic effect of paracetamol on ethanol-induced gastric damage in rats." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1989. http://hub.hku.hk/bib/B31209415.
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Dowdy, Janet A. "Effects of acetaminophen on estrogen-responsive alkaline phosphatase in Ishikawa endometrial cancer cells." Morgantown, W. Va. : [West Virginia University Libraries], 2000. http://etd.wvu.edu/templates/showETD.cfm?recnum=1565.
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Thesis (M.S.)--West Virginia University, 2000.Title from document title page. Document formatted into pages; contains vii, 79 p. : ill. (some col.). Includes abstract. Includes bibliographical references (p. 68-79).
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Miao, Lei. "Synthesis of Amphibian Alkaloids and Development of Acetaminophen Analogues." ScholarWorks@UNO, 2009. http://scholarworks.uno.edu/td/985.
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The focus of these studies has been toward the development of new synthetic methods and procedures for the synthesis of novel compounds with unique biological properties. This research has led to the development of two new synthetic strategies for the construction of two novel amphibian alkaloids. In addition, the efforts have led to the large-scale process for the preparation of a novel analgesic compound. The regioselective ring opening of lactones (δ-valerolactone and γ-butyrolactone) with aryllithium reagents is reported for the construction of a series of δ-hydroxyarylketones and γ-hydroxyarylketones. Both the R and S enantiomers of the amphibian alkaloid noranabasamine were prepared in >30% overall yield with 80% ee and 86% ee, respectively. An enantioselective iridium-catalyzed N-heterocyclization reaction with either (R)- or (S)-1-phenylethylamine and 1-(5-methoxypyridin-3-yl)-1, 5-pentanediol was employed to generate the 2-(pyridin-3-yl)-piperidine ring system in 69-72% yield. A cis-2, 5-disubstitued pyrrolidine building block derived from (-)-Cocaine•HCl was prepared. We utilized this compound as a chiral building block for the formal synthesis of (+)-gephyrotoxin. Using this pyrrolidine building block, Kishi's intermediate was obtained enantiospecifically in 15 steps and 9.4% overall yield. A large-scale process for the preparation of the analgesic compounds SCP-123 and its sodium salt, SCP-123ss•monohydrate has been developed. The process for the preparation of SCP-123 required three synthetic steps with no chromatography, while the process for the preparation of SCP-123ss required four synthetic steps and no chromatography. The overall yields for both SCP-123 and SCP-123ss were 47% and 46%, respectively, and both compounds were obtained in exceptionally high purity (>99%).
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Chowdhary, Vivek K. "Role of miR-122 in Acetaminophen Induced Liver Injury." The Ohio State University, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=osu1494133473685399.
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Relli-Dempsey, Vincent M. T. Relli-Dempsey. "A Thermometric Titration Study of Acetaminophen and Sodium Hypochlorite." Ohio Dominican University Honors Theses / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=oduhonors152621864170557.
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Kim, Seol-Hee. "Acetaminophen Associated Neurotoxicity and its Relevance to Neurodevelopmental Disorders." Scholar Commons, 2017. http://scholarcommons.usf.edu/etd/6717.
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Autism is a lifelong neurodevelopmental disorder. The etiology of autism still remains unclear due to the heterogeneous and complex nature of the disorder, however synergistic actions between genetic components and environmental factors have been suggested. Acetaminophen (APAP) is one of the most popular over-the-counter drugs that possess antipyretic and analgesic effects. It is considered a relatively safe and effective within therapeutic doses. Recently, early exposure to APAP has been suggested to be one of the underlying cause of autism. Children are often prescribed APAP to lessen fever or irritability after vaccination during the first year, and APAP may adversely affect the normal brain development. In order to better understand the association with APAP and autism, we used an inbred mouse strain BTBR T+tf/J (BTBR). BTBR exhibits behavioral deficits that mimic the core behavioral deficits of human autism. In the study, investigated 1) if BTBR mice showed differences in thiol biochemistry and EAAT3 levels in brain compared with C57BL/6J (C57) mice, 2) if early exposure to APAP induced behavioral changes worsening the autistic phenotypes of BTBR in adolescence, and 3) if APAP exposure in neonatal mice induced possible toxicity at various doses. As a result, we observed that BTBR mice have significantly lower plasma sulfate levels and EAAT expression levels in the frontal cortex compared to C57 mice. Surprisingly, neonatal therapeutic dose of APAP administration did not induce behavioral changes in both C57 and BTBR in adolescence. However, we showed that a supratheraputic dose of APAP significantly elevated levels of oxidative stress marker in the brain. Overall, the results suggested that BTBR mice would be a useful mouse model to investigate effects of various environmental factors that have been associated with autism. In addition, early exposure to APAP at supratherapeutic doses may negatively affect normal brain development.
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Anoopkumar-Dukie, Shailendra. "Serotonin-melatonin interactions in acetaminophen and N,N-dimethylformamide toxicity." Thesis, Rhodes University, 2000. http://hdl.handle.net/10962/d1003957.
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Acetaminophen and N,N-dimethylformamide (DMF) are compounds which are extremely toxic to the liver. Acetaminophen is a drug which is well known for its analgesic and antipyretic properties. However, the abuse potential of this agent as a non-narcotic analgesic in alcoholics is well known. It is also the leading cause of overdose in England. DMF toxicity results mainly from occupational exposure. At present there are no known reports of an antidote for DMF poisoning, while N-acetylcysteine, the antidote for acetaminophen poisoning, is known to produce adverse effects. The present study evaluates the potential of melatonin as an antidote for acetaminophen and DMF poisoning. This study also investigates the mechanism underlying acetaminophen addiction and abuse. Initial studies involved in vitro techniques in an attempt to remove the complexities of organ interactions. The photodegradation studies, using ultraviolet (UV) light, revealed that melatonin accelerates the rate of acetaminophen degradation in the presence of air, and reduces the rate of degradation in the presence of nitrogen. This study also revealed that melatonin is rapidly degraded in the presence of air, following UV irradiation. The effect of DMF on hydroxyl radical generation was also determined. DMF was shown to act as a free radical scavenger, rather that a generator of free radicals. The in vitro studies were followed by lipid peroxidation determination. DMF (0.4ml/kg and 0.8ml/kg) did not produce any significant increases in lipid peroxidation in the liver. Three different doses of acetaminophen (30mg/kg, 100mg/kg, and 500mg/kg) were administered to rats for seven days. Acetaminophen (500mg/kg) was shown to significantly increase (p<0.05) lipid peroxidation in the liver. Melatonin (2.5mg/kg) was not able to significantly reduce the damage. The lower doses of acetaminophen (30mg/kg and 100mg/kg) did not increase lipid peroxidation. Electron microscopy studies showed that DMF adversely affects the liver, and in particular, the endoplasmic reticulum. Co administration of melatonin (2.5mg/kg) was able to reduce the damage. Further experiments need to be performed before an accurate assessment can be made on the ability of melatonin as an antidote for DMF and acetaminophen poisoning. Several experiments were done in an attempt to uncover the biochemical mechanism underlying acetaminophen addiction and abuse. The first experiment targeted the liver enzyme tryptophan-2,3-dioxygenase (TDO). This enzyme is the major determinant of tryptophan levels in vivo. Acetaminophen administration (100mg/kg for three hours) was shown to significantly inhibit (p<0.05) the activity of TDO, indicating increased peripheral levels of tryptophan. This experiment was followed up with determination of brain serotonin and pineal melatonin. Brain serotonin was determined using the ELISA technique. Melatonin was estimated using this technique as well as with pineal organ culture. Acetaminophen administration (100mg/kg for three hours) significantly increased (p<0.05) brain serotonin levels. Using organ culture where exogenous (3H) tryptophan is metabolised to (3H) melatonin, acetaminophen (100mg/kg for three hours) was shown to significantly increase (p<0.05) pineal melatonin concentrations. However, the ELISA technique did not reveal any changes in endogenous pineal melatonin levels. The final experiment was the determination of urinary 5-hydroxyindole acetic acid (5- HIAA), the major metabolite of serotonin, following acetaminophen administration (100mg/kg for three hours). Acetaminophen was shown to significantly reduce 5-HIAA levels (p<0.05) suggesting reduced catabolism of serotonin. The findings of this study indicate that acetaminophen mimics the actions of an antidepressant. This compelling finding has important clinical implications, and needs to be examined further.
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Zhao, Ping. "The influence of alcohol on acetaminophen hepatotoxicity : CYP2E1 induction and selective mitochondrial glutathione depletion /." Thesis, Connect to this title online; UW restricted, 2002. http://hdl.handle.net/1773/7952.
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Kühnel, Claudia [Verfasser]. "Analgesic effect of acetaminophen in neonates : systematic review / Claudia Kühnel." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2015. http://d-nb.info/1071088548/34.
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Chen, Weiqiao. "Mechanistic studies on the formation of oxidative metabolites of acetaminophen /." Thesis, Connect to this title online; UW restricted, 1998. http://hdl.handle.net/1773/8162.
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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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Drachuk, V. M. "The nephroprotective activity of glutathione in acetaminophen-induced acute renal injury." Thesis, БДМУ, 2021. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/18899.
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Keaveney, Alexis A. "Acetaminophen, Affect, and Risk: An Analysis of Psychological and Neurochemical Mechanisms." The Ohio State University, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=osu1477054183340724.
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Maharaj, Himant. "An investigation into the neuroprotective properties of acetylsalicylic acid and acetaminophen." Thesis, Rhodes University, 2005. http://hdl.handle.net/10962/d1003247.
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The potent analgesic property of acetylsalicylic acid and acetaminophen makes these the most commonly used analgesics in the world. Easy accessibility and cost effectiveness of these agents are attractive to patients seeking pain relief. However, the abuse of nonnarcotic analgesics such as acetaminophen and acetylsalicylic acid by alcoholics and patients seeking to relieve dysphoric moods is well documented. These agents therefore impact on the brain neurotransmitter levels and therefore all processes involved in the synthesis and metabolism of neurotransmitters may be affected. The use of non-narcotic analgesics has been reported to reduce the incidence of neurodegenerative disorders such as Alzheimer’s disease (AD) and Parkinson’s disease (PD). The mode of action by which acetylsalicylic acid and acetaminophen elicit neuroprotection is however unclear as many mechanisms of action have been inconclusively postulated. The first part of this study aims to elucidate the various mechanisms by which acetylsalicylic acid and acetaminophen affect the enzymes responsible for the catabolism of tryptophan, which is a precursor for the mood elevating neurotransmitter serotonin, as well as to investigate whether these agents alter the interplay between serotonin and pineal indole metabolism. The second part of this study focuses on the neuroprotective properties of acetylsalicylic acid and acetaminophen utilizing the neurotoxic metabolite of the kynurenine pathway, quinolinic acid and the potent Parkinsonian neurotoxin, 1-methyl-4-phenylpyridinium (MPP+). The ability of acetylsalicylic acid and acetaminophen to alter TRP metabolism was determined by investigating the effects of these agents on the primary enzymes of the kynurenine pathway i.e. tryptophan 2, 3-dioxygenase and indoleamine 2,3-dioxygenase as well as to investigate whether these agents would have any effects on 3-hydroxyanthranilic acid oxygenase. 3-Hydroxyanthranilic acid oxygenase is the enzyme responsible for the synthesis of quinolinic acid. Acetylsalicylic acid and acetaminophen alter tryptophan metabolism by inhibiting tryptophan 2, 3-dioxygenase and indoleamine 2,3-dioxygenase thus increasing the availability of tryptophan for the production of serotonin. Acetylsalicylic acid and acetaminophen also inhibit 3-hydroxyanthranilic acid oxygenase thus implying that these agents could reduce quinolinic acid production. Acetaminophen administration in rats induces a rise in serotonin and norepinephrine in the forebrain. Acetylsalicylic acid curtails the acetaminophen-induced rise in brain norepinephrine levels as well as enhances serotonin metabolism, indicating that analgesic preparations containing both agents would be advantageous, as this would prevent acetaminophen-induced mood elevation. The results from the pineal indole metabolism study show that acetylsalicylic acid enhances pineal metabolism of serotonin whereas acetaminophen induces an increase in melatonin levels in the pineal gland. Neuronal damage due to oxidative stress has been implicated in several neurodegenerative disorders such as AD and PD. The second part of the study aims to elucidate and characterize the mechanism by which acetylsalicylic acid and acetaminophen afford neuroprotection. The hippocampus is an important region of the brain responsible for memory. Agents such as quinolinic acid that are known to induce stress in this area have detrimental effects and could lead to various types of dementia. The striatum is also a vulnerable region to oxidative stress and hence (MPP+), which is toxic for this particular region of the brain, was also used as a neurotoxin. The results show that ASA and acetaminophen alone and in combination, are potent superoxide anion scavengers. In addition, the results imply that these agents offer protection against oxidative stress and lipid peroxidation induced by several neurotoxins in rat brain particularly, the hippocampus and striatum. Histological studies, using Nissl staining and Acid fuchsin, show that acetylsalicylic acid and acetaminophen are able to protect hippocampal neurons against quinolinic acidinduced necrotic cell death. Immunohistochemical investigations show that QA induces apoptotic cell death in the hippocampus, which is inhibited by ASA and acetaminophen. In addition, ASA and acetaminophen inhibited MPP+ induced apoptotic cell death in the rat striatum. The study also sought to elucidate possible mechanisms by which ASA and acetaminophen exert neuroprotective effects in the presence of MPP+ as these agents are shown to prevent the MPP+-induced reduction in dopamine levels. The results show that acetylsalicylic acid and acetaminophen inhibit the action of this neurotoxin on the mitochondrial electron transport chain, a common source of free radicals in the cell. In addition, these agents were shown to block the neurotoxic effects of MPP+ on the enzymatic defence system of the brain i.e. superoxide dismutase, glutathione peroxidase and catalase. The reduction in glutathione levels induced by MPP+ is significantly inhibited by acetylsalicylic acid and acetaminophen. The results imply that these agents are capable of not only scavenging free radicals but also enhance the cell defence mechanism against toxicity in the presence of MPP+. These agents also block the MPP+-induced inhibition of dopamine uptake into the cell. This would therefore reduce auto-oxidation of dopamine thus implying another mechanism by which these agents exert a neuroprotective role in MPP+-induced neurotoxicity. The discovery of neuroprotective properties of acetylsalicylic acid and acetaminophen is important considering the high usage of these agents and the increased incidence in neurological disorders. The findings of this thesis point to the need for clinical studies to be conducted as the results show acetylsalicylic acid and acetaminophen to have a definite role to play as antioxidants. This study therefore provides novel information regarding the neuroprotective effects of these agents and favours the use of these agents in the treatment of neurodegenerative disorders, such as AD and PD, in which oxidative stress is implicated.
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Manyike, Peter Tsakani. "CYP2E1 : mechanism of induction by isoniazid and role in acetaminophen oxidation /." Thesis, Connect to this title online; UW restricted, 1999. http://hdl.handle.net/1773/7936.
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Schaer, Stephanie. "Acetaminophen as a marker of oroduodenal transit in healthy unweaned calves /." [S.l.] : [s.n.], 2003. http://www.stub.unibe.ch/html/haupt/datenbanken/diss/bestell.html.
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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.
Full textAbstract:
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.
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Bruschi, Sam A. "Investigations into mechanisms of paracetamol-induced toxicity using ìn vitro' systems /." Title page, abstract and table of contents only, 1987. http://web4.library.adelaide.edu.au/theses/09PH/09phb192.pdf.
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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.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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McCarthy, Tara. "Comparing Robotic-Assisted and Laparoscopic Hysterectomy Conducted with and without Intravenous Acetaminophen." Kent State University Honors College / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=ksuhonors1399632027.
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Gadd, Samantha. "Acetaminophen-induced proliferation of estrogen-responsive breast cancer cells is associated with increased c-mcy RNA expression and NF-kB activity." Morgantown, W. Va. : [West Virginia University Libraries], 2001. http://etd.wvu.edu/templates/showETD.cfm?recnum=2016.
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Thesis (Ph. D.)--West Virginia University, 2001.Title from document title page. Document formatted into pages; contains xi, 147 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references (p. 128-143).
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Wade, James Patrick. "Biotic and Abiotic Remediation of Acetaminophen with Woodchip and Biochar-amended Woodchip Adsorbents." Thesis, Virginia Tech, 2015. http://hdl.handle.net/10919/64157.
Full textAbstract:
Pharmaceuticals and personal care products found in the environment pose a significant hazard to human and ecosystem health. While there has been significant work on the fate and remediation of pharmaceuticals and personal care products in wastewater treatment, relatively little work has explored the fate, transport and remediation of these compounds in non-point source input. This is concerning given the increasing use of pharmaceuticals in livestock production and wastewater treatment derived biosolids frequently applied to land. These experiments aimed to quantify the abiotic adsorption and biotic transformation and uptake potential of woodchips and biochar-amended woodchips as a potential sorbent strategy for diffuse acetaminophen (ACT) pollution.
Batch reactions were created in triplicate, supplied with 5 mM ACT, and analyzed over an eight hr period using ultraviolet spectrophotometry (298 nm). Ultraviolet absorbance readings for each time step then were compared to standard curves and solution ACT concentration was determined. Decreases in ACT from initial concentrations were the result of either abiotic and/or biotic. Overall, the woodchips and biochar-amended woodchips showed similar removal efficiency (16-21% of initial concentration). Whole model ANOVA analysis showed biologic activity having no significant effect on ACT solution concentration. However, within group ANOVA comparison showed significant differences between abiotic and biotic WC and abiotic and biotic WC treatments (controlling for media). Thus, the media effect could have masked the effect of biology on ACT removal. Species capable of degrading ACT exist and further study into their ability to grow and survive on these sorbents requires further work.Master of Science
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Knight, Tamara, and Hartmut Jaeschke. "Peroxynitrite formation and sinusoidal endothelial cell injury during acetaminophen-induced hepatotoxicity in mice." BioMed Central, 2004. http://hdl.handle.net/10150/610125.
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INTRODUCTION:Vascular injury and accumulation of red blood cells in the space of Disse (hemorrhage) is a characteristic feature of acetaminophen hepatotoxicity. However, the mechanism of nonparenchymal cell injury is unclear. Therefore, the objective was to investigate if either Kupffer cells or intracellular events in endothelial cells are responsible for the cell damage.RESULTS:Acetaminophen treatment (300 mg/kg) caused vascular nitrotyrosine staining within 1 h. Vascular injury (hemorrhage) occurred between 2 and 4 h. This paralleled the time course of parenchymal cell injury as shown by the increase in plasma alanine aminotransferase activities. Inactivation of Kupffer cells by gadolinium chloride (10 mg/kg) had no significant effect on vascular nitrotyrosine staining, hemorrhage or parenchymal cell injury. In contrast, treatment with allopurinol (100 mg/kg), which prevented mitochondrial injury in hepatocytes, strongly attenuated vascular nitrotyrosine staining and injury.CONCLUSIONS:Our data do not support the hypothesis that acetaminophen-induced superoxide release leading to vascular peroxynitrite formation and endothelial cell injury is caused by activated Kupffer cells. In contrast, the protective effect of allopurinol treatment suggests that, similar to the mechanism in parenchymal cells, mitochondrial oxidant stress and peroxynitrite formation in sinusoidal endothelial cells may be critical for vascular injury after acetaminophen overdose.
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Wells, Larry Kevin. "Efficacy of Ibuprofen and Ibuprofen/Acetaminophen on Postoperative Pain in Symptomatic Necrotic Teeth." The Ohio State University, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=osu1283354429.
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Balzer, Stephen. "IBUPROFEN/ACETAMINOPHEN VERSUS SPRIX IN TEETH DIAGNOSED WITH PULPAL NECROSIS AND SYMPTOMATIC APICAL PERIODONTITIS." The Ohio State University, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=osu153191176802337.
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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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Paterson, Andrea Beth. "Mechanisms of acetaminophen-induced hepatotoxicity, effects of mitochondrial glutathione, protein thiols and oxidative phosphorylation." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/mq22375.pdf.
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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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Wu, Meng-Jie, and 吳孟潔. "Electo-oxidation of Acetaminophen." Thesis, 2011. http://ndltd.ncl.edu.tw/handle/25760232195482962113.
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碩士國立屏東科技大學
環境工程與科學系所
99
This study investigated degradation of acetaminophen (ACP) in water using electrochemical oxidation. The experimental results showed that the degradation rate of ACP on tested anodes was in order Pt > platinized > DSA. Increasing electrode area or temperature increased ACP degradation . The electrochemical degradation of ACP was better using an 1 M sodium sulfate solution as the electrolyte than using 1 M H2SO4. Cyclic voltammetry (CV) analysis showed that the higher the pH, the lower the potential required for ACP oxidation; moreover, in phosphate buffer solutions, the ACP electro-oxidation efficiency was in order basic > neutral > acidic. In the divided cell, the ACP electro-oxidation efficiency was in order 1 M Na2SO4 (90 min electro-oxidation efficiency = 95%) > 0.5 M Na2SO4 + 0.5 M NaOH > 1 M NaOH > 1 M H2SO4 > 0.5 M H2SO4 + 0.5 M Na2SO4, whereas that in the undivided cell was 1 M NaOH (90 min electro-oxidation efficiency = 95%) > 0.5 M NaOH + 0.5 M Na2SO4 > 1 M Na2SO4 > 1 M H2SO4 > 0.5 M H2SO4 + 0.5 M Na2SO4. The influence of ACP initial concentration on its electro-oxidation relied on anolyte, current, anode, and operating time. In 1 M Na2SO4, the ACP electro-oxidation was better in the divided cell than in the undivided cell, but a reverse tendency was observed in 1 M H2SO4. Partial electro-oxidized ACP was mineralized/converted to CO2. The addition of sulfate in sulfuric acid enhanced the ACP electro-oxidation efficiency.
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Pan, Yi-Chuan, and 潘一全. "Oxidative Degradation of Acetaminophen." Thesis, 2012. http://ndltd.ncl.edu.tw/handle/34585471035980533713.
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碩士國立屏東科技大學
環境工程與科學系所
100
The Contents of Abstract in This Thesis: In this study, electro-regeneration of Ce(IV) from Ce(III) in prepared and spent Cr-ehtching solutions used in TFT-LCD manufacturing processes was performed. The regenerated Ce(IV) was used in a Ce(IV)-mediated electrochemical oxidation (MEO) process which was then compared with direct electro-oxidation for the degradation of acetaminophen. The results showed that the magnitude of acetaminophen degradation rate on tested anodes was in order PbO2/Sn2O3SnO2/Ti > Pt > BDD, while that in the electrolytic cell using different separators was in order Nafion212 > AMX > CMX. The magnitude of Ce(IV) yield (from Ce(III) electro-oxidation) in prepared solutions follow the order of PbO2/ Sn2O3-SnO2/Ti(b) ≒PbO2/ Sn2O3-SnO2/Ti(a) > Pt > PbO2/Ti > diamond > BDD. At 25oC, the Ce(IV) reached 100% for the electrolysis of 0.2 M Ce(III) in 4 M HNO3 for 4-hr using the PbO2/Sn2O3-SnO2/Ti anode (1cm2, at 0.88 A) in a divided cell equipped with an AMI-7100 separator, In 4×10-4 M H2SO4 and 10-3 M HNO3, the optimal dosages of Ce(IV) were the same (1500 ppm) for the degradation of acetaminophen. In 4 M HNO3, the addition of 1500 ppm Ce(IV), Ce(IV) electro-regenerated in prepared solution, or Ce(IV) electro-regenerated in spent Cr-ehtching solution achieved complete oxidation/degradation of acetaminophen at 60 min; moreover, the oxidation/degradation efficiencies of p-benzoquinone (one of intermediates from the acetaminophen oxidative degradation) were 95%, 99%, and 95%, respectively, in 240 min reaction. Keywords: Acetaminophen,Ce(IV)-MEO, Cr-etching solution, Ce(IV) electro-regeneration, Ce(IV) yield, degradation
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Hossain, Mohammad. "Evaluation of gastrointestinal transit time and novel oral acetaminophen product formulation." Thesis, 1991. http://hdl.handle.net/1957/37368.
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Gastrointestinal (GI) transit data were collected using pigs
as animal models. Density and size effects of non-disintegrating
dosage forms on GI transit were investigated. Total GI transit
times range from 2 to 33 days for 22 administrations of these nondisintegrating
dosage forms. Pigs are found to not be an
appropriate animal model for studying bioavailability or GI transit
of non-disintegrating, non-erodible oral release dosage forms.
Development of controlled release dosage forms where the
mechanism of drug release is diffusion through polymeric membrane
formed via film coating utilizing fluid-bed technology requires
optimization of several processing and formulation variables. The
influence of a processing variable (nozzle orifice opening) and a
few formulation variables (individual vs. combination plasticizer,
or a water-insoluble additive) on dissolution of a model drug
(acetaminophen) spray coated with Aquacoat® were studied.
Pharmacodynamic and pharmacokinetic information for a model
drug (acetaminophen) and computer simulation were used to develop a
dosage form with a 12 hour sustained release for oral administration
to children and adults for maximum analgesic and
antipyretic effect. Simulated plasma acetaminophen concentration-time
curves were similar to observed bioavailability study
profiles. In vitro and preliminary in vivo results from an adult
human volunteer indicate that sustained therapeutic saliva
acetaminophen concentration is possible using the newly developed
acetaminophen molded tablet dosage form.
The bioavailability of the new, oral controlled release
acetaminophen molded tablet relative to a commercially available
product (Extra-Strength Tylenol® caplet) was evaluated in 8
healthy, adult volunteers. Multiple doses of these two products
were administered in a two-way cross-over design. Bioavailability
of the new sustained release molded tablet is comparable to that of
the immediate release product. Polymer coated acetaminophen beads
were effective in maintaining saliva acetaminophen concentrations
of 5 μ/ml over a 12 hour dosing interval.Graduation date: 1991
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HUANG, DONG-YU, and 黃東裕. "Studies on the nitrosation reaction of acetaminophen." Thesis, 1988. http://ndltd.ncl.edu.tw/handle/70417958503494794207.
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Youssefi, Mohammed. "The Effect of acetaminophen on isoniazid metabolism." Thesis, 1992. http://hdl.handle.net/2429/2350.
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Acetaminophen (APAP, paracetamol, N-acetyl-p-aminophenol), an analgesic and antipyretic drug, causes liver necrosis in overdose. Isoniazid (INH, isonicotinyl hydrazide), an antituberculous drug, also causes liver damage in some patients at therapeutic doses. The two medications are likely to be taken concurrently. Previously we reported that, depending on the condition, INH inhibits or induces the toxic pathway of APAP metabolism. In this study the influence of APAP on INH metabolism was investigated in ten healthy volunteers. INH, 300 mg, was ingested daily for 7 days. APAP, 500 mg, was ingested on the day before starting INH (day 0) and on day 7 of INH ingestion. INH and its major metabolites in urine (days 6 and 7) were analyzed by reversed-phase high-performance liquid chromatography. Two metabolites, isonicotinic acid (INA) and isonicotinylglycine (ING), were analyzed directly by using an isocratic mobile phase system; propionylisoniazid was used as an internal standard. INH and its hydrazine metabolites, hydrazine (Hz) and acetylhydrazine (AcHz), were derivatized with m-anisaldehyde and subsequently analyzed by using a gradient mobile phase system; 9-fluorenone was a standard. A different procedure was used to analyze acetylisoniazid (AcINH) and diacetylhydrazine (DiAcHz). The INH, AcHz, and Hz present in the samples were converted to hydrazones by reaction with p-chlorobenzaldehyde. The hydrazones were then extracted with methylene chloride. The AcINH and DiAcHz remaining in the aqueous layer were then converted to INH and AcHz, respectively, by partial acid hydrolysis. The partial hydrolysis products were derivatized with m-anisaldehyde and then analyzed as above. The 2-tailed paired-sample t test suggested that concomitant APAP ingestion had no effect on the metabolism of INH, but this conclusion is far from certain. A number of explanations are given.
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Wang, Ching-Tsung, and 王慶宗. "A Study on Acetaminophen Taste Masked Preparation." Thesis, 2011. http://ndltd.ncl.edu.tw/handle/89246161831696405260.
Full textAbstract:
碩士高雄醫學大學
藥學研究所碩士在職專班
99
Acetaminophen is commonly used as antipyretic. However, its bitter taste hastened it used. In order to decrease the bitter taste of acetaminophen and increase the compliance of patient, spray drying process is used to find out the optimal bitter taste masking formulation and procedure. The formulation contained 90% of Acetaminophen, 6.85 to 8.65% of Starch, 0.15% of Stearic acid, and 1.2 to 3.0% of PVP K-30. Starch and PVP K-30 accounted for 9.85%. The percentage of starch decreased as the portion of PVP K-30 increased. Spray drying was used to optimize process for formulation and human tests were proceeded for the effectiveness of taste masking. Result revealed that under the conditions of 90% of Acetaminophen, 7.45% of Starch 1500, 0.15% of Stearic Acid, 2.4% of PVP K-30, 52% of slurry concentration, 230°C inlet temperature, 130°C outlet temperature, 16000 rpm atomization rate, 25 rpm (about 50 mL/min) feed rate, the bitter taste masking had the best effect. 220 to 230°C Inlet temperature was better than 180°C and 170°C. 16000 rpm or 19500 rpm atomization rate is more suitable. Feed rate had to adjust according to atomization rate. Spray drying can produce better bitter taste masking for acetaminophen and increase compliance of patient. Further, it can aid in the value and competitiveness of the medicines to create more product benefit.
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Chang, An-Tzu, and 張安慈. "Degradation of Acetaminophen by Different Fenton Processes." Thesis, 2011. http://ndltd.ncl.edu.tw/handle/91023766163948422044.
Full textAbstract:
碩士嘉南藥理科技大學
環境工程與科學系暨研究所
99
A new approach for increasing ferric reduction efficiency using different electro-Fenton and photoelectro-Fenton processes has been developed to degrade organic toxic contaminants. Over the past decade, human and veterinary Pharmaceuticals and Personal Care Products (PPCPs) have received increasing attention as POPs in waters. These emerging pollutants are continuously introduced into the aquatic environment at ng-μg L-1 levels by several routes including emission from production sites, direct disposal of overplus drugs in households and hospitals, excretion from drug-using human and animals, and water treatments in fish farms. There are some available data indicating that some drugs can alter the endocrine system of fish as well as exert toxic effects on algae and invertebrates, even benefit the proliferation of multiresistant strains of microorganisms. The common conventional sewage treatment plants provide low efficient destruction to PPCPs because they are usually resistant to biodegradation, which means the adoption of oxidation technologies is needed due to it can ensure PPCPs being removed from the environment. Chemical oxidants such as Cl2, ClO2, and O3 can react with drugs and their metabolites, but they are unable to promote the mineralization completely.The use of UVA light and electric current as electron donors can encourage the efficiency, which named the Fenton reaction. Acetaminophen (ACT) is the target compound in this study because it was used with extensive, considerable quantities. Effects of initial pH (pHi), Fe2+ loading, H2O2 concentration are determined by the photoelectro-Fenton process. Increase the ferrous ion concentration from 0.01 to 0.1mM leading to increase the hydroxyl radicals, and then raising the degradation efficiency of ACT. The optimal H2O2 concentration for ACT degradation in this study is 25mM. The final COD removal efficiencies are 34%, 38% and 40% using Fenton, electro-Fenton and photoelectro-Fenton processes, respectively. The final TOC removal efficiencies are 14%, 23% and 23% using Fenton, electro-Fenton and photoelectro-Fenton processes, respectively.