J. A. Hinson
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Also affiliated: University of Copenhagen (1990); National Institutes of Health (1975–1982); United States Food and Drug Administration (1984–1989); University of Arkansas Medical Center (2000); Rigshospitalet (1990); National Heart, Lung, and Blood Institute (1975–1976); University of Missouri (1993)
Research Areas
Biomedical Subjects
Biography and Research Information
OverviewAI-generated summary
J. A. Hinson's research has focused on the biochemical mechanisms underlying acetaminophen toxicity, particularly the role of reactive metabolites. Investigations have explored the reactions of N-acetyl-p-benzoquinonimine (NAPQI), the primary toxic metabolite of acetaminophen, with glutathione, a critical endogenous antioxidant. Studies have employed techniques such as stopped-flow kinetics to elucidate the reaction rates and pathways involved in the detoxification of NAPQI by glutathione.
Further research has examined the formation of protein adducts resulting from NAPQI's reaction with cellular proteins, contributing to liver injury. Immunohistochemical methods have been utilized to localize and quantify these adducts in models of acetaminophen-induced hepatotoxicity. The broader context of covalent and noncovalent interactions in cell toxicity has also been a subject of investigation. Additionally, work has delved into the oxidative metabolism of acetaminophen, including its conversion to NAPQI catalyzed by enzymes like horseradish peroxidase and cytochrome P-450, as well as prostaglandin H synthase.
Metrics
- h-index: 20
- Publications: 33
- Citations: 1,642
Selected Publications
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New insights into the mechanisms of acetaminophen toxicity (2010)
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Acetaminophen-Associated Hepatic Injury: Evaluation of Acetaminophen Protein Adducts in Children and Adolescents With Acetaminophen Overdose (2008)
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Western Blot Analysis for Nitrotyrosine Protein Adducts in Livers of Saline-Treated and Acetaminophen-Treated Mice (2000)
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Role of Covalent and Noncovalent Interactions in Cell Toxicity: Effects on Proteins (1992)
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Acetaminophen-induced alterations in pancreatic β cells and serum insulin concentrations in B6C3F1 mice (1990)
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Mechanism of paracetamol toxicity (1990)
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Pretreatment with mixed‐function oxidase inducers increases the sensitivity of the hepatocyte/DNA repair assay (1989)
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Utility of solution electrochemistry mass spectrometry for investigation the formation and detection of biologically important conjugates of acetaminophen (1989)
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The spontaneous and enzymatic reaction of N-acetyl-p-benzoquinonimine with glutathione: A stopped-flow kinetic study (1988)
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Direct analysis of rat bile for acetaminophen and two of its conjugated metabolites via thermospray liquid chromatography/mass spectrometry (1987)
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Fast atom bombardment mass spectrometry and fast atom bombardment mass spectrometry/mass spectrometry of three glutathione conjugates of acetaminophen (1987)
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Mechanisms of acetaminophen oxidation to N-acetyl-P-benzoquinone imine by horseradish peroxidase and cytochrome P-450. (1987)
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The 1- and 2-electron oxidation of acetaminophen catalyzed by prostaglandin H synthase. (1987)
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High resolution mass spectrometric and high-field nuclear magnetic resonance spectroscopic studies of the herbicide propanil, itsN-oxidative decomposition products and related compounds (1986)
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Identification of acetaminophen polymerization products catalyzed by horseradish peroxidase. (1985)
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