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Drug-induced liver toxicity is a significant problem in getting new drugs on the market. A major factor for this is that mechanisms of drug-induced liver toxicities are poorly understood. A significant focus of our laboratory is investigating mechanisms of liver toxicity (necrosis) produced by the commonly used analgesic/antipyretic drug acetaminophen. Acetaminophen is sold under a variety of trade names including Tylenol®. Whereas the drug is safe at therapeutic doses, in overdose it can produce a liver toxicity leading to death. The toxicity is mediated by conversion of the drug to a metabolite that reacts with glutathione leading to its depletion and covalently binds to protein. We have shown that these events lead to oxidative/nitrosative stress causing mitochondrial dysfunction and subsequent necrosis. We are investigating mechanisms of how the reactive metabolite induces oxidative/nitrosative stress and how these events cause mitochondrial dysfunction and death of the cell.
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Paul Erhardt,Kenneth Bachmann,Donald Birkett, Michael Boberg,Nicholas Bodor,Gordon Gibson, David Hawkins, Gabrielle Hawksworth,Jack Hinson,Daniel Köehler,Brian Kress,Amarjit Luniwal,
IUPAC Standards Online (2022)
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Paul Erhardt,Kenneth Bachmann,Donald Birkett, Michael Boberg,Nicholas Bodor,Gordon Gibson, David Hawkins,Gabrielle Hawksworth,Jack Hinson,Daniel Köehler,Brian Kress,Amarjit Luniwal,
IUPAC Standards Online (2022)
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PURE AND APPLIED CHEMISTRYno. 3 (2021): 273-403
Toxicology Reports (2017): 134-142
Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Associationno. 4 (2016): 555-562.e3
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