M
Mitchell R. McGill
Researcher at University of Kansas
Publications - 84
Citations - 6732
Mitchell R. McGill is an academic researcher from University of Kansas. The author has contributed to research in topics: Liver injury & Acetaminophen. The author has an hindex of 35, co-authored 75 publications receiving 5677 citations. Previous affiliations of Mitchell R. McGill include University of Arkansas for Medical Sciences & University of Texas Southwestern Medical Center.
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Journal ArticleDOI
Oxidant stress, mitochondria, and cell death mechanisms in drug-induced liver injury: Lessons learned from acetaminophen hepatotoxicity
TL;DR: The formation of oxidants and the defense mechanisms available for cells are addressed and knowledge is applied to better understand mechanisms of drug hepatotoxicity, especially acetaminophen-induced liver injury.
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The mechanism underlying acetaminophen-induced hepatotoxicity in humans and mice involves mitochondrial damage and nuclear DNA fragmentation.
Mitchell R. McGill,Matthew R. Sharpe,C. David Williams,Mohammad Taha,Steven C. Curry,Hartmut Jaeschke +5 more
TL;DR: It is suggested that mitochondrial damage and nuclear DNA fragmentation are likely to be critical events in APAP hepatotoxicity in humans, resulting in necrotic cell death.
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Metabolism and disposition of acetaminophen: recent advances in relation to hepatotoxicity and diagnosis
TL;DR: Recent data providing novel insights into these processes, particularly in humans, are reviewed in the context of earlier work, and the effects of altered metabolism and reactive metabolite formation are discussed.
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Acetaminophen-induced liver injury in rats and mice: comparison of protein adducts, mitochondrial dysfunction, and oxidative stress in the mechanism of toxicity.
TL;DR: The hypothesis that mitochondrial dysfunction is critical for the development of necrosis after APAP treatment is supported, as rats were highly resistant to APAP toxicity and mitochondrial protein adducts were significantly lower in rats.
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Molecular forms of HMGB1 and keratin-18 as mechanistic biomarkers for mode of cell death and prognosis during clinical acetaminophen hepatotoxicity
Daniel J. Antoine,Rosalind E. Jenkins,James W. Dear,Dominic P. Williams,Mitchell R. McGill,Matthew R. Sharpe,Darren G. Craig,Kenneth J. Simpson,Hartmut Jaeschke,B. Kevin Park +9 more
TL;DR: K18 and HMGB1 represent blood-based tools to investigate the cell death balance clinical APAP hepatotoxicity and were identified and quantified by novel LC-MS/MS assays in APAP overdose patients and were associated with worse prognosis.