M
Mary K. Bruno
Researcher at University of Connecticut
Publications - 14
Citations - 844
Mary K. Bruno is an academic researcher from University of Connecticut. The author has contributed to research in topics: Acetaminophen & Glutathione. The author has an hindex of 10, co-authored 14 publications receiving 799 citations. Previous affiliations of Mary K. Bruno include College of the Holy Cross.
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Journal ArticleDOI
Protection against Acetaminophen Toxicity in CYP1A2 and CYP2E1 Double-Null Mice ☆
Hani Zaher,Jeroen Buters,Jerrold M. Ward,Mary K. Bruno,Angela M. Lucas,Stephan T. Stern,Steven D. Cohen,Frank J. Gonzalez +7 more
TL;DR: The protection against APAP toxicity afforded by deletion of both CYP2E1 and CYP1A2 likely reflects greatly diminished production of the toxic electrophile, NAPQI.
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Reduced Hepatotoxicity of Acetaminophen in Mice Lacking Inducible Nitric Oxide Synthase: Potential Role of Tumor Necrosis Factor-α and Interleukin-10
Carol R. Gardner,Jeffrey D. Laskin,Donna M. Dambach,Michael Sacco,Stephen K. Durham,Mary K. Bruno,Steven D. Cohen,Marion K. Gordon,Donald R. Gerecke,Peihong Zhou,Debra L. Laskin +10 more
TL;DR: Data demonstrate that nitric oxide is important in hepatotoxicity induced by acetaminophen, and some of its effects may be mediated by altering production of pro- and antiinflammatory cytokines and proteins important in tissue repair.
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Exaggerated hepatotoxicity of acetaminophen in mice lacking tumor necrosis factor receptor-1. Potential role of inflammatory mediators
Carol R. Gardner,Jeffrey D. Laskin,Donna M. Dambach,Donna M. Dambach,Hawjyh Chiu,Stephen K. Durham,Peihong Zhou,Mary K. Bruno,Donald R. Gerecke,Marion K. Gordon,Debra L. Laskin +10 more
TL;DR: The role of tumor necrosis factor receptor 1 (TNFR1) in pro-and anti-inflammatory mediator production and liver injury induced by acetaminophen was analyzed in this article.
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Purification, antibody production, and partial amino acid sequence of the 58-kDa acetaminophen-binding liver proteins.
John B. Bartolone,Raymond B. Birge,Steven J. Bulera,Mary K. Bruno,Ervant V. Nishanian,Steven D. Cohen,Edward A. Khairallah +6 more
TL;DR: The amino acid sequence of two cyanogen bromide/tryptic peptide fragments revealed that the major immunochemically detectable acetaminophen target in the cytosol is homologous to a selenium-binding protein which has been recently sequenced.
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Contribution of acetaminophen-cysteine to acetaminophen nephrotoxicity in CD-1 mice: I. Enhancement of acetaminophen nephrotoxicity by acetaminophen-cysteine.
Stephan T. Stern,Mary K. Bruno,Gayle E. Hennig,Robert A. Horton,Jeanette C. Roberts,Steven D. Cohen,Steven D. Cohen +6 more
TL;DR: It is demonstrated that APAP-CYS treatment alone depleted renal but not hepatic glutathione (GSH) in a dose-responsive manner, suggesting that depletion of renal GSH may predispose the kidney to APAP nephrotoxicity by diminishing GSH-mediated detoxification mechanisms.