Increased mitochondrial ROS formation by acetaminophen in human hepatic cells is associated with gene expression changes suggesting disruption of the mitochondrial electron transport chain. Issue 2 (16th April 2015)

• Record Type: Journal Article
• Authors: Jiang, Jian; Briedé, Jacob J.; Jennen, Danyel G.J.; Van Summeren, Anke; Saritas-Brauers, Karen; Schaart, Gert; Kleinjans, Jos C.S.; de Kok, Theo M.C.M.
• Is Part Of: Toxicology letters. Volume 234:Issue 2(2015)
• Page Start: 139
• Page End: 150
• Publication Date: 2015-04-16
• Subjects: Toxicology -- Periodicals; 363.179
• DOI: 10.1016/j.toxlet.2015.02.012
• Languages: English
• ISSNs: 0378-4274

Abstract

<abstract abstract-type="author-highlights" id="abs0005"> <title id="sect0005">Highlights</title> <sec> <p id="spar0095"> <list id="lis0005"> <list-item id="lsti0005"> <label></label> <p id="par0005">Toxic doses of acetaminophen (APAP) boost the formation of mitochondrial reactive oxygen species (ROS).</p> </list-item> <list-item id="lsti0010"> <label></label> <p id="par0010">Toxic doses of APAP disrupt the expression of many genes encoding the subunits of electron transport chain (ETC) complexes, and reduce the expression of SOD2, a mitochondria-specific antioxidant enzyme.</p> </list-item> <list-item id="lsti0015"> <label></label> <p id="par0015">Toxic doses of APAP reduce the ATP yield of human liver cells.</p> </list-item> </list> </p> </sec> </abstract>