Ramsay R R, Rashed M S, Nelson S D
Department of Biochemistry and Biophysics, University of California, San Francisco.
Arch Biochem Biophys. 1989 Sep;273(2):449-57. doi: 10.1016/0003-9861(89)90504-3.
Acetaminophen, an analgesic and antipyretic, is toxic in overdose to liver and kidney. The effects on mitochondrial respiration of acetaminophen, its less toxic analog, 3-hydroxyacetanilide, and metabolites which arise from these compounds have been investigated. The parent compounds inhibited NADH-linked respiration reversibly, whereas the metabolites inhibit all mitochondrial respiration, apparently in the Complex III region of the respiratory chain. The quinone derivatives, 4-acetamido-o-benzoquinone and 2-acetamido-p-benzoquinone, are the best inhibitors, with the onset of inhibition dependent on active respiration, suggesting interaction of these compounds with oxidized components of the electron transport chain.
