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Estimation of ROS production in isolated mitochondria after treatment with an acetaminophen metabolite

Authors: Roušarová Erika | Vrbová Martina | Roušar Tomáš | Čapek Jan | Kučera Otto | Červinková Zuzana

Year: 2015

Type of publication: ostatní - přednáška nebo poster

Page from-to: nestránkováno

Titles:

Language	Name	Abstract	Keywords
eng	Estimation of ROS production in isolated mitochondria after treatment with an acetaminophen metabolite	Acetaminophen (APAP) is a frequently used analgetic and antipyretic drug. After overdose, it may cause a number of pathophysiological processes that can even lead to acute liver and/or kidney failure. The cause of toxicity can be recognized in its metabolic activation but the entire mechanism of acetaminophen toxicity is still unknown. APAP is metabolized in hepatocytes through various pathways. The most important pathway acting in overdose is oxidation of APAP by cytochrome P450 to a substance, which is detoxified by reaction with glutathione