Skip to main content

Login for students

Login for employees

Publication detail

Acetaminophen conjugate induces mitochondria-related oxidative impairment in HK-2 cells,
Authors: Vrbová Martina | Roušarová Erika | Čapek Jan | Roušar Tomáš
Year: 2015
Type of publication: ostatní - přednáška nebo poster
Page from-to: nestránkováno
Titles:
Language Name Abstract Keywords
eng Acetaminophen conjugate induces mitochondria-related oxidative impairment in HK-2 cells, Acetaminophen (APAP) belongs to the most used analgetic and antipyretic drugs. APAP overdose causes liver injury and that is why it is the most frequent cause of acute liver injuries in the Western countries. In some cases, it is also associated with renal impairment occurring with frequency 1-2% of patients with acetaminophen overdose [1,2]. Acetaminophen is detoxified by three major pathways, glucuronidation, sulfation and oxidation by cytochrome P450. At therapeutic doses, a small portion of APAP dose is oxidized by cytochrome P450 to a reactive electrophilic molecule (NAPQI). After overdose, APAP is metabolized predominantly through the oxidation pathway and production of the oxidation product is enhanced. NAPQI is considered to be the toxic metabolite causing cell impairment [3]. However, based on our preliminary results, we postulated, that another metabolite could also cause toxicity.