Publikace detail

Acetaminophen conjugate induces mitochondria-related oxidative impairment in HK-2 cells,

Autoři: Vrbová Martina | Roušarová Erika | Čapek Jan | Roušar Tomáš

Rok: 2015

Druh publikace: ostatní - přednáška nebo poster

Strana od-do: nestránkováno

Tituly:

Jazyk	Název	Abstrakt	Klíčová slova
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.

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