Publikace detail

Estimation of oxidative stress in acetaminophen treated rat hepatocytes in culture.

Autoři: Roušar Tomáš | Kučera Otto | Křiváková Pavla | Lotková Halka | Červinková Zuzana

Rok: 2009

Druh publikace: ostatní - článek ve sborníku

Název zdroje: Acta Medica (Hradec Králové)

Název nakladatele: Univerzita Karlova v Praze

Místo vydání: Praha

Strana od-do: 48-49

Tituly:

Jazyk	Název	Abstrakt	Klíčová slova
cze	Estimation of oxidative stress in acetaminophen treated rat hepatocytes in culture.	Our project was focused on the optimization of fluorimetric methods and consequently on their use in estimation of oxidative stress. We introduced the spectrofluorimetric glutathione assay which become. Another aim of our project was to investigate the role of oxidative stress in acetaminophen liver injury. Acetaminophen (APAP; paracetamol) is one of the mostly used antipyretics and analgesics. After overdose, the toxic effect will appear as the centrilobular liver necrosis that may lead to the acute liver failure. At 3 h of treatment, the GR activity was inhibited to 88%, 78% and 58% of control activity in 1, 5 and 20 mM APAP, respectively. This finding has not been published anywhere yet. Thus, we have been trying to find the cause of the GR inhibition. It seems that the inhibition may be caused by a metabolite of APAP metabolism as our preliminary results showed, that is why we will continue in the study of the APAP toxicity.
eng	Estimation of oxidative stress in acetaminophen treated rat hepatocytes in culture.	Our project was focused on the optimization of fluorimetric methods and consequently on their use in estimation of oxidative stress. We introduced the spectrofluorimetric glutathione assay which become. Another aim of our project was to investigate the role of oxidative stress in acetaminophen liver injury. Acetaminophen (APAP; paracetamol) is one of the mostly used antipyretics and analgesics. After overdose, the toxic effect will appear as the centrilobular liver necrosis that may lead to the acute liver failure. At 3 h of treatment, the GR activity was inhibited to 88%, 78% and 58% of control activity in 1, 5 and 20 mM APAP, respectively. This finding has not been published anywhere yet. Thus, we have been trying to find the cause of the GR inhibition. It seems that the inhibition may be caused by a metabolite of APAP metabolism as our preliminary results showed, that is why we will continue in the study of the APAP toxicity.	Glutathione; acetaminophen; oxidative stress.

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