S-adenosylmethionin vykazuje protektivní účinek na thioacetamidem navozené poškození hepatocytů potkana v primární kultuře

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11150%2F07%3A00003620" target="_blank" >RIV/00216208:11150/07:00003620 - isvavai.cz</a>

Výsledek na webu

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DOI - Digital Object Identifier

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Jazyk výsledku

angličtina

Název v původním jazyce

S-adenosylmethionine exerts a protective effect against thioacetamide-induced injury in primary cultures of rat hepatocytes

Popis výsledku v původním jazyce

S-adenosylmethionine(SAMe) was demonstrated to protect hepatocytes from toxic injury experimental induced in animals and isolated hepatocytes.Thioacetamide(TAA) is a frequently used model hepatotoxin causing in vivo centrilobular necrosis.The aim of ourstudy was to determine the protective mechanisms of SAMe on TAA-induced hepatocyte injury using primary culture.The release of LDH from cells incubated with TAA for 24 h was lowered by contemporary treatment with SAMe for 24 h in a dose depdendent manner.The inhbibitory effect of SAMe on lipid peroxidation paralleled the effect on cytotoxicity.Decrease in mitochondrial membrane potential was prevented too.Attenuation of TAA-induced glutathione(GSH) depletion was determined at the following incubation periods of 48 and 72 h as a potential consequence of increase in GSH production during the continuation of SAMe treatment.

Název v anglickém jazyce

S-adenosylmethionine exerts a protective effect against thioacetamide-induced injury in primary cultures of rat hepatocytes

Popis výsledku anglicky

S-adenosylmethionine(SAMe) was demonstrated to protect hepatocytes from toxic injury experimental induced in animals and isolated hepatocytes.Thioacetamide(TAA) is a frequently used model hepatotoxin causing in vivo centrilobular necrosis.The aim of ourstudy was to determine the protective mechanisms of SAMe on TAA-induced hepatocyte injury using primary culture.The release of LDH from cells incubated with TAA for 24 h was lowered by contemporary treatment with SAMe for 24 h in a dose depdendent manner.The inhbibitory effect of SAMe on lipid peroxidation paralleled the effect on cytotoxicity.Decrease in mitochondrial membrane potential was prevented too.Attenuation of TAA-induced glutathione(GSH) depletion was determined at the following incubation periods of 48 and 72 h as a potential consequence of increase in GSH production during the continuation of SAMe treatment.

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

ED - Fyziologie

OECD FORD obor

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Projekt

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Návaznosti

Z - Vyzkumny zamer (s odkazem do CEZ)

Rok uplatnění

2007

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

ATLA-Alternatives to Laboratory Animals

ISSN

0261-1929

e-ISSN

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Svazek periodika

35

Číslo periodika v rámci svazku

3

Stát vydavatele periodika

GB - Spojené království Velké Británie a Severního Irska

Počet stran výsledku

9

Strana od-do

363-371

Kód UT WoS článku

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EID výsledku v databázi Scopus

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