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Protective effect of S-adenosylmethionine on mitochondrial membrane injury induced by hepatotoxic substances in hepatocyte primary culture.
Autoři: Lotková Halka | Křiváková Pavla | Kučera Otto | Roušar Tomáš | Červinková Zuzana
Rok: 2008
Druh publikace: článek ve sborníku
Název zdroje: Progress in Biochemistry and Biophysics (Shengwu Huaxue yu Shengwu Wuli Jinzhan)
Název nakladatele: Science Press
Místo vydání: Beijing
Strana od-do: 289
Tituly:
Jazyk Název Abstrakt Klíčová slova
cze Protektivní efekt S-adenosylmethioninu na poškození mitochondriální membrány indukované hepatotoxiny in vitro Protektivní efekt S-adenosylmethioninu na poškození mitochondriální membrány indukované hepatotoxiny in vitro.
eng Protective effect of S-adenosylmethionine on mitochondrial membrane injury induced by hepatotoxic substances in hepatocyte primary culture. S-adenosylmethionine has been demonstrated to protect hepatocytes from toxic injury in patients, animals or isolated hepatocytes. The mechanisms by which SAMe protects hepatocytes may result from the pathways of SAMe metabolism. Mitochondria are a target for oxidative stress following hepatotoxic injury. Unfortunately, the data documenting the protective effect of SAMe against the decrease of mitochondrial membrane potential are not widely available. The aim of our study was to determine the protective effect of SAMe from decrease of mitochondrial membrane potential induced by hepatotoxin agents. Primary cultures of hepatocytes were incubated in medium with 70 mM thioacetamide (TAA), 40 mM galactosamine (GalN) and 2.5 mM acetaminophen (AAP), respectively in combination with SAMe in concentrations of 5, 25, 50 or 1000 mg/l for 24 hours. Then the membrane potential was measured using Rhodamine 123, MitoCapture or JC-1 accumulation in mitochondia. Moreover, glutathione content, and lipid peroxidation in hepatocytes and mitochondrial respiration were measured. While our results documented the protective effect of SAMe from hepatocyte toxic injury induced by TAA and GalN, the effect on AAP-induced mitochondrial membrane injury was not improved. Nevertheless, SAMe abolished the AAP?induced decrease of mitochondrial respiration. Hepatocytes in culture, S-adenosylmethionine, oxidative damage.

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