Publication detail

The in vitro effect of S-adenosyl-L-methionine on the function of rat hepatocytes damaged by D-galactosamine.

Year: 2005

Type of publication: článek ve sborníku

Name of source: Clinica Chimica Acta

Publisher name: Elsevier Science BV

Place: Amsterdam

Page from-to: 152

Titles:

Language	Name	Abstract	Keywords
cze	Vliv S-adenosylmethioninu na funkci hepatocytů potkanů poškozených D-galaktosaminem	Protože S-adenosylmethionin (SAMe) má možný hepatoprotektivní efekt, zjišťovali jsme schopnost SAMe zlepšit funkci hepatocytů potkanů poškozených D-galaktosaminem (GalN). Izolované hepatocyty potkanů byly umístěny v mediu a byla zjištěna jejich funkční kapacita a integrita (via měření sekrece albuminu, syntesa urey, LDH aktivity a aktivita mitochondriálních dehydrogenas). Z výsledků vyplynulo, že SAMe snižuje toxicitu indukovanou GalN na dávce dependentním způsobem.	S-adenosyl-L-methionin; hepatocyty; D-galactosamin.
eng	The in vitro effect of S-adenosyl-L-methionine on the function of rat hepatocytes damaged by D-galactosamine.	Being a key intermediate in transmethylation and transsulphuration reactions, S-adenosyl-L-methionine (SAMe) exerts a possible hepatoprotective effect. We evaluated the ability of SAMe to improve the functions of rat hepatocytes damaged by D-galactosamine (GalN). Hepatocytes were isolated from Wistar rats (220 ? 250 g) by collagenase perfusion and cultured in William´s E medium. After cell attachment GalN (40 mM) +/- SAMe (50 and 1000 mg/L) were added to media. Hepatocyte functional capacity and integrity were analysed by albumin secretion activity (ELISA kit, Bethyl Lab.), urea synthesis (kit, Sigma Aldrich) and lactate dehydrogenase (LDH) activity (kit, Sigma Aldrich) in cultivation media after 24 and 48 h incubation. Activities of mitochondrial dehydrogenases were determined by colorimetric assay based on the cleavage of the tetrazolium salt WST?1. GalN increased significantly LDH leakage from the cells during 24 h and 48 h incubation and decreased albumin secretion activity. SAMe significantly reduced LDH leakage and enhanced mitochondrial dehydrogenase activities in GalN-exposed cells in dose-dependent manner (both at 24 and 48 h), however, during 24 h it did not influence albumin and urea secretion. Increase of urea synthesis in SAMe treated hepatocytes appeared within 48 h. These findings indicate that SAMe attenuates GalN-induced toxicity to rat hepatocytes in dose-dependent manner. Whether this effect is caused more by regulation of membrane fluidity via methylation of membrane phospholipids or by maintenance of the glutathione homeostasis in hepatocytes will be the subject of further studies.	S-adenosyl-L-methionine; rat hepatocytes; D-galactosamine.

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