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Dadun > Depósito Académico > CIMA (Centro de Investigación Médica Aplicada) > Área de Terapia génica y Hepatología > Hepatología experimental > DA - CIMA - Terapia génica y Hepatología - Hepatología experimental - Artículos de revista >

S-adenosyl-L-methionine protects the liver against the cholestatic, cytotoxic, and vasoactive effects of leukotriene D4: a study with isolated and perfused rat liver
Authors: Cincu, R.N. (Rafael N.)
Rodriguez-Ortigosa, C.M. (Carlos M.)
Vesperinas, I. (Idoia)
Quiroga, J. (Jorge)
Prieto, J. (Jesús)
Keywords: Cholestasis/prevention & control
Leukotriene D4/toxicity
Liver/drug effects
S-Adenosylmethionine/pharmacology
Issue Date: 1997
Publisher: Wiley-Blackwell
Publisher version: http://onlinelibrary.wiley.com/doi/10.1002/hep.510260212/abstract
ISSN: 1527-3350
Citation: Cincu RN, Rodriguez-Ortigosa CM, Vesperinas I, Quiroga J, Prieto J. S-adenosyl-L-methionine protects the liver against the cholestatic, cytotoxic, and vasoactive effects of leukotriene D4: a study with isolated and perfused rat liver. Hepatology 1997 Aug;26(2):330-335.
Abstract
Cysteinyl-leukotrienes can cause cholestasis and liver damage when administered at nanomolar concentrations. Using the isolated and perfused rat liver we analyzed whether S-adenosyl-L-methionine (SAMe) may protect this organ against the noxious effects of leukotriene-D4 (LTD4). We observed that a 2 nmol bolus of this compound decreased bile flow (-12.6% +/- 1.6%, P < .02), and bile salt excretion (-23.5% +/- 2.2%, P < .02; both compared with baseline values), caused the release of glutamic-oxaloacetic transaminase (GOT) and lactic dehydrogenase (LDH) to the hepatic effluent, and increased significantly the perfusion pressure as compared with a control group not receiving LTD4 (6.0 +/- 1.1 vs. 0.2 +/- 0.02 mm hg, respectively; P < .001). The cholestatic effect of LTD4 was attenuated by infusion of SAMe which, at rates of 67 and 100 microg/min, totally prevented the decrease in bile salt excretion. Likewise, in SAMe infused livers, the release to the effluent of GOT and LDH was lower than in the group receiving LTD4 only, and was even lower than in the control group. We also found that the increase in perfusion pressure induced by LTD4 was prevented by SAMe in a dose-dependent manner. Of interest, SAMe increased the biliary excretion of the eicosanoid in a dose-related fashion. We conclude that SAMe reverts the cholestatic, cytotoxic, and hemodynamic effects of LTD4 on the liver, and that these protective effects might be partly because of a stimulation of the biliary excretion of the leukotriene.
Permanent link: http://hdl.handle.net/10171/23284
Appears in Collections:DA - CUN - Hepatología - Artículos de revista
DA - CIMA - Terapia génica y Hepatología - Hepatología experimental - Artículos de revista

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