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Titre du document / Document title

Changes in hepatic nitrogen metabolism in isolated perfused liver during the development of thioacetamide-induced cirrhosis in rats

Auteur(s) / Author(s)

MASUMI S. (1 2) ; MORIYAMA M. (1) ; KANNAN Y. (1) ; OHTA M. (1) ; KOSHITANI O. (2) ; SAWAMOTO O. (2) ; SUGANO T. (1) ;

Affiliation(s) du ou des auteurs / Author(s) Affiliation(s)

(1) Department of Veterinary Physiology, College of Agriculture, Osaka Prefecture University, Gakuen-cho 1-1, Sakai, Osaka, JAPON
(2) Division of Drug Safety Evaluation, Naruto Research Institute, Otsuka Pharmaceutical Factory, Inc., Tateiwa 115, Muya-cho, Naruto, Tokushima, JAPON

Résumé / Abstract

Changes in hepatic nitrogen metabolism in isolated perfused liver were studied during the induction of experimental cirrhosis by thioacetamide in female Sprague-Dawley rats. Cirrhosis of the micronodular type developed during 12-week administration of thioacetamide. Despite an increase in food consumption for 4 weeks after the end of administration, the physiological changes characteristic of cirrhosis were maintained. The rate of urea excretion per unit liver weight was significantly decreased compared with pair-fed control rats both during and after thioacetamide treatment. During 4 weeks of thioacetamide treatment, the rate of urea production in perfused liver from a combination of 0.25 mM NH4Cl and I mM glutamine decreased slightly, without a decrease in the maximum rate of urea production from 10 mM NH4Cl. In cirrhotic rats, the rate of urea production in perfused liver from NH4Cl and/or glutamine decreased, with a decrease in the maximum rate of urea production. The Km of ureagenesis for NH3 was unchanged in cirrhotic livers. During 4 weeks of thioacetamide treatment, glutamate dehydrogenase activity decreased, but the thioacetamide-induced cirrhotic state had no effect on glutamate dehydrogenase or glutaminase activity. Glutamine synthetase activity was decreased in rats treated with thioacetamide for 4 or 12 weeks. These results are consistent with the hypothesis that the capacity for urea production from NH3 and amino acids is decreased in the development of cirrhosis.

Revue / Journal Title

Toxicology    ISSN  0300-483X   CODEN TXICDD 

Source / Source

1999, vol. 135, no1, pp. 21-31 (1 p.1/4)

Langue / Language

Anglais

Editeur / Publisher

Elsevier, Kidlington, ROYAUME-UNI  (1973) (Revue)

Mots-clés anglais / English Keywords

Toxicity

;

Metabolism

;

Cirrhosis

;

Rat

;

Animal

;

Liver

;

Nitrogen

;

Urea

;

Glutamate dehydrogenase

;

Glutamate-ammonia ligase

;

Glutaminase

;

Hyperammonemia

;

Rodentia

;

Mammalia

;

Vertebrata

;

Oxidoreductases

;

Enzyme

;

Carbon-nitrogen ligases

;

Ligases

;

Hydrolases

;

Digestive diseases

;

Hepatic disease

;

Mots-clés français / French Keywords

Thioacétique acide amide

;

Toxicité

;

Métabolisme

;

Cirrhose

;

Rat

;

Animal

;

Foie

;

Azote

;

Urée

;

Glutamate dehydrogenase

;

Glutamate-ammonia ligase

;

Glutaminase

;

Hyperammoniémie

;

Rodentia

;

Mammalia

;

Vertebrata

;

Oxidoreductases

;

Enzyme

;

Carbon-nitrogen ligases

;

Ligases

;

Hydrolases

;

Appareil digestif pathologie

;

Foie pathologie

;

Mots-clés espagnols / Spanish Keywords

Toxicidad

;

Metabolismo

;

Cirrosis

;

Rata

;

Animal

;

Hígado

;

Nitrógeno

;

Urea

;

Glutamate dehydrogenase

;

Glutamate-ammonia ligase

;

Glutaminase

;

Hiperamonemia

;

Rodentia

;

Mammalia

;

Vertebrata

;

Oxidoreductases

;

Enzima

;

Carbon-nitrogen ligases

;

Ligases

;

Hydrolases

;

Aparato digestivo patología

;

Hígado patología

;

Localisation / Location

INIST-CNRS, Cote INIST : 15984, 35400008599756.0030

Nº notice refdoc (ud4) : 1901550



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