Abstract
Exposure to the toxin thioacetamide (TAA) causes acute hepatic encephalopathy (HE), changes in the functioning of systemic organs, and an imbalance in a number of energy metabolites. The deferred effects after acute HE development are poorly understood. The study considers the balance of the tricarboxylic acid (TCA) cycle metabolites in the blood plasma, liver, kidneys, and brain tissues of rats in the post-rehabilitation period. The samples of the control (n = 3) and TAA-induced groups of rats (n = 13) were collected six days after the administration of a single intraperitoneal TAA injection at doses of 200, 400, and 600 mg/kg. Despite the complete physiological recovery of rats by this date, a residual imbalance of metabolites in all the vital organs was noted. The results obtained showed a trend of stabilizing processes in the main organs of the animals and permit the use of these data both for prognostic purposes and the choice of potential therapeutic agents.
Subject
Inorganic Chemistry,Organic Chemistry,Physical and Theoretical Chemistry,Computer Science Applications,Spectroscopy,Molecular Biology,General Medicine,Catalysis
Reference35 articles.
1. Hepatic encephalopathy-Definition, nomenclature, diagnosis, and quantification: Final report of the Working Party at the 11th World Congresses of Gastroenterology, Vienna, 1998;Ferenci;Hepatology,2002
2. Hepatic encephalopathy: Diagnosis and management;Amodio;Liver Int.,2018
3. Energy metabolism in brain cells: Effects of elevated ammonia concentrations;Hertz;Metab. Brain Dis.,2007
4. Brain α-ketoglutarate dehydrogenase complex: Kinetic properties, regional distribution, and effects of inhibitors;Lai;J. Neurochem.,1986
5. Hepatic encephalopathy in patients with acute decompensation of cirrhosis and acute-on-chronic liver failure;Montagnese;J. Hepatol.,2015
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