ACTIVITY OF THE THIOREDOXIN SYSTEM IN THE LIVER OF RATS UNDER CONDITIONS OF PARTIAL HEPATECTOMY AFTER TOXIC INJURY
DOI:
https://doi.org/10.31861/biosystems2024.02.186Keywords:
thioredoxin, thioredoxin reductase, selenocysteine β-lyase, partial hepatectomy, acetaminophen, toxic injury, liverAbstract
The work is dedicated to evaluating the activity of thioredoxin, thioredoxin reductase, and selenocysteine β-lyase in the cytosolic fraction of rat liver under conditions of partial hepatectomy after toxic injury by acetaminophen. The experiments were carried out on white non-linear rats, which were divided into two groups by the method of randomization: control animals, which received partial hepatectomy according to the Mitchell and Willenbring method (C/PH), and rats, which had partial resection of 2/3 of the liver tissue following acute toxic injury by acetaminophen through prior two-day administration at a dose of 1250 mg/kg of animal body weight (TI/PH). The study was performed at 0 hours (control), 24 hours (initiation phase), 48 hours (proliferative phase), 72 hours (termination phase), and 168 hours (distant period) after partial hepatectomy. The performance of partial hepatectomy after acetaminophen-induced injury modeling (TI/PH) is accompanied by a statistically significant decrease in thioredoxin activity in liver cells at the initial stages of regeneration (24 h and 48 h) compared to control values (0 h). The established changes occur against the background of suppression of selenium-dependent thioredoxin reductase and selenocysteine β-lyase activities during the initiation period (24 h), active cell proliferation (48 h), and termination (72 h). Depletion of the functional reserves of the thiol-dependent thioredoxin redox system and the suppression of selenide production efficiency, due to the demonstrated impairment in the conversion of organic selenium forms involving selenocysteine β-lyase in animals with acetaminophen-induced injury following partial hepatectomy (TI/PH), can be considered one of the factors reducing the regenerative potential of the liver under conditions of toxic injury.
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