Biochemical markers of the functional liver state in rats with toxic hepatitis under the conditions of germanium citrate administration
Journal Title: Біологія тварин - Year 2017, Vol 19, Issue 1
Abstract
Activity of rats’ liver marker enzymes under the conditions of acetaminophen-induced toxic liver injury and influence of germanium citrate was studied. Hepatitis was modeled in these rats by per os acetaminophen administration (1 g/kg in 2 % starch suspension for 2 days using a special catheter). Serum sorbitol dehydrogenase activity was determined by the kinetic method in the reaction of NADH-dependent reduction of D-fructose to D-sorbitol. Serum alanine aminotransferase (ALT) activity and aspartate aminotransferase (AST) was evaluated using a kit of reagents (Filicit-Diagnostica,Ukraine). It is shown that under the conditions of modeled toxic liver injury an increase of the enzymatic activity of sorbitol dehydrogenase, alanine transaminase and aspartate transaminase along with the elevation of De Ritis ratio was observed. Administration of germanium citrate to the intact animals have shown that studied compound is devoid of hepatotoxic properties since the activity of the enzymatic markers of liver state (sorbitol dehydrogenase, AST, ALT) and De Ritis ratio remains on the control level. Study of the hepatoprotector properties of the germanium citrate have shown that in animals with the previously modeled toxic liver injury and administration of germanium citrate a decrease by 2.5times of sorbitol dehydrogenase activity along with the restoration of transaminases activity and De Ritis ratio down to the control values was observed comparing to the animals which weren’t administered with studied compound. Established decrease of the enzymatic activities of marker liver enzymes opens the new perspectives for the study of biochemical mechanisms of the hepatoprotector properties of germanium citrate.
Authors and Affiliations
G. P. Kopylchuk, O. M. Voloshchuk, O. V. Balandyuk
Keywords
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- EP ID EP262623
- DOI 10.15407/animbiol19.01.059
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