Abstract
Activity of the mitochondrial isoenzymes of endogenous aldehydes catabolism under the conditions of acetaminophen-induced hepatitis
Highlights
Today it is known that mitochondrion is the key metabolic center of the cell [1], because it carries out a number of important biological functions: provides the oxidative phosphorylation and β-oxidation of fatty acids, participates in the maintaining of the cell calcium homeostasis, biosynthesis of lipids, heme, iron-sulfur clusters and some amino acids, etc. [2, 3]
There is an aldehyde dehydrogenase pathway of endogenous aldehydes catabolism, which function is the oxidation of aldehydes to carboxylic acids, and aldehyde reductase pathway that catalyzes the reduction of endogenous aldehydes to alcohols [7, 8]
The aim of the current work was to determine the activity of aldehyde dehydrogenase (EC 1.2.1.3), aldehyde reductase (EC 1.1.1.21), the content of thiobarbituric acid (TBA) reactive substances and protein carbonyl derivatives in the rat liver mitochondrial fraction under the conditions of acetaminophen-induced hepatitis on the background of dietary protein deprivation
Summary
Today it is known that mitochondrion is the key metabolic center of the cell [1], because it carries out a number of important biological functions: provides the oxidative phosphorylation and β-oxidation of fatty acids, participates in the maintaining of the cell calcium homeostasis, biosynthesis of lipids, heme, iron-sulfur clusters and some amino acids, etc. [2, 3]. Mitochondria are considered as the main source of reactive oxygen species which can influence intracellular signaling, regulation of cell functions and non-specific immune response [4, 5]. Due to their high oxidation potential, the reactive oxygen species are capable of damaging cell structure and inducing a number of chain reactions leading to the uncoupling of integration functions in the organism [6]. The aim of the current work was to determine the activity of aldehyde dehydrogenase (EC 1.2.1.3), aldehyde reductase (EC 1.1.1.21), the content of TBA reactive substances and protein carbonyl derivatives in the rat liver mitochondrial frac-
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