The ratio of ubiqiunon redox forms in the liver mitochondria under toxic hepatitis induced on the background of alimentary protein deficiency

• Voloshchuk Oksana N.
• Kopylchuk Galina P.

Abstract

The level of the total ubiqiunon and redox forms CoQ in the rat liver mitochondria under the conditions of alimentary protein deficiency and toxic hepatitis, induced on the background protein deficiency has been investigated. Research has been carried out on 36 white non-linear rats, divided into 4 groups: 1 – rats, maintained on the complete semisynthetic ration; 2 – rats, fed low-protein ration; 3 – rats with acute acetaminophen-induced hepatitis, maintained on complete ration; 4 – rats with acetaminophen-induced hepatitis, maintained under the conditions of protein deficiency. The content of total and oxidized ubiqiunon was determined spectrophotometrically at λ=275 nm (molar extinction coefficient 12.25 Mm-1×sm-1). Reduced ubiqiunon content was determined by the difference between total and oxidized ubiqiunon content. The amount of tyrosine in the liver was measured in deproteinised by 6% sulfosalicylic acid extracts of liver tissue on an automated amino acid analyzer. The decrease of the total ubiqiunon content in liver mitochondria by 35% on the background of 2-fold decrease of oxidized ubiqiunon and preservation of reduced ubiqiunon amount has been estimated under the conditions of low-protein diet. Simultaneously the 5-fold decrease of liver content of tyrosine – the ubiqiunon precursor – has been observed. It has been shown, that under the conditions of acetaminophen-induced hepatitis the content of total ubiqiunon and its redox forms in the liver mitochondria of rats fed complete diet didn’t change significantly comparing to control. A decrease of total ubiqiunon by 60% on the background of acute (18-fold) decrease of reduced ubiqiunon in liver mitochondria of rats with hepatitis, fed low-protein diet, has been observed. Established changes of the content of redox ubiquinone forms (a key component of the oxidative phosphorylation system in the liver mitochondria) can be considered as one of the mechanisms of malfunction of energy biotransformation system under the conditions of toxic liver injury in animals with protein deficiency.

Keywords:protein deficiency, toxic hepatitis, ubiqiunon, rats

All articles in our journal are distributed under the Creative Commons Attribution 4.0 International License (CC BY 4.0 license)