G. P. Kopylchuk, O. M. Voloshchuk

Yuriy Fedkovych Chernivtsi National University
Institute of Biology, Chemistry and Natural Resources, Ukraine;
e-mail: kopilchuk@gmail.com

The rate of superoxide anion radical, hydroxyl radical and hydrogen peroxide generation, the level of oxidative modification of mitochondrial proteins in the liver of rats with toxic hepatitis was investigated on the background of alimentary protein deficiency. We did not find significant increases of the intensity of free radical processes in liver mitochondria of rats maintained on the protein-deficient ration. The most significant intensification of free radical processes in liver mitochondria is observed under the conditions of toxic hepatitis, induced on the background of alimentary protein deprivation. Under these conditions the aggravation of all studied forms of reactive oxygen species generation was observed in liver mitochondria. The generation rates were increased as follows: O₂ – by 1.7 times, Н₂О₂ – by 1.5 times, ^•ОН – practically double on the background of accumulation of oxidized mitochondria-derived proteins. The established changes in thiol groups’ redox status of respiratory chain proteins insoluble in 0.05 M sodium-phosphate buffer (pH 11.5), and changes of their carbonyl derivatives content may be considered as one of the regulatory factors of mitochondrial energy-generating function.

Keywords: acetaminophen, alimentary protein deficiency, induced liver injury, mitochondrial proteins, oxidative protein modification, reactive oxygen species